1. No category

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B L 00
OCTOBER,
The Journal
VOL.
Hemolytic
Anemia
with
Blood
Cells
Due
to a New
Normal
Human
Serum
By
DAUSSET,
JEAN
JEAN
to
be
involved.
by
It is necessary
is acquired
through
enon)
and
form
which
is
vitro
respective
The
spontaneous
in the
studied
an
irrespective
between
the
the
blood
groups.
to
infection
was
In
is obtained.
in 1927
found
agglutinable
by
T,
of
so
was
associated
a thrombocytopenic
with
seven
old
had
anemia
only
was
who
attempts
clinical
have
medicine
T has
From
sur
les
the
been
Centre
Maladies
Submitted
the
autoantibodies.
been
on
spontaneous
the
that
red
all
human
phenomblood
which,
with
may
an
be
this
by
their
a grave
source
all
findings
these
cases
are
of
abscess,3
of the
In one
a generalized
case the poly-
hemolytic
anemia
peculiar
case
is that
serologic
ag-
There
In most
pelvic
another
there
was
normal.7’11
In one
ir-
that
anti-T
in human
beings.
the literature.6#{176}
acquired
This
cells
sera,
showed
septicemia,6
In
made
the
National
du
June
revealed
Sang
18, 1958;
basis
authors
have
through
de
de
to explain
same
Thomsen-Friedenreich.
Some
patients
with polyagglutinability
antigen
which
with
pyogenous
infection
infection,15
salpingitis.1#{176}
an
purpura.
cells
groups
of
an
comof a
acquired
polyagglutinability
temporary.
Many
in
child14
with
case
1930
observed
septicemia
urinary
aglutinahility
plicated
with
the
this
bacteria
pneumococcal
infection,9
meningitis,13
from
reacting
group
in
syphilis
was
present7;
in
of the cases
were
apparently
weeks’
certain
of the blood
polyagglutinability
evident:
in
capable
case,
congenital
cancer.17
Two
hemolvtic
red
ABO
phenom-
by
Friedenreich5
polyagglutinability
postahortional
uterine
skin,10
pneumococcal
the
polyagglutinability
patients.
become
contamination
determination
cases
of
in
of certain
of
panagglutinability
as the sample
later
Thomsen24
10
BERNARD
tendency
sera,
in certain
uncover
an antigen,
present
in all adult
sera.
of error
14 well
these
called
can
due
the
JEAN
NO.
of
(Hubener-Thomsen-Friedenreich
appears
a while
is
enzymes,
glutinin
distinguish
for
of
phenomenon
human
in vitro
often
occasionally
enon
is observed
as soon
Hubener1
in 1925 and
in
all
to
aging
which
AND
is meant
agglutinated
XIV,
Polyagglutinahility
Factor
Present
(Anti-Tn)
MOULLEC
Y POLYAGGLUTINABILITY
kept
of Hematology
1959
Acquired
Red
B
D
accepted
them
Sanguine,
l’Association
Claude
for
polyagglutinability
the
phenomenon
have
shown
that
the same behavior
aging
Transfusion
the
as
publication
red blood
as the red
in vitro.7’9’12’13’15
Paris,
Bernard,
and
the
Centre
H#{244}pital Saint-Louis,
Apr.
27,
observed
of
Hubenercells
from
cells whose
Reepmaker15
de
Recherches
Paris.
1959.
1079ThIS
One
\
W7H5- LEL-9XRX
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1080
DAUSSET,
isolated
from
capable
in
These
was
the
urine
vitro
of
cells
have
modified
by
of
making
then
the
in all
absorbed
by
by
red
way
the
cells
cases.
cases
in which
agglutinable
of Vibrio
those
Thus
Henningsen1’
were
not
Actinomyces.
It
is also
was
observed
the
with
those
to
interpret
difficult
T
concluded
that
identical
sera.
antigen
polyagglutinability
this conclusion
believed
erythrocytes
polyagglutinability
He
was
human
whose
comma.
BERNARD
which
all
by
as
phenomenon
and
identical.
However
possibly
by
cells
AND
streptococcus
characteristics
of a culture
patient’s
treated
a hemolytic
blood
same
filtrate
studied
his
patient
red
the
the Hubener-Thomsen-Friedenreich
very
closely
related
and
reached
his
MOULLEC
that
was
were
not
agglutinins
absorbed
in
in apparently
this
normal
subjects.
The
case
presented
below
Polyagglutinability
nomenon
observed
thrombocytopenia
polyagglutinability
differs
in
this
patient
for
nine
consecutive
essentially
from
apparently
years
and
and a chronic
hemolytic
and the severe
hemolytic
is also
discussed
capable
of
further
agglutinating
relation
with
known
so far.
the
anti-T
in this
paper.
the
patient’s
agglutinins
CASE
The
previously
substance
blood
can
by
The relationship
displayed
by
present
cells
be
cited
linked
ones.
a permanent
accompanied
anemia.
anemia
red
nor
the
represented
phe-
leukopenia,
the
between
patient
in normal
has
to
serum
neither
any
any
agglutinins
cor-
HISTORY
M. T., 65 years
old, who had
apparently
had no previous
disease,
suffered
in 1946
while
in Mexico
from
an acute
infection
of undetermined
etiology
which
lasted
about
10 days. This episode
was accompanied
by a severe
anemia
(about
1,400,000
red blood
cells per cubic
millimeter).
He was given
five transfusions,
one of which
caused
a very
marked
reaction.
Since
that time,
the anemia
has never
disappeared.
The skin has been
pale
and
yellow-tinged.
The
patient
always
felt tired
and
had
alternative
periods
of
improvement
and relapse.
In 1946, splenomegaly
had been discovered,
the lower
border
of the spleen
being
felt
at two or three
fingerhreadth
below
the left costal
margin.
At that
time,
blood
counts
revealed
a hematologic
picture
of pancytopenia:
RBC,
3,090,000
per cubic
millimeter,
hemoglobin
82 per cent, hematocrit
32 per cent,
M.C.V.
106 cubic
microns,
reticulocytes
1.3 per cent and 5 per cent. WBC,
2,900
per cubic
millimeter
with the following
differential: neutrophils
34 per cent,
eosinophils
1 per cent,
basophils
1 per cent,
lymphocytes
63 per cent, monocytes
1 per cent. Ameth’s
classification
showed
a shift to the left. The
platelets
were
130,000
per cubic
millimeter.
Differential
counts
of bone
marrow
showed
an increase
of erythroblastic
elements
(50
per
cent).
Osmotic
resistance
was
normal
(4.8 - 3.2).
No sickling
of red blood
cells was noted.
The
icterus
Index
was 9 on one
occasion
and 23.8 on another
occasion
(normal:
2 to 4). The qualitative
Van den Bergh’s
reaction
was strongly
positive.
Urobilinogen
was present
In the urine
to a dilution
of 1/15.
There
was no hemosiderin
in the urinary
sediment.
No occult
blood
was found
in the
urine
or in the stools.
The bleeding
time was 3 to 4 minutes.
The clotting
time was 13
minutes.
Prothrombin
time
was normal.
The thymol
turbidity
test gave
a result
of 8.1
units.
Bromsulfalein
retention
was 40 to 80 per cent.
Blood
urea was 0.19 per 1000 ml.
serum
proteins:
71 Gm. per 1000 ml. (albumin
46 Gm. per 1000 ml., globulin
25 Gm.
per 1000 ml.).
Alkaline
phosphatase:
10 units.
Biopsy
of the liver
did not show
any
lesion
compatible
with
a diagnosis
of cirrhosis.
Cholecystography
was
done
but
the
gallbladder
was
not
visualized.
To
summarize:
there
was
at that
time
a marked
pancytopenia
with signs of increased
destruction
of blood
cells and accelerated
regeneration,
confirming
the diagnosis
of hemolytic
anemia.
Because
of the palpable
spleen,
the
diagnosis
of splenic
neutropenia
was made.
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ACQUIRED
HEMOLYTIC
ANEMIA
AND
1081
ANTI-TN
Between
1946 and 1952, the red blood
counts
have ranged
from 2,100,000
to 3,350,000
per cubic
millimeter,
the mean
being
2,500,000.
The white
blood
counts
oscillated
between
3,900
and
1,300
per cubic
millimeter,
with
a mean
of 2,200.
Neutrophils
were
always
around
45 per cent,
lymphocytes
around
40 per cent.
Reticulocyte
count
was 10
per cent on one occasion,
but it was low usually.
The general
condition
of the patient
was
never
very satisfactory
during
that period
and the course
of the disease
was interspersed
with episodes
of fatigue
and increased
icterus.
However,
these
pathologic
manifestations
were so important
as to keep the patient
away
from his work.
One of us noted
in 1950 the polyagglutinability
of the patient’s
red blood
cells.
It
could
be ascertained,
however,
that the patient
was of group
B because
his serum
contamed
an anti-A
agglutinin.
On the same
occasion,
marked
ovalocytosis
was discovered
(20 per cent of the erythrocytes
were ovalocytes
of Gunther’s
group
IV).
On the first examination,
in 1951,
the following
results
were
found:
RBC,
2,715,000
per cubic
millimeter;
hematocrit,
30; mean
diameter
of red cells, 7 to 8 microns;
M.C.V.,
[08 cubic
microns;
reticulocyte
count,
8 per cent. The red cells had a tendency
to autoagglutinate.
There
was
marked
anisocytosis
with
ovalocytosis.
The
hemoglobin
was 60
per cent and the color index
1.1. M.C.H.
was 32 micromicrograms
and M.C.H.C.
29 per
cent.
The osmotic
fragility
test showed
initial
lysis at 5.4 and complete
lysis at 3.4 per
1000 ml. The
mechanical
resistance
of erythrocytes
was
slightly
decreased.
Acid-serum
test,
Crosby’s
test and
autohemolysis
study
gave
normal
results.
Donath-Landsteiner’s
test was negative.
The WBC was 2,800 per cubic
millimeter
with the following
differential:
neutrophils,
42 per cent,
eosinophils,
2 per cent,
lymphocytes,
46 per cent,
monocytes,
8 per cent,
acidophilic
normoblasts,
2 per cent.
The platelets
were
112,000
per cubic
millimeter.
Hemostasis
studies
showed
a bleeding
time at 4 minutes,
a clotting
time
at
8 minutes,
a normal
clot retraction,
a prothrombin
time at 75 per cent, a slightly
diminished
prothrombin
consumption
and also a slightly
diminished
heparin
tolerance.
Serologic
studies
showed
the persistence
of polyagglutinability.
There
was no panagglutinin in the serum
as seen in acquired
hemolytic
anemia.
However
a certain
degree
of
autoagglutination
was noted
under
the microscope.
The search
for hemolysins,2’
as well
as the Donath-Landsteiner’s
test, remained
negative.
In the serum
a cold thromboagglutinin was detected,
but no leukoagglutinin
was found
at that time.
During
the following
months
the general
condition
of the patient
remained
unchanged.
In 1952, as well as on a few occasions
afterwards,
attacks
of acute
gouty
arthritis
supervened.
Because
of the
persistence
of the anemia,
it was
decided
in 1953
to give the
patient
a
few
transfusions
of
washed
B,
Rh-negative
red
cells.
These
were
perfectly
tolerated
at a frequency
of one transfusion
of 200 ml. every
two weeks.
The RBC reached
3,200,000
per cubic
millimeter,
but the \VBC
remained
at 1,200
per cubic
millimeter
and platelet
count
at 120,000.
Some time later,
an acute
infection
provoked
a fall of the RBC to 1,500,000
per cubic
millimeter.
Six transfusions
of washed
cells were
then
necessary.
At that point
a leukoagglutinin
was found
in the serum.
In 1955,
the patient
was treated
with
cortisone
(from
200 to 350 mg. per day for
three
weeks)
and then with prednisone
(from
20 to 50 mg. per day).
Improvement
was
remarkable
and transfusions
could
be discontinued.
Following
that,
RBC
was between
2 and 3 million
per cubic
millimeter,
WBC
between
2,500
and
3,000
and platelet
count
around
200,000
per cubic
millimeter.
In 1956,
the patient
began
to complain
of a lasting
pain in the right
hypochondrlum.
No lesion
has been
found
to explain
it,
and the
general
condition
of the patient
has
remained
satisfactory
since then.
Briefly,
this is an acquired
hemolytic
anemia
with persistent
leukopenia.
The beginning
of the
disease
dates
back
to 12 years
ago and seems
to be related
to an acute
infection
of undetermined
etiology.
From the serologic
point of view, this case is remarkable
because
of the
persistence
of the polyagglutinability
phenomenon,
observed
since
1950.
Transfusions of washed
erythrocytes
have
been
given
with
success,
washed
cells
being
used
in
order
not to give the patient
the substance
which
is present
in normal
plasma
and has
the power
of agglutinating
his own red blood
cells. Corticoid
therapy
has been
effective
and has made
transfusions
unnecessary
for over two years.
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1082
DAUSSET,
SERoi.ocIC
MOULLEC
AND
BERNARD
STUDY
Erythrocytes
Polyagglutinability.-ExIsTENCE
blood
group,
agglutinated
by
only
The
A cells.
all
be
their
has
group:
AB
agglutinin
which
have
them.
The
been
with
came
of 40 sera
also
from
were
absorbed
BY
the
by
chimpanzee
did
cells
and
sheep
have
agglutinin
also
genotype
action
OTHER
his
degree
now
of
absorbing
did
not
Since
erythrocytes
developed
was
in the
BLOOD
from
after
the
the
of
or A
agglutinin.
observed
was
of anti-Tn
16
no
at
the
relation
newborn
cells, the
infants
in-
maximum
of whom
anti-B
ABO
agglutinin
found
on normal
on
human
comma,
are
1/16.
However,
The
anti-C;
anti-E,
secreted
sensitized
a goat,
been
human
red
capable
the
cells
of
serum
agof
conditions.
anti-D,
had
from
have
Because
of polyagglutinability,
system-could
be made
at all the
patient
Sera
rabbits
absorption
same
probably
as follows:
33
of 0
anti-B
SPECIES.
methods.
absorb
in rabbits
thus
that
com-
studied;
titers
absorption
GROUPS.
the
the
as
490
subjects
Their
different
after
absorption
but
agglutinins.
that
probable
secretor.
cells,
sera,
through
capable
antiLua
ANIMAL
several
blood
patient-apart
agglutinins,
concluded
any
THE
especially
were
anti-Fyt
and
OF
of the
indirectly,
same
showed
groups.
subjects
step.
DIFFERENT
and
red
abThis
agglutinated
been
of
groups
20 of other
FIIOM
adult
Until
(from
frequently
CORD
and
patient’s
not
from
have
the filtrate
of a culture
of Vibrio
patient’s
erythrocytes
to a dilution
of
DETERMINATION
grouping
SERA
A
erythrocytes.
found
that
the titer
had
of the donor.
BLOOD.
The
serum
from
as a preliminary
a chimpanzee
Horse
modified
glutinating
group
the
agglutiwhatever
have
been
AB serum.
strongly
the
absorption
most
FROM
of
sera
of B or AB
titer
sera
have
groups)
after
beforehand
a horse,
patient’s
weakly
or not at all the patient’s
red
have
been
performed
on 28 newborn
of B or AB
erythrocytes.
AB
tested
SERA
agglutinates
contain
The abnormal
adult
sera,
agglutinins.
incompatible
The
very
Studies
to agglutinate
B or
laboratory.
It was
Rh or Duffy
groups
BY
agglutinates
not
agglutinins
action
as
All
and
anti-B
128.
AGGLUTINABILITY
a sheep,
marked
and
the
ABO,
agglutinates
being
1/2.
were
quite
2 to
with
are
serum
do
the
SERA.
Sixteen
been
the
his serum
as
erythroeytes
subjects
of
eight
Tn
of
determining
erythrocytes
anti-Tn.
from
AGGLUTINABILITY
fants
titer
is
subjects
have
the
which
natural
the same
ADULT
against
Negroes.
Titration
temperature
whatever
called
anti-A
(from
from
groups)
ranging
be
tested
cells
agglutinates
whose
have
COMPATiBLE
natural
sera
them
strongly
subjects,
red cells,
agglutination
obtained
patible
serum
0
BY
group
AB
red
but
therefore
to the B group.
cells is present
in all human
will
AGGLUTINABILITY
on
patient’s
The
sera,
the
of
effect
On
PHENOMENON.
noted:
anti-A+B
be
no
belongs
his red
group
A or
corresponding
abnormal
and
cannot
but
THE
are
anti-B
patient
antigen.
The patient
nm which
acts on
Sera from
sorbed
by
reactions
anti-A,
A or A2 cells
may
OF
abnormal
patient’s
anti-e,
anti-Kell
anti-c,
antiC%v,
substance
the
with
B N CDe/CDe
Leb
only
red
blood
and
anti-P
B, it could
antigen.
patient’s
pp kk Fy
An
red
cells.
Leb+
be
anti-N
The
Lu”
From www.bloodjournal.org by guest on December 22, 2014. For personal use only.
HEMOLYTIC
ACQUIRED
ANEMIA
AND
1.-Iso-
TABLE
Tn
In
red
1083
ANTI-TN
and Autoagglutination
cells
saline
not
(degrees
18
37
of the
Tn Red
CelLs
trypsinized
In albumin
C.)
4
(degrees
C.)
18
37
With
Indirect
Coombs
test
4
I
A
I
A
I
A
I
A
I
A
I
A
I
Normal
adult
ABserum
0
1
0
16
1
16
0
4
0
16
0
32
0
0
Tnserum
0
0
0
0
0
1
1
0
0
0
1
1
Tn
In saline
A
Normal
adult
ABserum
0
Tn
1
serum
I
iso-red
A
Each
2
cells
= Tn
corresponds
CONSTANCY
the
128
OF
red
cells
titer
THE
with
of this
with
other
Anti-Tn
4
A
I
A
I
A
64
512
0
4
64
512
0
4
64
256
8
0
1
64
4
dilution
still
OVER
the
serum
case
of normal
at 4 than
at this
latter
ACTION
the
it in
I
A
0
0
anti
E
0
(table
serum
previously
absorbed
which
was
bovine
added
Differences
pnditions
1/4
ACTION
on
cells
was
negative
used
in several
erythrocytes,
Coombs
negative
on
with
both
dilutions:
all
the
extent
to
the
same
test
after
patient’s
a degree
at
red
situation
manifests
weakest
has
been
red
can
The
in
of
minimal.
be comconstant
comparison
The
agglutinating
itself
in saline
more
sera)
it is still present
cells
also
cells
to
Coombs
test
of the
methods,
the
tube
globulin
rabbit
sera
by the antiglobulin
Tn erythrocytes.
be
incubation
in
spontaneously
the
in pure
in the
which
after
not
in
and
titer
normal
proved
with
could
and
and
anti-human
as
studied
in saline
C. the
37
and
rabbit
blood
it
constant
and
antigens.
AMPUTUDE.
albumin,
tile
is further
incubation
which
been
nature.
patient’s
environment.
The direct
ANTIGLOBULIN.
Variations
have
unidentical
titer
or human
in a colloid
OF
group
agglutinability
1).
between
the titers
obtained
have
been
very
slight.
At
became
The
7 years.
last
subject
Tn erythrocytes
(except
for the
Agglutinin
COLLOIDS.
result.
PERIOD.
the
same
an
positive
LONG
to be quantitatively
view
with
blood
adult
sera on
at 37 C., but
a
during
of
keeps
temperature
OF
giving
A
constant
cases which
were
of temporary
agglutinin
of normal
sera.-THERMAL
power
strongly
to
With
indirect
Coombe
test
C.)
I
1
PHENOMENON
remained
involved
seems
that
point
of
phenomenon
test
A
red cells.
to the maximum
has
obtained
The
antigen
pared
from
positive
being
(degrees
18
37
I
8
1
In albumin
4
A
0
128
C.)
cells.
auto-red
number
of Tn
I
0
red cells trypsinized
(degrees
18
37
I
1
A
saline,
same
human
other
was
in
AB
serum
to
albumin.
experimental
1/1 in saline
patient’s
red
blood
antiglobulin
sera
do.
being
agglutinate
The
Tn
absence
neutralization
The
indirect
normal
of
serum
agglutinated
a
test
Coombs
diluted
remained
negative.
OF
ACTION
red
cells
treated
red
cells
not
ABSORPTION
the
patient’s
PROTEOLYTIC
ENZYMES.
by trypsin
submitted
AND
red
has
to
ELUTION.
blood
cells
Agglutination
occurred
the action
of
It is possible
and
elute
by normal
at only
slightly
the enzyme
to absorb
it
afterwards
serum
higher
titers
of patient’s
than
with
(table
1).
the anti-Tn
agglutinin
by
the
usual
methods.
on
From www.bloodjournal.org by guest on December 22, 2014. For personal use only.
1084
DAUSSET,
2.-Cross
TABLE
Absorption
MOULLEC
BERNARD
Anti-A
and
of Anti-Tn
AND
Normal
adult
B serum
(Agglutination-titer)
Nonabsorbed
with
and
A1
Tn
=
Absorbed
and tested
eluate
red
cells.
OF
pH.
OF
AGING
several
months
cells
16
1
Tn
red
IN
ago
by
are
pH
by
When
adult
Relations
between
the
glutinin
does
not
as was
shown
by
Anti-H
anti-Tn
seem
to
have
differential
Agglutinin.
anti-Tn
it
contained,
NONSPECIFIC
any
besides
correlation
glutinin.
It
anti-Tn
with
easy
agglutinin
absorbed
cold
agglutinin.
Anti-T
Agglutinin.
absorption
own
serum,
studies
both
the
of a culture
red cells
filtrate
filtrate)
To
were
having
of a culture
for one hour
no
hour
half
or
effect
on
at
the
sera.
even
Aging
anti-B
sera
are
prepared
agglutinated
if the latter
still has
of sera
thus
seems
other
agglutinius
(table
of
The
anti-A
its
to
human
anti-Tn
agagglutinin,
2).
is not
three
absorbed
by
the
H
sub-
agglutinin
and
by
substance
between
with
adult
absorbed
comma
group
of Vibrio
comma
at the temperature
either
or
the
from
been
that
of
the
other.
H, it probably
has
anti-Tn
normal
on
patient’s
B erythrocytes
(4
agglutinin.
able to find
anti-Tn
not
have
independently
differentiate
been
the
We
of cold
one
performed
of Vibrio
and normal
antibodies,
Agglutinins.
titer
absorb
is not
an incomplete
filtrate
Patient’s
the
to
other
Cold
between
is
studies
an
saliva
of secretor
group
0 subjects.
The serum
anti-B
and anti-H
agglutinins,18
of which
anti-B
had the same
effect
as a normal
serum
(Race).
the
AGCLUTININS.
half
Agglutinins.
with
natural
agglutinin
on other
at 56 C. for
for
and
and
System
relation
absorption
The
stance
which
is present
in the
of a patient
containing
anti-A,
had been
absorbed
previously,
Thus
agglutinin
ABO
any
AGGLUTININS.
heating
erythrocytes
only by the anti-B
serum
and not by the anti-A,
agglutinating
power
on A2B red cells
intact.
diminish
the titer of the anti-Tn
agglutinin.
Serum.-SPECIFIC
no action
9 have
anti-A
patient’s
has
C.
6 and
normal
the
by
at 65
certain
utilized,
but
modified
heating
between
cells
VITIIO.
erythrocytes,
is not
of
of patient’s
ACTION
1
8
it is destroyed
Variations
OF
64
32
agglutinin
The
HEAT.
agglutination
cells
agglutinates
an hour.
However,
70 C. for 10 minutes.
ACTION
red
by Tn red
with =
A1 red cells
Tn red cells
specifically
ACTION
cells
by A1 red cells
with =
A1 red cells
Tn red cells
Absorbed
and tested
The
tested
red
and
sera
erythrocytes
anti-Tn
the
no relation
anti-T,
and
ag-
Since
the
crossed
patient’s
by
modified
red cells.
were
treated
by
the
volumes
of cells
for 1 volume
of
of the laboratory.
Absorption
of sera
From www.bloodjournal.org by guest on December 22, 2014. For personal use only.
HEMOLYTIC
ACQUIRED
ANEMIA
AND
3.-Specificity
TABLE
of the
Titration
1/1
Normal
adult
1085
ANTI-TN
1/2
Rabbit
of
1/4
the
s erum
Anti-Tn
Serum
pr eviously
diluted
1/20
1/8
1/16
1/32
1/64
1/128
1/256
1/612
sera
average:
BM
-
-
-
-
-
-
-
-
-
-
BN
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
(+)
-
-
-
-
-
-
-
-
-
-
BMN
Tn
non
absorbed
Rabbit
anti-Tn
+
sera:
BM
(+)
BN
++
++
+++
BMN
Tn
anti-Tn
Rabbit
atsorbed
+
+
+++
+
-
-
-
-
-
-
(+)
-
-
-
-
-
-
-
-
-
-
++
++
++
+
(+)
+++
+++
-
(+)
sera
with
BMN
cells:
BM
-
-
-
-
-
-
-
-
-
-
BN
BMN
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
++
++
-
-
-
-
was
made
on
serum),
with
sera
in
group
either
the
were
the
-
+++
Tn
red
or not
procedure.
The
cells
by the
red blood
cells.
the four varieties
absorption
incubation.
+++
B normal
modified
patient’s
added
-
+++
(1
was
of
A similar
To successive
of erythrocytes
was
repeated
(+)
volume
filtrate.
Reading
procedure
+
dilutions
which
made
five
cells
for
1 volume
procedure
on
times
was
of these
had been
tile
with
after
of
foUowed
absorbed
employed
one
constantly
hour
the
of
same
results.
It
was
while
found
that
unmodified
nins
are
thus
modified
Tn
normal
erythrocytes
have
red
cells
not
absorbed
have
anti-T.
not
agglutinin
which
absorbed
anti-Tn,
The
two
aggluti-
is active
against
distinct.
The
normal
patient’s
modified
serum
contains
red cells.
an
anti-T
Two
anti-Tn
ability
other
methods
have
been
employed
to study
the relations
between
and anti-T:
(1)
Attempts
have
been
made
to transmit
polyagglutinbut without
success;
(2)
culture
of the patient’s
blood
has remained
sterile.
Tn
Antigen.-ANTIGENICITY
rabbits
an
with
Tn
anti-N
cells
agglutinin,
N antigen.
one
finds
After
in it
consequently
which
seems
normal
of Vibrio
comma.
weakly
agglutinates
by
the
filtrate.
specifically
abolished
We
by
have
When
agglutinates
absorption
also
prepared
have
technic.
that
the
a strong
patient’s
it is absorbed
on
Tn
Tn
several
a number
obtained
erythrocytes
have
tried
by trypsin
rabbit
serum
(absorbed
erythrocytes
which
have
on
serum
by
3).
have
BMN
The
of
contains
the
erythrocytes,
Tn substance
antigenicity.
We
as modffied
only
sensitized
The
serum
diluted
1/20
agglutinin
(table
ANTIGEN.
antigens
Anti-Tn
the
usual
proves
TN
We
ANIMALS.
the
of the
anti-Tn
to have
OF
from
using
absorption
a specific
DIFFERENTIATION
antigen
IN
red
red
red
sera
cells
by
on normal
red
been
trypsinized
cells
erythrocytes.
(table
injecting
to differentiate
or the filtrate
treated
This
by
agglutination
the
Tn
of a culture
blood
or
the
cells)
treated
filtrate,
it
can
be
4).
into
rabbits
B erythrocytes
From www.bloodjournal.org by guest on December 22, 2014. For personal use only.
1086
DAUSSET,
4.-Differentiation
Trypsin
TABLE
Rabbit
by
Absorbed
serum
Between
Cholera
or by
the T n Antigen
Filtrate
by Means
anti-Tn
Tested
with
red
cells
B red cells
treated
by
B non
Tn
cholera
filtrate
Tn
red
filtrate
filtrate
filtrate
filtrate
Filtrate
Rabbit
anti-cholera
Absorbed
red
has
that
power
the
Tn
RELATIONS
metabolism
-
++
-
(+)
-
+
(+)
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
Tn Antigens
Anti-Cholera
treated
red
and the
Filtrate
cell
serum
Tested
with
B
non
B
trypsinized
Normal
Treated
Antigens
Treated
Red Cell Serum
Normal
adult
treated
+
+
+
cells
1
cholera
non
Tn
±
of a culture
4
4
filtrate
filtrate
16
treated
cholera
0
0
0
0
0
filtrate
cholera
Tn
B serum
0
cholera
B non
Tn
Tn +
by
(Agglutination-titer)
Tn
filtrate
treated
0
0
8
treated
cholera
filtrate
cholera
filtrate
of Vibrio
comma.
by the
for the
After
absorption
filtrate
red
and
blood
Tn
cells
on normal
erythrocytes,
treated
by
it
the
5).
A normal
the
-
+++
-
+
-
cells and then
on red cells treated
found
that
the sera were
specific
(table
-
-
-
-
B +
SECRETION.
-
-
(+)
-
B non
filtrate
-
++
-
-
cells
filtrate
-
+++
-
+
-
(+)
(+)
B
by the
-
+
1/128
-
-
Red cells treated
by cholera
filtrate
treated
-
++
1/64
-
-
B
red
was
++
1/32
by
-
Tn
Tn red
++
Treated
-
by
Normal
-
-
+++
__+
filtrate
-
BERNARD
-
Between
the
Means
of Rabbit
by
-
-
+++
serum
1/16
1/8
+++
+++
-
of the
AND
Antigens
Anti-Tn
1/4
+++
-
-
+++
Tn
B + cholera
Tn + cholera
Cholera
+++
+
+++
++
+++
filtrate
filtrate
treated
5.-Differentiation
TABLE
-
+++
B + cholera
Tn + cholera
B non treated
cells
1/2
+
Tn
B + cholera
Tn + cholera
and the Normal
of Rabbit
Serum
Dilution
1/1
B trypsinized
Normal
MOULLEC
of
antigen
WITH
of
B serum
absorbed
agglutinating
is not
THE
Tn
the
saliva
It
can
of
the
patient
thus
be
still
concluded
secreted.
RECEPTORS
certain
on
erythrocytes.
FOR
bacteria,
VIRUS.
INFLUENZA
influenza
viruses
can
Like
the
induce
products
of
agglutination
of human
red
blood
cells.
Our
hypothesis
that
polyagglutinability
of Tn
erythrocytes
was due to a modification
of surface
antigens
led us to determine
if Tn erythrocytes
are
agglutinated
by influenza
viruses.
This
part
of the
work
was
done
by Miss
and A’ and mumps
virus.
by those
viruses
remains
the
Tn
antigen
RELATIONS
which
have
are
WITH
been
both
Cateigne,
It was
intact.
present
MODIFICATIONS
modified
by
who
used
strains
of influenza
virus
A
found
that
the agglutinability
of the cells
Thus
the
receptors
for influenza
virus
and
on the
surface
INDUCED
enzymes
of Tn
BY
or
through
red
ENZYMES.
the
cells.
Normal
action
of
red
virus
cells
prod-
From www.bloodjournal.org by guest on December 22, 2014. For personal use only.
ACQUIRED
HEMOLYTIC
ucts
bodies,
become
even
used
out
or
by
of which
the
can
it
No
STUDY.
could
examine
alive.
None
since
group.
grouping
tests
The
possibility
of
Patient’s
that
25
has
Tn
of
the
56
members
individuals
were
easily
of discovering
THE
ON
when
PATIENT’S
have
been
always
to note
than
the
teresting
active
cells
have
ACTION
been
ON
occurs
more
a panel
treated
OTHER
by
RED
evident
of red
tests
at
cells
a Coombs
ence
of
test on
an anti-E
transfusions.
patient’s
red
ferent
normal
enzyme
CELLS.
\Vith
that
and
containing
4
C.
cells
These
all
temperatures
(4,
which
the
with
To
specific
summarize:
for the
treated
weak
with
complete
The
patient’s
a proteolytic
antibody
18 and
pH
is
which
have
Tn
However,
which
studies
any
for
patient’s
red
is
is
after
with
is weak
in-
more
the
red
active
were
incubation
(1)
when
substance
optimum
of
Coombs
a substance
these
cells
behaves
20 C.
not
but
C.,
with
Through
the presto previous
against
made
at
for
in a second
step,
provoke
sensitization
serum
contains
cells,
especially
treated
trypsinized
at 37
antigens.
to visualize
to be due
C. after
been
performed
known
by an indirect
red cells.
enzyme.
That
with
a thermal
reached
of agIt
not
were
hemolysin
hemolysins
37 C. or at 37
may
be detected
use of trypsinized
has
enzyme,
serum
true
a
treatment
as in al-
laboratory.
reverse
presently
or by replacing,
serum
does
not
serum
before
as well
normal
red cells
it was
possible
which
was
considered
Tn serum
does
not contain
cells
or other
red cells.
Tests
Tn
of
1).
negative.
is observed
almost
trypsinized
antibody
the
red
the
AB
was
Unfortunate-
a proteolytic
trypsin,
(table
are
always
agglutination
C.
of
with
of the
antigen
serum,
the titers
But the maximum
sera.
still
patient
The
serum
agglutinin.
CELLS.
to
are
the
family.
RED
Tn
temperature
the
18
time
at 4 C.) at different
serum
by complement.
autoerytkrocytes
this same
test
the
as
erythrocytes
in saline
submitted
However,
who
one
was
a family
the
OWN
by the
that,
before
treatment
patient’s
serum
and
an enzyme,
the
cells
a nonspecific
but
at
in
red
cannot
France.
anomaly
no
of
like
antigen
family
that
marriage.
adults,
a Tn
patient’s
own
at any
temperature,
they
in
the
same
exists
from
normal
red cells are strongly
agglutinated
higher
than
those
obtained
with
glutination
the
marriage
the
lives
of
aging
behave
Tn
anti.
are
type
through
not
the
performed
and
the existence
a consanguine
serum.-ACTI0N
do
patient
had
incomplete
of this
eliminated
Therefore
of
the
been
erythrocytes
as trypsin.
by trypsin.
there
are no children
as is the case for all
However,
these
being
sera
containing
is saline.
If sera
relative
out
weak
action
on
a proteolytic
enzyme,
bumin.
by
red
agglutinin
seen
a
with
anti-Rh
medium
anti-Tn
close
these
because
ly, however,
niece
contained,
only
by
be
25
1087
ANTI-TN
by an enzyme
such
to an antigen
modified
FAMILY
increased
AND
agglutinable
the suspension
dilution,
cells treated
be likened
we
if
ANEMIA
the
dif-
a certain
the
of
test
patient’s
iso- or
or
by
which
is
have
been
only
like
a
also like an
incomplete
antibody
which
is fixed by the antigen
modified
with
trypsin
and
is not detected
by the indirect
Coombs
test.
It also
contains
(2)
another
substance
which
is active
against
all varieties
or erythrocytes.
It has been
possible,
through
a technic
of crossed
absorption,
to differentiate
these
two
substances.
It may
be
seen
(table
6)
that
trypsinized
Tn
erythro-
From www.bloodjournal.org by guest on December 22, 2014. For personal use only.
1088
DAUSSET,
6.-Differentiation
TABLE
Between
Present
Specific
tile
in the Patient’s
MOULLEC
Autoantibody
Serum
by
and
Cross
AND
the
BERNARD
Aspecific
Antibody
Absorption
Agglutination
Serum
Nonabsorbed
tested
with:
Normal
trypsinized
red
Tn trypsinized
red cells
Absorbed
by normal
trypsinized
Normal
trypsinized
red
Tn trypsinized
red cells
Absorbed
by Tn trypsinized
Normal
trypsinized
red
Tn trypsinized
red cells
cytes
absorb
sorb
only
these
two
both
the
second.
TFER
OF
titer
4
2
32
red
cells
and
tested
0
64
0
32
1
1
0
1
with:
cells
red
cells
and
tested
with:
cells
and
Thus,
are
Tn
that
red
different
normal,
cells
from
Dosage
trypsinized
passes
each
both
erythrocytes
antigens
ab-
and
therefore
an
abnormal-
other.
of complement
has
not
shown
(1/16).
CONCENTRATION
OF
to make
and
the
PLASMA
dilutions
titer
to
normal
At
87’C
256
COMPLEMENT.
used
found
titer
At
20’C
cells
substances
substances
ly low
Tn
of
be
COLLOIDAL
of a serum
this
agglutinin
similar
to
in
that
The
FACTOR.
containing
serum
obtained
patient’s
serum
an incomplete
was
by
determined.
diluting
has
anti-Rh
the
been
antibody,
The
result
anti-Rh
was
serum
with
serum.
ELECTROPHORETIC
gave
in
and
5.55
alpha-i
Gm.;
ANALYSIS
1952
the
gamma
In 1954,
of the
beta
THE
PATIENT’S
results:
globulins,
34.04
gamma
globulins,
alpha-2
and
Charbonnier).
increase
OF
following
total
Gm.;
alpha-2
Gm.
21.05
globulins
a paper
(Antweiller’s
64.6 Gm.;
SERUM
serum
proteins,
globulins,
There
was
and
a decrease
electrophoresis
of
3.94 Gm.;
therefore
of
serum
method)
albumin
beta
globulins,
an increase
beta-globulins
proteins
showed
of
(Dr.
an
globulins.
Platelets
The
at
patient’s
4
C.
not
against
the
Dausset
and
ing
of the
not
inhibit
found,
serum
only
contains
against
patient’s
own
Malinvaud.19
serum
at
62
the
cold
thromboagglutinin
platelets
platelets.
C.
for
30
pH
patient’s
is
serum
(44
This
Complement
agglutination.
and
a
foreign
was
is not
minutes
not
has
and
detected
by
necessary
the
important.
no
which
No
inhibitory
is
tested)
varieties
to
the
its
absorption
also
technic
action.
on
has
on
of
Heat-
BaSO4
thrombolysin
action
active
but
clot
do
been
retrac-
tion.
Leukocytes
A.
out
The
patient’s
of three
sera
globulin
leukocytes
known
to
consumption
test
have
contain
been
found
to be agglutinable
immune
isoleukoagglutinins.
performed
with
the
patient’s
by two
The
anti-
leukocytes
was
in
but
negative.22
B.
The
patient’s
serum
contained
no
isoleukoagglutinins2#{176}
1953,
From www.bloodjournal.org by guest on December 22, 2014. For personal use only.
ACQUIRED
HEMOLYTIC
following
against
of
ANEMIA
7 transfusions
patient’s
white
leukocytes.
One
AND
a
blood
year
1089
ANTI-TN
leukoagglutinin
cells,
but
after
the
appeared
against
active
last
transfusion,
45
that
which
out
of
was
52
inactive
varieties
leukoagglutinin
had
disappeared.
DIScUSSION
Here
one
munologic
of
finds
a combination
nature
is suggested
permanent
unknown
until
main
problem
to one another.
First
we
is to
has occurred
group
antigen.
but would
study
of
that
in
an
between
eliminated,
AB
group.
would
then
be
can
be
red
This
a relationship
anemia,
since
have
their
been
are
an
all
im-
which
has
extremely
by
rare
patient
human
sera,
belong
to
Tjb antigen
possess
an
anti-Tj
which
is not
very
trypsin.
This
fact
antigen.
not
leads
us
to
group
to be
group
antigen,
been
systems
who
almost
there
which
encountered
the known
the subjects
patient
Tn
could
That
the
Actually
red cell anomaly
of the
specifically
agglutinates
our
any
of an AB
considered
agglutinates
likely.
However,
not give
the family
who
of polyagglutinability.
has
of
since
another.
autoantibodies
genes.
does
of
are
an extremely
rare
acquired
anomaly,
since
any
one
with
group
of the
anomalies
from
anemia
and the existence
individuals
was
those
adult
an
between
the
his
serum
two
independent
blood
cells
not
constitute
family
hypothesis
treated
whose
a phenomenon
factor
those
of one of the patient’s
unfortunately
incomplete,
be
by
extent
one of the members
exhibits
the phenomenon
the
serum
first
and
serum
hemolytic
does
not seem
to
be identical
with
in
This
No
to
detected
have
anemia,
studies
a normal
anomalies
may
limited
grossly
cells.
what
polyagglutinability
since
none
of
yet. This
antigen
groups.
It cannot
TjbTjt)
to
a patient
whose
red
This
antigen
would
support
to this hypothesis.
have
their
group
determined
of the
to
acquired
merely
be a product
the family,
which
is
A confusion
could
be
due
know
two
suppose
hemolytic
serologic
now.
hypothesi&-The
Then
acquired
an
the
polyagglutinability
remained
The
related
of
by
all
seems
and his
erythrocytes
consider
of
are
human
to exist
hemolytic
which
a second
hy-
pothesis.
Second
hypothesis.-The
hemolytic
anemia
According
to
be compared
against
all
for
two
is due
this
to
one
another.
of
our
patient
could
in which
there
co-exists
a nonspecific
antibody
red
cells
and
a specific
one
(anti-e
or
active
anti-D,
hypothesis,
to the
varieties
cases
of
when
the
instance,
anomalies
to a specific
are
anti-Tn
the
related
hemolytic
erythrocytes
of
The
autoantibody.
anemia
the
subject
possess
the
antigen
e or D).
The
against
stance
they
of
serum
normal
of
which
is
have
their
been
nature,
our
patient
compatible
strongly
red
active
trypsinized.
these
stance
which
is active
like the panantibodies
contains:
cells
Even
substances
against
all
of acquired
(1)
treated
against
if
seem
a substance
by trypsin,
Tn
erythrocytes,
we
have
to
behave
varieties
hemolytic
of
which
is active
and
(2)
a sub-
not
like
trypsinized
anemias.
especially
given
a
antibodies.
red
after
formal
proof
The
cells
sub-
behaves
From www.bloodjournal.org by guest on December 22, 2014. For personal use only.
1090
DAUSSET,
The
substance
erythrocytes
same
which
to
seems
serologic
is
be
an
characters
adult
serum.
This
specific
specifically
immune
as
the
autoantibody
its
has
structure.
This
serum
if the
a genetically
transmitted
According
our
patient
the
Tn
to
hypothesis,
be
at
in
the
normal
antigen
antigen.
action
limited
It is possible,
of a virus
or
unmasking
antibody
have
present
a group
actually
immune
not
own
it
more
probable,
which
present
in
a
modifying
or
since
would
have
not
the patient,
were
antigen.
second
then
or
as it is found
group
this
to
BERNARD
patient’s
does
is
unmasked
transitory
seems
an
it
that
antigen,
alternative
contains
Tn antigen,
would
an
a latent
second
the patient’s
been
formed
to
AND
the
since
anti-Tn
either
rare
or
permanent
modified
against
anti-Tn
natural
corresponds
to one family
and extremely
as a matter
of fact,
that
the
micro-organism
active
MOULLEC
due
the
the
to
hemolytic
action
of an
observed
anemia
immune
antibody
in
against
antigen.
CONCLUSIONS
The
case
we
terpretation
patient
may
in
normal
adult
acteristics
this time.
of
been
presented
serum
here
unmasked
is
of
finding
a new
by
against
the
agent
the
Tn
an
that
of the
against
Although
antigen
has
the
anemia
is due
patient’s
char-
unknown
induced
the
to
own
in-
in our
existence
up
if the new
Tn
or an antigen
has
the
our
the
which
to determine
to one family,
that
the persistence
autoantibody
active
against
one.
polyagglutinability
us to show
(anti-Tn)
active
impossible
restricted
or modified
unique
a
permanent
has brought
substance
antibody
it has been
group
antigen,
anemia.
It appears
likely
ment
of an immune
probably
of
a complete
Unfortunately
is a very
rare
has
have
of the
phenomenon
be challenged,
this
to
antigen
which
hemolytic
the
develop-
erythrocytes,
antigen.
SUMMARY
A case of acquired
manent
polyagglutinability
1. Polyagglutinability
erythrocytes
of an
dependent
antigen
letters
of
be
was
present
absent
antibody,
inducing
studies
strate
being
massive
and
that
and
H
of 12 years’
duration
9 years,
is presented.
presence
up to
and
enzymes.
is not secreted
erythrocytes
of 25 members
which
induces
agglutination
the
weak
serum
in
active
in
clumping
through
anti-T
T
by proteolytic
Tn substance
in
or
is due to the
unknown
antigens
modified
Tn. The
anemia
at least
for
antigen
been
found
on the
2. The substance
to
hemolytic
of
28
473
sera
from
cord’s
anti-Tn
in
are
rabbits,
distinct.
a per-
on the surface
of the patient’s
the present
time,
which
is in-
does
It
not
behave
like
a
normal
has
been
designated
in saliva.
This
antigen
by
has
of the patient’s
family.
(natural
anti-Tn)
was
adults
and
blood.
we
33
It
saline
at the temperature
of Tn red cells.
Through
sensitization
and
white
showing
acts
adult
like
of laboratory
absorption
have
been
able
the
not
found
Negroes.
a complete
and
and
to
then
elution
demon-
It
From www.bloodjournal.org by guest on December 22, 2014. For personal use only.
ACQUIRED
3.
HEMOLYTIC
There
against
are
Tn
(b )
Tn;
a
ANEMIA
in
nonspecific
incomplete
all
anti-E;
(d )
a cold
three
last
4. To explain
agglutinability,
anemia
has
group
antigen,
is directly
and
Tn
varieties
to
antigen,
revealed
are
to
last
by
probably
the
existence
one
Tn
immune
the
causal
Es presettate
annos
con
minus
un caso
manifestation
of
IN
immune
the
antileukocyte
and polyhemolytic
the
patient
of
(b)
The
hemolytic
on
our
and
incomplete
anemia
acquired
anti-Tn
a very
patient’s
antibody
antigen
rare
anemia
red
cells
against
the
or
an
antigen
disease.
INTERLINGUA
acquirite
anemia
(Ic polyagglutinabilitate
polyagglutinabilitate
in
superficie
del
erythrocytos
viemente
essite
describite,
e que
non
proteolytic.
secernite
in
2.
de
Esseva
esseva
adultos
28 seros
illo
es
hemnolytic
in
active
de un
permitnente
duration
Ic
presentia,
Iste
le
substantia
in
le
solution
sahn
de
al
durante
Le
que
sequente
substantia
anti-E
temperatura
es
specificamente
in
active
anti
leucocytos.
probabilemente
4.
Pro
Le
le effecto
explicar
plmeiiomneiio
de
acquirite
anemia
de tin rarissime
le
tres
de
anticorpores
racia
a
superficie
del
(anti-Tn
blanc
dehile
anticorpore
laboratorio
e de
grados)
complete,
e induce
Tn. Per
sensibilisation
medio
in
i.e.
subse-
de studios
in
23
de
conilios,
nos
distincte.
Ic
contra
tractate
con trypsina.
II es possibile
que
non-specific
anticorpore
incomplete,
plus
omne
varietates
de erythrocytos
tractate
anti-E.
(d) Un substantia
de cryoactivitate
imnmun
del
es entitates
presente
H,
enzymas
Tn non
agglutination
(Ic
un
de erythrocytos
experimentos
de
e anti-Tn
entitates
le
presente
como
pre-
patiente.
adultos
(o
al
trovate
del
al
non
T e antigeno
modificate
per
Tn. Le substantia
esseva
457
ha
que
antigeno
induce
que
de
seros
al
de
non
familia
del
per
antigeno
un
antigeno
normal
per le litteras
antigeno
membros
que
causate
(Ic
es independente.
massive
aggregation
e de elution
e per
demonstrate
Un
que
presente
es
CS()
de racia
negre.
Illo esseva
absente
ab sanguine
de cordon.
Illo age
quentemente
absorption
3.
iste
patiente,
como
un
designate
le saliva.
25 altere
trovate
natural)
del
se comporta
Illo ha essite
erythrocytos
ha
to transfusions.
an
9 annos.
1. Le
es
de
due
anti-
anti-Tn
(c )
an
group
active
immune
the
hemolytic
( a ) The
a
agent
than
antigen
either
an
(e )
in
an
being
specifically
be
trypsin;
family.
of the
of
SUMMARIO
12
and
an acquired
presented:
existence
antigen
or modified
may
by
of
are
to
development
this
substance
treated
very
confined
to the
the
cells
combination
hypotheses
relationship
a
this
weaker
substance;
antibodies
related
trypsin;
antibody
of red
perhaps
(a )
:
by
antiplatelet
the
two
no
is due
serum
treated
against
109i
ANTI-TN
patient’s
erythrocytes
active
antibody.
These
our
AND
sero
(Ic
nostre
erythrocvtos
patiente:
Tn
que
(a)
ha
essite
anti-Tn
immun.
(h)
Un
le anti-Tn
e active
contra
COIl
trypsina.
(c)
Un incomplete
antiplachettal.
E (e) Ull anticorpore
isto
es
(Iehilc
un
que
nientionate
sIll)
(c),
((I),
c (c)
es
transfusiones.
combination
polyagglutinahilitate,
hemolytic
ha nulle
antigeno
de gruppo
(IC
tin
acquirite
ancniia
hemolvtic
(Iuo hypotheses
es Presenttte:
relation
con le existentia,
in iste
que es possibilemente
restringite
con
(a)
Le
patiente,
a un
sol
From www.bloodjournal.org by guest on December 22, 2014. For personal use only.
1092
DAUSSET,
familia.
del
(b)
Le
antigeno
anemia
Tn
hemolytic
super
es directemente
le erythrocvtos
de
disveloppamento
de un anticorpore
le caso del secunde
(Ic iste hypotheses,
gruppo
un
0
antigeno
revelate
o
AND
relationate
nostre
e es
contra
Tn
per
le
BERNARD
COn Ic existentia
patiente
immun
anti-Tn
Ic antigeno
modificate
MOULLEC
causate
le antigeno
esserea
tin
agente
per
le
Tn.
in
de
antigeno
del
causal
nlorbo.
ACKNO\VLEDGMENTS
We
and
are
greatly
patient’s
family
We
has
indebted
Seigneurin,
also
We
this
very
are
Professors
have
living
in
Rumania,
to
us,
wish
been
to
who
to
thank
helpful
very
helped
very
grateful
Nicolai
us
study
to
Israel,
Brazil
sincerely
and
I)rs.
who
to l)r.
and
the
R.
Jacques
France.
Race
and
the
l)rs.
Van
the
Gold
members
Loghem
personally
had
Junqucira,
different
J. J.
to study
who
to
of
and
agreed
Boulay,
also
Gurevitch,
blood
the
(lifficult
of
whose
advice
patient’s
task
our
blood.
of
translating
paper.
REFERENCES
1.
G.:
Huebener,
Untersuchungen
Berflcksichtigung
weichungen
von
0.:
Agens
Em
als
genie
glutinatorischen
Verhaltens
Blutkorperchen,
eine
bekannte
Quelle
mung.
der
Au
d’un
capable
ules
de
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die
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con-
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Thomsen
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Munskgaard,
1930,
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porary
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Katzin,
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of
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C.,
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of
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Basil-Jones,
B.,
Walsh,
R. J.:
An
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tin
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Nature
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E.,
D.
Loutit,
B.:
J.
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Polyagglutinabic
an(l
of
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de
J.Clin.
R.,
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chez
Rev.
une
d’H#{233}inat.
1952.
J. J.:
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rouges.
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M#{233}d.Exp. 21:213-217,
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polyagglutinabilit#{233}
#{233}rythrocytes
groupe
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cas
des
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des
between
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de,
7:372-380,
\‘an
Rev.
1951.
the
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patiente
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K.
C.
cells.
chez
phenomenon.
de:
red
17.
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semaines.
6:316-333,
5:266-270,
Nluralt,
and
L.:
accompagn#{233}e
de
Friedenreich
H.
factor
6:149-
thrombocytop#{233}nique,
and
Poly-
A.,
Acta.
aigu#{235}provoqtie
auto-anticorps,
J.:
H.:
agglutinable
Pneumokok-
Holijinder,
et
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1943.
der
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Paediat.
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Polyagglutinabilitats
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Copen-
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h#{233}molytique acquise
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beigeord-
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Van
M.:
rode
Holl#{228}nder,
glob96:556-
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des
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und
vol.
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43-47,
155,
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hagen,
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(laccroisse-
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-:
J. J.,
Loghem,
et
1927.
neter
6.
Van
52:85-
agent
Landsteinerschen
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12.
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558,
case
Biill.Lab.Bloedtr.Ned.Rode
sujet
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1949.
roten
tin-
K.:
glutinable
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red
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ment
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der
bisher
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Henningsen,
iso-ag-
Ztschr.f.Immunit#{228}tsf.
107,
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des
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782-788,
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Ver#{228}nderer
158:446-447,
1946.
Grubb,
R.: Abnormal
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in pyoAimJ.Clin.Path.
19:
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11.
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45:223-248,
1926.
3.
10.
Gruppenschema.
Ztschr.f.Immunit#{228}tsf.
2.
red
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Ab-
Iso-agglutination
Y.
M.,
Fl.
M.,
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Path.
1951.
R.,
C.
K.,
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R.,
W.
related
Lancet
Dausset,
to
the
262:903-904,
J.,
fluence
tion
AND
de
et
et dans
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chronic
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720,
1952.
l’agitation
sur
Son
C.:
In-
plaquettaire
du test
(note
liminaire).
Nenna,
agglutinins.
-,
22.
-,
l’agglutina-
utilit#{233}pour
Le
de Coombs
technique
Sang
pr#{233}-
25:847-851,
A.,
and Brecy,
H.:
V. Leuko-agglutinins
in
symptomatic
in paroxysmal
hemoglobinuria.
noc-
Blood
9:696-
1954.
malades
p#{233}niesidiopathiques.
Leuko-
or
and
Colombani,
J. et Evelin,
J.: Technique
de recherche
des auto-h#{233}molysines
immunologiques.
Rev.
Franc.
Et.clin.et
biol. 2:735-745,
1957.
and
Brecy,
H.:
Test direct
de consommation
de l’antiglobuline
stir les
leucocytes
et les plaquettes
de certains
1954.
-,
21.
des thrombo-agglutinines
la pratique
idiopathic
pancytopenia
system.
Malinvaud,
thrombocytaire.
la recherche
20.
1093
ANTI-TN
Morgan,
W. T. J., and Watkins,
M.: A “new”
blood
group
char-
acter
19.
ANEMIA
197-203,
1958.
atteints
de
Vox
pancyto-
Sang.
3(3):
From www.bloodjournal.org by guest on December 22, 2014. For personal use only.
1959 14: 1079-1093
Acquired Hemolytic Anemia with Polyagglutinability of Red Blood Cells
Due to a New Factor Present in Normal Human Serum (Anti-Tn)
JEAN DAUSSET, JEAN MOULLEC and JEAN BERNARD
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