T-cell early developmental stages and alternative options: GATA-3 is depicted as an intrathymically induced, specific inhibitor of access to the B-lineage pathway. Recognized stages in early intrathymic T-cell development are shown, along with the degrees of access to the B-cell program and other alternative programs that the cells can demonstrate at these stages if the extrinsic barrier of Notch/Dll4 signaling (red line) is removed. Red bricks represent GATA-3 when expressed at critical levels, and purple bricks represent other T-lineage commitment factors (eg, Bcl11b) that are activated later. Not shown are the positive roles of GATA-3 that permit the efficient generation of DN2 cells. Full commitment is complete by the DN2b stage

Rothenberg, Ellen V.

Caltech Authors - Main

doi:10.1182/blood-2013-01-477737
2013 121: 1673-1674
 
 
 
 
Ellen V. Rothenberg
 
GATA-3 locks the door to the B-cell option
 http://bloodjournal.hematologylibrary.org/content/121/10/1673.full.html
Updated information and services can be found at:
 (1838 articles)Free Research Articles   
Articles on similar topics can be found in the following Blood collections
 http://bloodjournal.hematologylibrary.org/site/misc/rights.xhtml#repub_requests
Information about reproducing this article in parts or in its entirety may be found online at:
 http://bloodjournal.hematologylibrary.org/site/misc/rights.xhtml#reprints
Information about ordering reprints may be found online at:
 http://bloodjournal.hematologylibrary.org/site/subscriptions/index.xhtml
Information about subscriptions and ASH membership may be found online at:
 Copyright 2011 by The American Society of Hematology; all rights reserved.
Washington DC 20036.
by the American Society of Hematology, 2021 L St, NW, Suite 900, 
Blood (print ISSN 0006-4971, online ISSN 1528-0020), is published weekly
 
 
 
 
 personal use only.
For at CALIFORNIA INST TECH/MILLIKAN LIBRARY on August 9, 2013. bloodjournal.hematologylibrary.orgFrom 
l l l IMMUNOBIOLOGY
Comment on Garcı´a-Ojeda et al, page 1749
GATA-3 locks the door to the B-cell option
-----------------------------------------------------------------------------------------------------
Ellen V. Rothenberg1 1CALIFORNIA INSTITUTE OF TECHNOLOGY
In this issue of Blood, Garcı´a-Ojeda et al demonstrate a key mechanism that drives
T and B lymphocytes to divergent fates from early in their development.1
T cells and B cells share manydevelopmental requirements, starting
with the parallel checkpoints in both pathways
that are dependent on the activation of
Rag1-Rag2 DNA recombinase and
Rag-mediated immune receptor gene
rearrangements. A close developmental
relationship has seemed self-evident: the ﬁrst
partially restricted hematopoietic progenitor
cell type to be deﬁned prospectively was the
common lymphoid precursor,2 a stem cell
descendant that retains both T- and B-lineage
potential while other potentials are reduced or
eliminated. Thus, it has remained perplexing
that, within the thymus, T-cell precursors
lose access to the B-cell developmental fate
substantially earlier than they lose access to
myeloid, dendritic, and NK cell fates.3,4 The
environmental signaling imposed on these
precursors through Notch1 Dll4 interaction is
known to block the B-cell developmental
program as long as the cells remain in situ.5
However, Notch signaling also limits access
to other fate alternatives during exposure to
Dll4. Yet even when early T-lineage
precursors are removed from the Dll4-rich
thymic environment, they prove to have
become unable to generate B cells at stages
when they can still generate myeloid or
dendritic cells in these conditions3,4 (see
ﬁgure). This implies that early T cells must
have activated an endogenous, speciﬁc
antagonist of the B-cell program. In this issue,
Garcı´a-Ojeda et al present compelling
evidence that it is the activation of GATA-3
in the precursors that accounts for this
profound barrier to B-cell fate.1
GATA-3 has long been a tempting
candidate for this role. It is expressed in
prethymic cells at a low level, and then
strongly upregulated by Notch signals as one
of the earliest events in T-cell development
(reviewed in Rothenberg et al6). Once turned
on, it is not highly dependent on continuing
Notch signals. Thus, it is upregulated around
the time that B-lineage exclusion is ﬁrst
imposed, and then it remains expressed (albeit
at modulating levels) in all subsequent stages
of T-cell development. It is one of the few
transcription factors in T cells that do not
have a family member shared between any
phases of B- and T-cell lineage programs
(unlike family members TCF-1/LEF-1 and
Bcl11b/Bcl11a, as well as other factors that
are explicitly shared). Furthermore, forced
GATA-3 expression profoundly antagonizes
B-cell development,7,8 whereas without this
factor, Gata32/2 precursors can generate
some B cells even when weak Notch signals
are present.1 However, the dose effects of
GATA-3 have complicated the arguments for
a speciﬁc role in B-lineage exclusion. First,
GATA-3 becomes so important for T-lineage
precursor survival and development at an
early stage that the Gata3 loss of function
depletes most of the cells that need to be
assayed.9 This has invited concern that any
B cells alleged to have emerged from GATA-
3–deﬁcient T-cell precursors might in fact be
products of contaminants. Second, GATA-3
overexpression not only inhibits B-cell
development, but it also inhibits T-cell
development itself.8,10
T-cell early developmental stages and alternative options: GATA-3 is depicted as an intrathymically induced, specific
inhibitor of access to the B-lineage pathway. Recognized stages in early intrathymic T-cell development are shown,
along with the degrees of access to the B-cell program and other alternative programs that the cells can demonstrate at
these stages if the extrinsic barrier of Notch/Dll4 signaling (red line) is removed. Red bricks represent GATA-3 when
expressed at critical levels, and purple bricks represent other T-lineage commitment factors (eg, Bcl11b6) that are
activated later. Not shown are the positive roles of GATA-3 that permit the efficient generation of DN2 cells. Full
commitment is complete by the DN2b stage.6
BLOOD, 7 MARCH 2013 x VOLUME 121, NUMBER 10 1673
insideblood
®
7 MARCH 2013 I VOLUME 121 , NUMBER 10
 personal use only.
For at CALIFORNIA INST TECH/MILLIKAN LIBRARY on August 9, 2013. bloodjournal.hematologylibrary.orgFrom 
Garcı´a-Ojeda et al have carefully
structured their case to circumvent these
problems.1 They have dissected the effects of
Gata3 deletion by using highly deﬁned
precursor cell populations, efﬁcient and
quantitative precursor frequency assays, gene
expression monitoring and T-cell receptor
gene rearrangement analyses, and temporally
controlled excision of Gata3 in cells that have
already reached a deﬁnitive T-lineage
developmental stage. Their results extend our
understanding of both the roles of GATA-3
in T-cell developmental progression and the
speciﬁc dependence of T-cell precursors on
GATA-3 for B-lineage fate exclusion. The
authors ﬁnd that a loss of GATA-3 function
at an early stage handicaps the generation of
deﬁnitive DN2-stage, T-lineage progenitors
from less-deﬁned DN1 precursors. The
inhibition is conﬁrmed by the reduced
expression of a suite of genes that normally
turn on during the transition to T-lineage
commitment (at DN2b stage) and just
afterward, that is, Cd3e, Itk, Bcl11b, Rag1,
and Ets1. However, some DN2 cells are made,
and these can be conﬁrmed to be of early
T-cell lineage through their robust expression
of Tcf7. Importantly, the GATA-3–deﬁcient
DN2 cells also show exaggerated, not
reduced, expression of Notch-activated genes
Dtx1 and Ptcra, proving that their Notch
signaling is not inhibited. The appropriate
cells exist, therefore, in which to ask whether
GATA-3 is truly an intrinsic requirement for
B-lineage exclusion.
When removed from Notch stimulation,
Gata32/2 DN2 cells indeed display B-lineage
potential along with reduced NK-lineage
potential.1 B-cell precursor activity is detected
at ;10% frequency (comparable to wild-type
NK precursor frequency), in marked contrast
to the complete lack of detectable B-cell
potential in normal DN2 cells. The converted
cells switch to a B-lineage transcriptional
proﬁle, eliminating any trace of previous
T-lineage gene expression. However, at least
some of them retain TCRb gene
rearrangements attesting to a T-lineage past.
The concern that they might represent the
outgrowth of an aberrant minority within the
mutant DN2 population is countered by using
an acute deletion system to remove Gata3
only after the cells have reached the DN2
stage with their GATA-3 function intact.
Such cells should have had the full
opportunity to activate GATA-3 as well as
many of the T-cell genes shown to be
dependent on GATA-3. Nevertheless, when
Gata3 is removed, they, too, reveal B-cell
precursor competence, a >102-fold increase
in frequency from GATA-3–replete DN2
cells that lack detectable B-cell potential.
These experiments may still be affected by
GATA-3 contributions to proliferation and
survival; however, Garcı´a-Ojeda et al
make a strong case that GATA-3 has
a nonredundant role in B-lineage exclusion
speciﬁcally, once cells have entered the T-cell
pathway. GATA-3 is not the answer for all
aspects of T-lineage commitment: loss of
GATA-3 reduces, rather than increases,
access to the NK pathway, and the conditions
used would not optimally reveal the role of
GATA-3 in access to myeloid- or dendritic-
cell fates. The steps in the pathway of lineage
conversion, especially for cells starting from a
normal DN2 stage, also remain to be deﬁned.
Nevertheless, GATA-3 induction and the
mechanisms that sustain its expression now
appear to constitute the key with which
common lymphoid precursors and any other
uncommitted progenitors that enter the
thymus are persuaded to lock the door to the
B-lineage pathway.
Conﬂict-of-interest disclosure: The author
declares no competing ﬁnancial interests. n
REFERENCES
1. Garcı´a-Ojeda ME, Klein Wolterink RGJ, Lemaıˆtre
F, et al. GATA-3 promotes T-cell speciﬁcation by
repressing B-cell potential in pro-T cells in mice.
Blood. 2013;121(10):1749-1759.
2. Kondo M, Weissman IL, Akashi K. Identiﬁcation of
clonogenic common lymphoid progenitors in mouse bone
marrow. Cell. 1997;91(5):661-672.
3. Wada H, Masuda K, Satoh R, et al. Adult T-cell
progenitors retain myeloid potential. Nature. 2008;
452(7188):768-772.
4. Bell JJ, Bhandoola A. The earliest thymic progenitors
for T cells possess myeloid lineage potential. Nature. 2008;
452(7188):764-767.
5. Mohtashami M, Shah DK, Nakase H, et al. Direct
comparison of Dll1- and Dll4-mediated Notch activation
levels shows differential lymphomyeloid lineage
commitment outcomes. J Immunol. 2010;185(2):867-876.
6. Rothenberg EV, Zhang J, Li L. Multilayered
speciﬁcation of the T-cell lineage fate. Immunol Rev. 2010;
238(1):150-168.
7. Heavey B, Charalambous C, Cobaleda C, et al.
Myeloid lineage switch of Pax5 mutant but not wild-type
B cell progenitors by C/EBPa and GATA factors.
EMBO J. 2003;22(15):3887-3897.
8. Taghon T, Yui MA, Rothenberg EV. Mast cell
lineage diversion of T lineage precursors by the essential
T cell transcription factor GATA-3. Nat Immunol. 2007;
8(8):845-855.
9. Hosoya T, Kuroha T, Moriguchi T, et al. GATA-3 is
required for early T lineage progenitor development. J Exp
Med. 2009;206(13):2987-3000.
10. Xu W, Carr T, Ramirez K, et al. E2A transcription
factors limit expression of Gata3 to facilitate T lymphocyte
lineage commitment. Blood. 2013.
l l l THROMBOSIS & HEMOSTASIS
Comment on Zhi et al, page 1858
The platelet Fc receptor:
a new role for an old actor
-----------------------------------------------------------------------------------------------------
Jose´ A. Lo´pez1 1PUGET SOUND BLOOD CENTER
In this issue of Blood, Zhi et al1 demonstrate an important role for Fc greceptor
IIa (FcgRIIa) in platelet functions dependent on integrin aIIbb3 outside-in signals.
Being typecast is a problem not only foractors but also for biological molecules.
For the former, a role may prove so
convincing to an audience or be played so
often that it is difﬁcult for the audience to
accept the actor in a different role. For
biological molecules, the problem more often
is associated with the names they carry. These
names were usually assigned based on the ﬁrst
biological role with which the molecule was
associated. Platelet-activating factor (PAF) is
a case in point. This bioactive phospholipid
was originally named for its ability to activate
platelets but extensive subsequent works
shows this to be only a minor component of
PAF’s biological roles, which span the gamut
from inﬂammation, to nociception, asthma,
cell death, bone metabolism, and even sperm
function.2 Fc receptors have been similarly
typecast, although their functions do relate
more closely to the function for which they
were named. Platelets contain 1 Fc receptor,
1674 BLOOD, 7 MARCH 2013 x VOLUME 121, NUMBER 10
 personal use only.
For at CALIFORNIA INST TECH/MILLIKAN LIBRARY on August 9, 2013. bloodjournal.hematologylibrary.orgFrom 


GATA-3 locks the door to the B-cell option

doi:10.1182/blood-2013-01-477737
2013 121: 1673-1674
 
 
 
 
Ellen V. Rothenberg
 
GATA-3 locks the door to the B-cell option
 http://bloodjournal.hematologylibrary.org/content/121/10/1673.full.html
Updated information and services can be found at:
 (1838 articles)Free Research Articles   
Articles on similar topics can be found in the following Blood collections
 http://bloodjournal.hematologylibrary.org/site/misc/rights.xhtml#repub_requests
Information about reproducing this article in parts or in its entirety may be found online at:
 http://bloodjournal.hematologylibrary.org/site/misc/rights.xhtml#reprints
Information about ordering reprints may be found online at:
 http://bloodjournal.hematologylibrary.org/site/subscriptions/index.xhtml
Information about subscriptions and ASH membership may be found online at:
 Copyright 2011 by The American Society of Hematology; all rights reserved.
Washington DC 20036.
by the American Society of Hematology, 2021 L St, NW, Suite 900, 
Blood (print ISSN 0006-4971, online ISSN 1528-0020), is published weekly
 
 
 
 
 personal use only.
For at CALIFORNIA INST TECH/MILLIKAN LIBRARY on August 9, 2013. bloodjournal.hematologylibrary.orgFrom 
l l l IMMUNOBIOLOGY
Comment on Garcı́a-Ojeda et al, page 1749
GATA-3 locks the door to the B-cell option
-----------------------------------------------------------------------------------------------------
Ellen V. Rothenberg1 1CALIFORNIA INSTITUTE OF TECHNOLOGY
In this issue of Blood, Garcı́a-Ojeda et al demonstrate a key mechanism that drives
T and B lymphocytes to divergent fates from early in their development.1
T cells and B cells share manydevelopmental requirements, starting
with the parallel checkpoints in both pathways
that are dependent on the activation of
Rag1-Rag2 DNA recombinase and
Rag-mediated immune receptor gene
rearrangements. A close developmental
relationship has seemed self-evident: the first
partially restricted hematopoietic progenitor
cell type to be defined prospectively was the
common lymphoid precursor,2 a stem cell
descendant that retains both T- and B-lineage
potential while other potentials are reduced or
eliminated. Thus, it has remained perplexing
that, within the thymus, T-cell precursors
lose access to the B-cell developmental fate
substantially earlier than they lose access to
myeloid, dendritic, and NK cell fates.3,4 The
environmental signaling imposed on these
precursors through Notch1 Dll4 interaction is
known to block the B-cell developmental
program as long as the cells remain in situ.5
However, Notch signaling also limits access
to other fate alternatives during exposure to
Dll4. Yet even when early T-lineage
precursors are removed from the Dll4-rich
thymic environment, they prove to have
become unable to generate B cells at stages
when they can still generate myeloid or
dendritic cells in these conditions3,4 (see
figure). This implies that early T cells must
have activated an endogenous, specific
antagonist of the B-cell program. In this issue,
Garcı́a-Ojeda et al present compelling
evidence that it is the activation of GATA-3
in the precursors that accounts for this
profound barrier to B-cell fate.1
GATA-3 has long been a tempting
candidate for this role. It is expressed in
prethymic cells at a low level, and then
strongly upregulated by Notch signals as one
of the earliest events in T-cell development
(reviewed in Rothenberg et al6). Once turned
on, it is not highly dependent on continuing
Notch signals. Thus, it is upregulated around
the time that B-lineage exclusion is first
imposed, and then it remains expressed (albeit
at modulating levels) in all subsequent stages
of T-cell development. It is one of the few
transcription factors in T cells that do not
have a family member shared between any
phases of B- and T-cell lineage programs
(unlike family members TCF-1/LEF-1 and
Bcl11b/Bcl11a, as well as other factors that
are explicitly shared). Furthermore, forced
GATA-3 expression profoundly antagonizes
B-cell development,7,8 whereas without this
factor, Gata32/2 precursors can generate
some B cells even when weak Notch signals
are present.1 However, the dose effects of
GATA-3 have complicated the arguments for
a specific role in B-lineage exclusion. First,
GATA-3 becomes so important for T-lineage
precursor survival and development at an
early stage that the Gata3 loss of function
depletes most of the cells that need to be
assayed.9 This has invited concern that any
B cells alleged to have emerged from GATA-
3–deficient T-cell precursors might in fact be
products of contaminants. Second, GATA-3
overexpression not only inhibits B-cell
development, but it also inhibits T-cell
development itself.8,10
T-cell early developmental stages and alternative options: GATA-3 is depicted as an intrathymically induced, specific
inhibitor of access to the B-lineage pathway. Recognized stages in early intrathymic T-cell development are shown,
along with the degrees of access to the B-cell program and other alternative programs that the cells can demonstrate at
these stages if the extrinsic barrier of Notch/Dll4 signaling (red line) is removed. Red bricks represent GATA-3 when
expressed at critical levels, and purple bricks represent other T-lineage commitment factors (eg, Bcl11b6) that are
activated later. Not shown are the positive roles of GATA-3 that permit the efficient generation of DN2 cells. Full
commitment is complete by the DN2b stage.6
BLOOD, 7 MARCH 2013 x VOLUME 121, NUMBER 10 1673
insideblood
®
7 MARCH 2013 I VOLUME 121 , NUMBER 10
 personal use only.
For at CALIFORNIA INST TECH/MILLIKAN LIBRARY on August 9, 2013. bloodjournal.hematologylibrary.orgFrom 
Garcı́a-Ojeda et al have carefully
structured their case to circumvent these
problems.1 They have dissected the effects of
Gata3 deletion by using highly defined
precursor cell populations, efficient and
quantitative precursor frequency assays, gene
expression monitoring and T-cell receptor
gene rearrangement analyses, and temporally
controlled excision of Gata3 in cells that have
already reached a definitive T-lineage
developmental stage. Their results extend our
understanding of both the roles of GATA-3
in T-cell developmental progression and the
specific dependence of T-cell precursors on
GATA-3 for B-lineage fate exclusion. The
authors find that a loss of GATA-3 function
at an early stage handicaps the generation of
definitive DN2-stage, T-lineage progenitors
from less-defined DN1 precursors. The
inhibition is confirmed by the reduced
expression of a suite of genes that normally
turn on during the transition to T-lineage
commitment (at DN2b stage) and just
afterward, that is, Cd3e, Itk, Bcl11b, Rag1,
and Ets1. However, some DN2 cells are made,
and these can be confirmed to be of early
T-cell lineage through their robust expression
of Tcf7. Importantly, the GATA-3–deficient
DN2 cells also show exaggerated, not
reduced, expression of Notch-activated genes
Dtx1 and Ptcra, proving that their Notch
signaling is not inhibited. The appropriate
cells exist, therefore, in which to ask whether
GATA-3 is truly an intrinsic requirement for
B-lineage exclusion.
When removed from Notch stimulation,
Gata32/2 DN2 cells indeed display B-lineage
potential along with reduced NK-lineage
potential.1 B-cell precursor activity is detected
at ;10% frequency (comparable to wild-type
NK precursor frequency), in marked contrast
to the complete lack of detectable B-cell
potential in normal DN2 cells. The converted
cells switch to a B-lineage transcriptional
profile, eliminating any trace of previous
T-lineage gene expression. However, at least
some of them retain TCRb gene
rearrangements attesting to a T-lineage past.
The concern that they might represent the
outgrowth of an aberrant minority within the
mutant DN2 population is countered by using
an acute deletion system to remove Gata3
only after the cells have reached the DN2
stage with their GATA-3 function intact.
Such cells should have had the full
opportunity to activate GATA-3 as well as
many of the T-cell genes shown to be
dependent on GATA-3. Nevertheless, when
Gata3 is removed, they, too, reveal B-cell
precursor competence, a >102-fold increase
in frequency from GATA-3–replete DN2
cells that lack detectable B-cell potential.
These experiments may still be affected by
GATA-3 contributions to proliferation and
survival; however, Garcı́a-Ojeda et al
make a strong case that GATA-3 has
a nonredundant role in B-lineage exclusion
specifically, once cells have entered the T-cell
pathway. GATA-3 is not the answer for all
aspects of T-lineage commitment: loss of
GATA-3 reduces, rather than increases,
access to the NK pathway, and the conditions
used would not optimally reveal the role of
GATA-3 in access to myeloid- or dendritic-
cell fates. The steps in the pathway of lineage
conversion, especially for cells starting from a
normal DN2 stage, also remain to be defined.
Nevertheless, GATA-3 induction and the
mechanisms that sustain its expression now
appear to constitute the key with which
common lymphoid precursors and any other
uncommitted progenitors that enter the
thymus are persuaded to lock the door to the
B-lineage pathway.
Conflict-of-interest disclosure: The author
declares no competing financial interests. n
REFERENCES
1. Garcı́a-Ojeda ME, Klein Wolterink RGJ, Lemaı̂tre
F, et al. GATA-3 promotes T-cell specification by
repressing B-cell potential in pro-T cells in mice.
Blood. 2013;121(10):1749-1759.
2. Kondo M, Weissman IL, Akashi K. Identification of
clonogenic common lymphoid progenitors in mouse bone
marrow. Cell. 1997;91(5):661-672.
3. Wada H, Masuda K, Satoh R, et al. Adult T-cell
progenitors retain myeloid potential. Nature. 2008;
452(7188):768-772.
4. Bell JJ, Bhandoola A. The earliest thymic progenitors
for T cells possess myeloid lineage potential. Nature. 2008;
452(7188):764-767.
5. Mohtashami M, Shah DK, Nakase H, et al. Direct
comparison of Dll1- and Dll4-mediated Notch activation
levels shows differential lymphomyeloid lineage
commitment outcomes. J Immunol. 2010;185(2):867-876.
6. Rothenberg EV, Zhang J, Li L. Multilayered
specification of the T-cell lineage fate. Immunol Rev. 2010;
238(1):150-168.
7. Heavey B, Charalambous C, Cobaleda C, et al.
Myeloid lineage switch of Pax5 mutant but not wild-type
B cell progenitors by C/EBPa and GATA factors.
EMBO J. 2003;22(15):3887-3897.
8. Taghon T, Yui MA, Rothenberg EV. Mast cell
lineage diversion of T lineage precursors by the essential
T cell transcription factor GATA-3. Nat Immunol. 2007;
8(8):845-855.
9. Hosoya T, Kuroha T, Moriguchi T, et al. GATA-3 is
required for early T lineage progenitor development. J Exp
Med. 2009;206(13):2987-3000.
10. Xu W, Carr T, Ramirez K, et al. E2A transcription
factors limit expression of Gata3 to facilitate T lymphocyte
lineage commitment. Blood. 2013.
l l l THROMBOSIS & HEMOSTASIS
Comment on Zhi et al, page 1858
The platelet Fc receptor:
a new role for an old actor
-----------------------------------------------------------------------------------------------------
José A. López1 1PUGET SOUND BLOOD CENTER
In this issue of Blood, Zhi et al1 demonstrate an important role for Fc greceptor
IIa (FcgRIIa) in platelet functions dependent on integrin aIIbb3 outside-in signals.
Being typecast is a problem not only foractors but also for biological molecules.
For the former, a role may prove so
convincing to an audience or be played so
often that it is difficult for the audience to
accept the actor in a different role. For
biological molecules, the problem more often
is associated with the names they carry. These
names were usually assigned based on the first
biological role with which the molecule was
associated. Platelet-activating factor (PAF) is
a case in point. This bioactive phospholipid
was originally named for its ability to activate
platelets but extensive subsequent works
shows this to be only a minor component of
PAF’s biological roles, which span the gamut
from inflammation, to nociception, asthma,
cell death, bone metabolism, and even sperm
function.2 Fc receptors have been similarly
typecast, although their functions do relate
more closely to the function for which they
were named. Platelets contain 1 Fc receptor,
1674 BLOOD, 7 MARCH 2013 x VOLUME 121, NUMBER 10
 personal use only.
For at CALIFORNIA INST TECH/MILLIKAN LIBRARY on August 9, 2013. bloodjournal.hematologylibrary.orgFrom 


English

https://authors.library.caltech.edu/39829/1/Blood-2013-Rothenberg-1673-4.pdf

GATA-3 locks the door to the B-cell option

Abstract

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