Research Topics
Genomes and Genes
Species | Jinfang ZhuSummaryAffiliation: National Institutes of Health Country: USA Publications
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Detail Information
Publications
Growth factor independent-1 induced by IL-4 regulates Th2 cell proliferationJinfang Zhu
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Immunity 16:733-44. 2002..The synergy of Gfi-1 and Gata3 provides a mechanism through which IL-4 could selectively promote Th2 cell expansion...
Independent roles for IL-2 and GATA-3 in stimulating naive CD4+ T cells to generate a Th2-inducing cytokine environmentHidehiro Yamane
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
J Exp Med 202:793-804. 2005..A MEK inhibition rescued early GATA-3 expression and responsiveness to IL-2; these cells were now capable of producing early IL-4 and undergoing subsequent Th2 differentiation...
CD4+ T cell plasticity-Th2 cells join the crowdJinfang Zhu
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Immunity 32:11-3. 2010....
Differentiation of effector CD4 T cell populations (*)Jinfang Zhu
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892 1892, USA
Annu Rev Immunol 28:445-89. 2010....
The transcription factor T-bet is induced by multiple pathways and prevents an endogenous Th2 cell program during Th1 cell responsesJinfang Zhu
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Immunity 37:660-73. 2012..Our study revealed redundancy and synergy among several Th1 cell-inducing pathways in regulating the expression of T-bet and IFN-γ, and a critical role of T-bet in suppressing an endogenous Th2 cell-associated program...
Heterogeneity and plasticity of T helper cellsJinfang Zhu
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Cell Res 20:4-12. 2010..In this review, we summarize recent reports on heterogeneity and plasticity of Th cells, and discuss potential mechanisms and implications of such features that Th cells display...
CD4 T cells: fates, functions, and faultsJinfang Zhu
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Blood 112:1557-69. 2008....
Transcriptional regulation of Th2 cell differentiationJinfang Zhu
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Immunol Cell Biol 88:244-9. 2010..Finally, the difference between in vitro and in vivo Th2 differentiation is discussed...
Gfi-1 plays an important role in IL-2-mediated Th2 cell expansionJinfang Zhu
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 103:18214-9. 2006..Reduced Th2 cell expansion in the absence of Gfi-1 was confirmed by the diminished frequency of IL-4-producing cells when these mice were infected with Schistosoma mansoni...
GATA-3 promotes Th2 responses through three different mechanisms: induction of Th2 cytokine production, selective growth of Th2 cells and inhibition of Th1 cell-specific factorsJinfang Zhu
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Cell Res 16:3-10. 2006....
Down-regulation of Gfi-1 expression by TGF-beta is important for differentiation of Th17 and CD103+ inducible regulatory T cellsJinfang Zhu
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
J Exp Med 206:329-41. 2009..Thus, Gfi-1 plays a critical role both in enhancing Th2 cell expansion and in repressing induction of Th17 and CD103(+) iTreg cells...
Conditional deletion of Gata3 shows its essential function in T(H)1-T(H)2 responsesJinfang Zhu
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Nat Immunol 5:1157-65. 2004..Thus, GATA-3 serves as a principal switch in determining T(H)1-T(H)2 responses...
Stat5 activation plays a critical role in Th2 differentiationJinfang Zhu
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Immunity 19:739-48. 2003..Stat5A binds to HSII and HSIII sites of the Il4 gene. Coinfection with STAT5A1*6-NGFR-RV and GATA-3-GFP-RV results in optimal Th2 priming...
Peripheral CD4+ T-cell differentiation regulated by networks of cytokines and transcription factorsJinfang Zhu
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 1892, USA
Immunol Rev 238:247-62. 2010..We also discuss the interactions of key transcription factors at both genetic and protein levels and the function of the resulting network(s) in regulating the expression of effector cytokines...
The sequential activity of Gata3 and Thpok is required for the differentiation of CD1d-restricted CD4+ NKT cellsLie Wang
Laboratory of Immune Cell Biology, Center for Cancer Research CCR, NCI, NIH, Bethesda, MD 20892 4259, USA
Eur J Immunol 40:2385-90. 2010..These findings identify the sequential activity of Gata3 and Thpok as a hallmark of CD4(+) T-cell differentiation, regardless of MHC restriction...
The transcription factor GATA3 actively represses RUNX3 protein-regulated production of interferon-gammaRyoji Yagi
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Immunity 32:507-17. 2010..Thus, the Runx3-mediated pathway, actively suppressed by GATA3, induces IFN-gamma production in a STAT4- and T-bet-independent manner...
IL-1 family members and STAT activators induce cytokine production by Th2, Th17, and Th1 cellsLiying Guo
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 106:13463-8. 2009....
Basophils produce IL-4 and accumulate in tissues after infection with a Th2-inducing parasiteBooki Min
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 10 Center Dr, Bldg. 10, Bethesda, MD 20892, USA
J Exp Med 200:507-17. 2004....
Genome-wide analyses of transcription factor GATA3-mediated gene regulation in distinct T cell typesGang Wei
Laboratory of Molecular Immunology, NHLBI, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892, USA
Immunity 35:299-311. 2011....
Elevating calcium in Th2 cells activates multiple pathways to induce IL-4 transcription and mRNA stabilizationLiying Guo
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
J Immunol 181:3984-93. 2008..p38 also regulates IL-4 production by mRNA stabilization. TCR stimulation also phosphorylates p38, partially through the calcium-dependent pathway; activated p38 is required for optimal IL-4 and IFN-gamma...
Interleukin 2 plays a central role in Th2 differentiationJavier Cote-Sierra
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 101:3880-5. 2004..Thus, IL-2 plays a critical role in the polarization of naive CD4 T cells to the Th2 phenotype...
Distinct functions for the transcription factors GATA-3 and ThPOK during intrathymic differentiation of CD4(+) T cellsLie Wang
Laboratory of Immune Cell Biology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892, USA
Nat Immunol 9:1122-30. 2008..We propose that GATA-3 acts as a specification factor for the CD4(+) lineage 'upstream' of the ThPOK-controlled CD4(+) commitment checkpoint...
The transcription factor Gfi1 regulates G-CSF signaling and neutrophil development through the Ras activator RasGRP1Maria De La Luz Sierra
Laboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda MD, USA
Blood 115:3970-9. 2010..These results uncover a previously unknown function of Gfi1 as a regulator of RasGRP1 and link Gfi1 transcriptional control to G-CSF signaling and regulation of granulopoiesis...
Global mapping of H3K4me3 and H3K27me3 reveals specificity and plasticity in lineage fate determination of differentiating CD4+ T cellsGang Wei
Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
Immunity 30:155-67. 2009..Our data suggest an epigenetic mechanism underlying the specificity and plasticity of effector and regulatory T cells and also provide a framework for understanding complexity of CD4(+) T helper cell differentiation...
In TH2 cells the Il4 gene has a series of accessibility states associated with distinctive probabilities of IL-4 productionLiying Guo
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, and Cancer Genetics Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 99:10623-8. 2002..This finding suggests a regulation of IL-4 expression keyed to the function of this cytokine in cell/cell interactions and in the regulation of threshold responses...
Opposing regulation of the locus encoding IL-17 through direct, reciprocal actions of STAT3 and STAT5Xiang Ping Yang
Molecular Immunology and Inflammation Branch, National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA
Nat Immunol 12:247-54. 2011..Thus, the balance rather than the absolute magnitude of these signals determined the propensity of cells to make a key inflammatory cytokine...
Transcription factor Gfi-1 induced by G-CSF is a negative regulator of CXCR4 in myeloid cellsMaria De La Luz Sierra
Laboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute NCI, National Institutes of Health NIH, Bethesda, MD 20892, USA
Blood 110:2276-85. 2007....
MicroRNA126 contributes to granulocyte colony-stimulating factor-induced hematopoietic progenitor cell mobilization by reducing the expression of vascular cell adhesion molecule 1Ombretta Salvucci
Laboratory of Cellular Oncology, CCR, NCI, NIH, Bethesda, MD 20892, USA
Haematologica 97:818-26. 2012..Since hematopoietic stem/progenitor cells represent a minority of all blood cells mobilized by granulocyte colony-stimulating factor, the underlying mechanisms need to be understood in order to develop selective drugs...
An updated view on transcription factor GATA3-mediated regulation of Th1 and Th2 cell differentiationRyoji Yagi
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Int Immunol 23:415-20. 2011....
Thpok-independent repression of Runx3 by Gata3 during CD4(+) T-cell differentiation in the thymusYumei Xiong
Laboratory of Immune Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
Eur J Immunol 43:918-28. 2013..Thus, in addition to its previously documented role in promoting CD4-lineage gene-expression, Gata3 represses CD8-lineage gene expression. These findings identify Gata3 as a critical pivot of CD4-CD8 lineage differentiation...
GATA3 controls Foxp3⁺ regulatory T cell fate during inflammation in miceElizabeth A Wohlfert
Mucosal Immunology Unit, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, Maryland, USA
J Clin Invest 121:4503-15. 2011..Overall, our work reveals what we believe to be a new facet in the complex role of GATA3 in T cells and highlights what may be a fundamental role in controlling Treg physiology during inflammation...
How are T(H)2-type immune responses initiated and amplified?William E Paul
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Nat Rev Immunol 10:225-35. 2010....
KLF13 sustains thymic memory-like CD8(+) T cells in BALB/c mice by regulating IL-4-generating invariant natural killer T cellsDazhi Lai
Laboratory of Cellular and Molecular Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
J Exp Med 208:1093-103. 2011..This work documents the impact of a small number of KLF13-dependent iNKT cells on the generation of memory-like CD8(+) T cells...
Molecular mechanisms of interleukin-4-induced up-regulation of type I collagen gene expression in murine fibroblastsTracy L McGaha
Department of Microbiology, Mount Sinai School of Medicine, One Gustave L Levy Place, New York, NY 10029, USA
Arthritis Rheum 48:2275-84. 2003..We therefore examined the effect of IL-4 on collagen synthesis in primary fibroblasts isolated from normal and TSK/+ mice, which spontaneously develop a scleroderma-like syndrome characterized by diffuse cutaneous hyperplasia...
Formation of IL-7Ralphahigh and IL-7Ralphalow CD8 T cells during infection is regulated by the opposing functions of GABPalpha and Gfi-1Anmol Chandele
Department of Immunobiology, Yale Medical School, New Haven, CT 06511, USA
J Immunol 180:5309-19. 2008....
IL-4 selectively enhances FcgammaRIII expression and signaling on mouse mast cellsHey Jin Chong
Department of Biology, Virginia Commonwealth University, Richmond, VA 23284-2012, USA
Cell Immunol 224:65-73. 2003..Selective regulation of mast cell FcgammaR by interleukin-4 could alter inflammatory IgG responses and subsequently disease severity and progression...
