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Article ; Online: Intricacies of TGF-β signaling in Treg and Th17 cell biology.

Wang, Junying / Zhao, Xingqi / Wan, Yisong Y

2023 Volume 20, Issue 9, Page(s) 1002–1022

Abstract: Balanced immunity is pivotal for health and homeostasis. ... ...

Abstract	Balanced immunity is pivotal for health and homeostasis. CD4
MeSH term(s)	Th17 Cells ; T-Lymphocytes, Regulatory ; Signal Transduction ; Transforming Growth Factor beta/metabolism ; Autoimmunity
Chemical Substances	Transforming Growth Factor beta
Language	English
Publishing date	2023-05-23
Publishing country	China
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2435097-7
ISSN	2042-0226 ; 1672-7681
ISSN (online)	2042-0226
ISSN	1672-7681
DOI	10.1038/s41423-023-01036-7
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: SKI Expression Suppresses Pathogenic Th17 Cell Response and Mitigates Experimental Autoimmune Encephalomyelitis.

Li, Ping / Guo, Zengli / Wan, Yisong Y

Frontiers in immunology

2021 Volume 12, Page(s) 707899

Abstract: Pathogenic Th17 cells are critically involved in many autoimmune diseases, while non-pathogenic Th17 cells are more immune regulatory. Understanding the mechanisms of the induction and maintenance of pathogenic Th17 cells will benefit the development of ... ...

Abstract	Pathogenic Th17 cells are critically involved in many autoimmune diseases, while non-pathogenic Th17 cells are more immune regulatory. Understanding the mechanisms of the induction and maintenance of pathogenic Th17 cells will benefit the development of therapeutic treatments of related diseases. We have shown that the transforming growth factor-β (TGFβ) induced SKI degradation and dissociation from Smad4 complex is a prerequisite for TGFβ-induced Th17 cell differentiation. However, it is unclear whether and how SKI regulates pathogenic Th17 differentiation, which does not require TGFβ cytokine. Here we showed that SKI expression was downregulated during pathogenic Th17 cell differentiation and the ectopic expression of SKI abrogated the differentiation of pathogenic Th17 cells. Functionally, using a knock-in mouse model, we found ectopic SKI expression specifically in T cells prevented myelin oligodendrocyte glycoprotein peptide (MOG
MeSH term(s)	Animals ; Cell Differentiation/immunology ; DNA-Binding Proteins/immunology ; DNA-Binding Proteins/metabolism ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Mice ; Mice, Inbred C57BL ; Proto-Oncogene Proteins/immunology ; Proto-Oncogene Proteins/metabolism ; Th17 Cells/immunology ; Th17 Cells/pathology ; Transforming Growth Factor beta/metabolism
Chemical Substances	DNA-Binding Proteins ; Proto-Oncogene Proteins ; Ski protein, mouse ; Transforming Growth Factor beta
Language	English
Publishing date	2021-07-15
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.707899
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Article ; Online: GATA3: a master of many trades in immune regulation.

Wan, Yisong Y

Trends in immunology

2014 Volume 35, Issue 6, Page(s) 233–242

Abstract: GATA3 has conventionally been regarded as a transcription factor that drives the differentiation of T helper (Th) 2 cells. Increasing evidence points to a function for GATA3 beyond controlling Th2 differentiation. GATA3 regulates T cell development, ... ...

Abstract	GATA3 has conventionally been regarded as a transcription factor that drives the differentiation of T helper (Th) 2 cells. Increasing evidence points to a function for GATA3 beyond controlling Th2 differentiation. GATA3 regulates T cell development, proliferation, and maintenance. Furthermore, recent studies have demonstrated important roles for GATA3 in innate lymphoid cells. Thus, GATA3 emerges as a factor with diverse functions in immune regulation, which are in some cases cell-type specific and in others shared by multiple cell types. Here, I discuss recent discoveries and the current understanding of the functions of GATA3 in immune regulation.
MeSH term(s)	Adaptive Immunity ; Animals ; GATA3 Transcription Factor/genetics ; GATA3 Transcription Factor/metabolism ; Gene Expression Regulation ; Humans ; Immunity/physiology ; Immunity, Innate ; Lymphocyte Activation ; Lymphocyte Subsets/immunology ; Lymphocyte Subsets/metabolism ; Signal Transduction
Chemical Substances	GATA3 Transcription Factor
Language	English
Publishing date	2014-04-28
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2036831-8
ISSN	1471-4981 ; 1471-4906
ISSN (online)	1471-4981
ISSN	1471-4906
DOI	10.1016/j.it.2014.04.002
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Article ; Online: SKI and SMAD4 are essential for IL-21-induced Th17 differentiation.

Zhang, Song / Zhang, Ge / Wan, Yisong Y

Molecular immunology

2019 Volume 114, Page(s) 260–268

Abstract: Th17 cells are essential for the pathogenesis of inflammatory and autoimmune diseases. In the presence of TGF-β, the differentiation of Th17 cells can be induced by inflammatory cytokines, especially IL-6, which is mainly produced by antigen presenting ... ...

Abstract	Th17 cells are essential for the pathogenesis of inflammatory and autoimmune diseases. In the presence of TGF-β, the differentiation of Th17 cells can be induced by inflammatory cytokines, especially IL-6, which is mainly produced by antigen presenting cells (APCs); or IL-21, which is derived from T cells. IL-21 is required for IL-6-induced Th17 cell differentiation. However, the key regulators and underlying mechanisms for IL-21-induced Th17 differentiation is still elusive. Here we show that SMAD4 is a key regulator in IL-21-induced Th17 differentiation. SMAD4 deficient naïve T cells can differentiate into Th17 cells in the absence of TGF-β signaling, and these Th17 cells are pathogenic during EAE. SMAD4 represses Rorc mRNA transcription to constrain IL-21-induced Th17 differentiation in the absence of TGF-β signaling. While in the presence of TGF-β, SMAD4 losses its suppressive ability due to the degradation of SKI. Mutation of Y429A or A432E on SMAD4 disrupts the interaction of SKI from SMAD4 and eliminates SMAD4 mediated suppression of Th17 differentiation. SMAD4 is indispensable for SKI binding to Rorc promoter region to regulate Th17 differentiation. Moreover, activin can induce Th17 differentiation in combination with IL-21, and the process is also subjected to the control of SKI and SMAD4. This study therefore elucidates critical mechanism for IL-21-induced Th17 differentiation to indicate SKI and SMAD4 as potential therapeutic targets for treating autoimmune diseases.
MeSH term(s)	Animals ; Autoimmune Diseases/immunology ; Cell Differentiation/immunology ; Cytokines/immunology ; Inflammation/immunology ; Interleukins/immunology ; Mice ; Mice, Inbred C57BL ; Signal Transduction/immunology ; Smad4 Protein/immunology ; Th17 Cells/immunology ; Transforming Growth Factor beta/immunology
Chemical Substances	Cytokines ; Interleukins ; Smad4 Protein ; Smad4 protein, mouse ; Transforming Growth Factor beta ; interleukin-21 (MKM3CA6LT1)
Language	English
Publishing date	2019-08-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	424427-8
ISSN	1872-9142 ; 0161-5890
ISSN (online)	1872-9142
ISSN	0161-5890
DOI	10.1016/j.molimm.2019.07.029
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Zs.A 166: Show issues

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Article ; Online: CD200

Wang, Xinxin / Zha, Haoran / Wu, Wei / Yuan, Ting / Xie, Shuanglong / Jin, Zheng / Long, Haixia / Yang, Fei / Wang, Zhongyu / Zhang, Anmei / Gao, Jianbao / Jiang, Ying / Wang, Lujing / Hu, Chunyan / Wan, Yisong Y / Li, Qi-Jing / Symonds, Alistair L J / Jia, Qingzhu / Zhu, Bo

Science translational medicine

2023 Volume 15, Issue 679, Page(s) eabn5029

Abstract: Anti-PD-1/PD-L1 therapy, either by anti-PD-1 antibody or anti-PD-L1 antibody, has efficacy by reinvigorating tumor-infiltrating ... ...

Abstract	Anti-PD-1/PD-L1 therapy, either by anti-PD-1 antibody or anti-PD-L1 antibody, has efficacy by reinvigorating tumor-infiltrating CD8
MeSH term(s)	Animals ; Mice ; T-Lymphocytes, Cytotoxic ; CD8-Positive T-Lymphocytes ; Tumor Microenvironment ; Neoplasms/therapy ; Immunotherapy ; B7-H1 Antigen ; Lymphocytes, Tumor-Infiltrating
Chemical Substances	B7-H1 Antigen
Language	English
Publishing date	2023-01-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2518854-9
ISSN	1946-6242 ; 1946-6234
ISSN (online)	1946-6242
ISSN	1946-6234
DOI	10.1126/scitranslmed.abn5029
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Zs.A 6941: Show issues

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Article ; Online: Regulatory T cells: immune suppression and beyond.

Wan, Yisong Y

Cellular & molecular immunology

2010 Volume 7, Issue 3, Page(s) 204–210

Abstract: Foxp3-expressing regulatory T cells (Tregs) were originally identified as critical in maintaining self-tolerance and immune homeostasis. The immunosuppressive functions of Tregs are widely acknowledged and have been extensively studied. Recent studies ... ...

Abstract	Foxp3-expressing regulatory T cells (Tregs) were originally identified as critical in maintaining self-tolerance and immune homeostasis. The immunosuppressive functions of Tregs are widely acknowledged and have been extensively studied. Recent studies have revealed many diverse roles of Tregs in shaping the immune system and the inflammatory response. This review will discuss our efforts as well as the efforts of others towards understanding the multifaceted function of Tregs in immune regulation.
MeSH term(s)	Animals ; Homeostasis ; Humans ; Immune Tolerance ; Inflammation/immunology ; T-Lymphocytes, Regulatory/immunology
Language	English
Publishing date	2010-04-12
Publishing country	China
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2435097-7
ISSN	2042-0226 ; 1672-7681
ISSN (online)	2042-0226
ISSN	1672-7681
DOI	10.1038/cmi.2010.20
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Article: Immune Cell Metabolism in Tumor Microenvironment.

Li, Yongsheng / Wan, Yisong Y / Zhu, Bo

Advances in experimental medicine and biology

2017 Volume 1011, Page(s) 163–196

Abstract: Tumor microenvironment (TME) is composed of tumor cells, immune cells, cytokines, extracellular matrix, etc. The immune system and the metabolisms of glucose, lipids, amino acids, and nucleotides are integrated in the tumorigenesis and development. ... ...

Abstract	Tumor microenvironment (TME) is composed of tumor cells, immune cells, cytokines, extracellular matrix, etc. The immune system and the metabolisms of glucose, lipids, amino acids, and nucleotides are integrated in the tumorigenesis and development. Cancer cells and immune cells show metabolic reprogramming in the TME, which intimately links immune cell functions and edits tumor immunology. Recent findings in immune cell metabolism hold the promising possibilities toward clinical therapeutics for treating cancer. This chapter introduces the updated understandings of metabolic reprogramming of immune cells in the TME and suggests new directions in manipulation of immune responses for cancer diagnosis and therapy.
MeSH term(s)	Carcinogenesis ; Cell Transformation, Neoplastic ; Humans ; Immune System/metabolism ; Neoplasms/immunology ; Tumor Microenvironment
Language	English
Publishing date	2017-09-05
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-94-024-1170-6_5
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: SKI and SMAD4 are essential for IL-21-induced Th17 differentiation

Zhang, Song / Zhang, Ge / Wan, Yisong Y

Molecular immunology. 2019 Oct., v. 114

2019

Abstract	Th17 cells are essential for the pathogenesis of inflammatory and autoimmune diseases. In the presence of TGF-β, the differentiation of Th17 cells can be induced by inflammatory cytokines, especially IL-6, which is mainly produced by antigen presenting cells (APCs); or IL-21, which is derived from T cells. IL-21 is required for IL-6-induced Th17 cell differentiation. However, the key regulators and underlying mechanisms for IL-21-induced Th17 differentiation is still elusive. Here we show that SMAD4 is a key regulator in IL-21-induced Th17 differentiation. SMAD4 deficient naïve T cells can differentiate into Th17 cells in the absence of TGF-β signaling, and these Th17 cells are pathogenic during EAE. SMAD4 represses Rorc mRNA transcription to constrain IL-21-induced Th17 differentiation in the absence of TGF-β signaling. While in the presence of TGF-β, SMAD4 losses its suppressive ability due to the degradation of SKI. Mutation of Y429A or A432E on SMAD4 disrupts the interaction of SKI from SMAD4 and eliminates SMAD4 mediated suppression of Th17 differentiation. SMAD4 is indispensable for SKI binding to Rorc promoter region to regulate Th17 differentiation. Moreover, activin can induce Th17 differentiation in combination with IL-21, and the process is also subjected to the control of SKI and SMAD4. This study therefore elucidates critical mechanism for IL-21-induced Th17 differentiation to indicate SKI and SMAD4 as potential therapeutic targets for treating autoimmune diseases.
Keywords	T-lymphocytes ; antigen-presenting cells ; autoimmune diseases ; cell differentiation ; interleukin-21 ; interleukin-6 ; messenger RNA ; mutation ; pathogenesis ; promoter regions ; therapeutics ; transcription (genetics) ; transforming growth factor beta
Language	English
Dates of publication	2019-10
Size	p. 260-268.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	424427-8
ISSN	1872-9142 ; 0161-5890
ISSN (online)	1872-9142
ISSN	0161-5890
DOI	10.1016/j.molimm.2019.07.029
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Multi-tasking of helper T cells.

Wan, Yisong Y

Immunology

2010 Volume 130, Issue 2, Page(s) 166–171

Abstract: CD4 T helper cells (Th) are critical in combating pathogens and maintaining immune homeostasis. Since the establishment of the Th1-Th2 paradigm in the 1980s, many types of specialized Th cells, including Th1, Th2, Th17, Th9, follicular helper T and ... ...

Abstract	CD4 T helper cells (Th) are critical in combating pathogens and maintaining immune homeostasis. Since the establishment of the Th1-Th2 paradigm in the 1980s, many types of specialized Th cells, including Th1, Th2, Th17, Th9, follicular helper T and regulatory T, have been identified. We have become accustomed to the idea that different Th cells are 'committed' to their paths but recent emerging evidence suggests that under certain conditions, seemingly committed Th cells possess plasticity and may convert into other types of effector cells. In this review, we will first introduce the major sub-types of Th cells that are involved in immune regulation. Then, we will describe in detail the inter-convertibility of Th cells among different sub-types under in vitro and in vivo conditions. Finally, we will discuss our current understanding of the underlying mechanisms on how a particular type of Th cells may convert into other types of Th cells.
MeSH term(s)	Animals ; Homeostasis/physiology ; Humans ; T-Lymphocytes, Regulatory/immunology ; Th1 Cells/immunology ; Th2 Cells/immunology
Language	English
Publishing date	2010-06-14
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	80124-0
ISSN	1365-2567 ; 0019-2805 ; 0953-4954
ISSN (online)	1365-2567
ISSN	0019-2805 ; 0953-4954
DOI	10.1111/j.1365-2567.2010.03289.x
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Ud II Zs.181: Show issues

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Article ; Online: Radiation-induced eosinophils improve cytotoxic T lymphocyte recruitment and response to immunotherapy.

Cheng, Jia-Nan / Luo, Wen / Sun, Chengdu / Jin, Zheng / Zeng, Xianghua / Alexander, Peter B / Gong, Zhihua / Xia, Xin / Ding, Xiaofang / Xu, Shouxia / Zou, Ping / Wan, Yisong Y / Jia, Qingzhu / Li, Qi-Jing / Zhu, Bo

Science advances

2021 Volume 7, Issue 5

Abstract: The efficacy of cancer immunotherapy is dictated by ... ...

Abstract	The efficacy of cancer immunotherapy is dictated by CD8
Language	English
Publishing date	2021-01-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.abc7609
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