Crucial role of interleukin-7 in T helper type 17 survival and expansion in autoimmune disease

Variation in the IL-7 receptor is associated with susceptibility to multiple sclerosis. Jingwu Zhang and his colleagues provide an explanation. They show that the cytokine IL-7 regulates the surival and proliferation of T helper type 17 cells—a cell type known to be involved in the pathogenesis of m...

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Published in	Nature medicine Vol. 16; no. 2; pp. 191 - 197
Main Authors	Liu, Xuebin, Leung, Stewart, Wang, Chunxia, Tan, Zhu, Wang, Ji, Guo, Taylor B, Fang, Lei, Zhao, Yonggang, Wan, Bing, Qin, Xia, Lu, Limin, Li, Runsheng, Pan, Heng, Song, Mingjuan, Liu, Ailian, Hong, Jian, Lu, Hongtao, Zhang, Jingwu Z
Format	Journal Article
Language	English
Published	New York Nature Publishing Group US 01.02.2010 Nature Publishing Group
Subjects	631/250/127/1213 631/250/1619/554/1898/1273 631/80/86 692/699/249/1313/1666 Animals Apoptosis Autoimmune diseases BAX protein Bcl-2 protein Biomedical and Life Sciences Biomedical research Biomedicine Cancer Research Care and treatment Cell Differentiation Cell survival Cytokines Development and progression Effector cells Encephalomyelitis Encephalomyelitis, Autoimmune, Experimental - immunology Experimental allergic encephalomyelitis Gene expression Health aspects Helper cells Infectious Diseases Interleukin 7 Interleukin-7 - immunology Interleukins Janus kinase Janus Kinases - metabolism Kinases Lymphocytes Lymphocytes T Medical schools Metabolic Diseases Mice Mice, Transgenic Molecular Medicine Multiple sclerosis Neurosciences Prevention Proteins Selectivity Signal transduction SOCS-1 protein Stat5 protein STAT5 Transcription Factor - metabolism Survival T-Lymphocytes, Helper-Inducer - cytology Transcription United States China
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ISSN	1078-8956 1546-170X 1546-170X
DOI	10.1038/nm.2077

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Abstract	Variation in the IL-7 receptor is associated with susceptibility to multiple sclerosis. Jingwu Zhang and his colleagues provide an explanation. They show that the cytokine IL-7 regulates the surival and proliferation of T helper type 17 cells—a cell type known to be involved in the pathogenesis of multiple sclerosis. The findings suggest that IL-7 antagonism could be useful in individuals with autoimmune diseases such as multiple sclerosis ( pages 166–168 ). Interleukin-7 receptor (IL-7R) is genetically associated with susceptibility to multiple sclerosis. Here we describe that IL-7 is essential for survival and expansion of pathogenic T helper type 17 (T H 17) cells in experimental autoimmune encephalomyelitis (EAE). IL-7 directly expanded effector T H 17 cells in EAE and human T H 17 cells from subjects with multiple sclerosis, whereas it was not required for T H 17 differentiation. IL-7R antagonism rendered differentiated T H 17 cells susceptible to apoptosis through the inhibition of Janus kinase–signal transducer and activator of transcription-5 (JAK-STAT5) pathway and altered expression of the prosurvival protein Bcl-2 and the proapoptotic protein Bax, leading to decreased severity of EAE. In contrast, T H 1 and regulatory T (T reg ) cells were less susceptible to or not affected by IL-7R antagonism in vivo . The selectivity was attributable to minimal expression of IL-7Rα in T reg cells and correlated with a high level of Socs1 (encoding suppressor of cytokine signaling-1) expression in T H 1 cells. The study reveals a unique, previously undescribed role of IL-7–IL-7R in T H 17 cell survival and expansion and has implications in the treatment of autoimmune disease.
AbstractList	Interleukin-7 receptor (IL-7R) is genetically associated with susceptibility to multiple sclerosis. Here we describe that IL-7 is essential for survival and expansion of pathogenic T helper type 17 ([T.sub.H]17) cells in experimental autoimmune encephalomyelitis (EAE). IL-7 directly expanded effector [T.sub.H]17 cells in EAE and human [T.sub.H]17 cells from subjects with multiple sclerosis, whereas it was not required for [T.sub.H]17 differentiation. IL-7R antagonism rendered differentiated [T.sub.H]17 cells susceptible to apoptosis through the inhibition of Janus kinase-signal transducer and activator of transcription-5 (JAK-STAT5) pathway and altered expression of the prosurvival protein Bcl-2 and the proapoptotic protein Bax, leading to decreased severity of EAE. In contrast, [T.sub.H]1 and regulatory T ([T.sub.reg]) cells were less susceptible to or not affected by IL-7R antagonism in vivo. The selectivity was attributable to minimal expression of IL-7Rα in [T.sub.reg] cells and correlated with a high level of Socs1 (encoding suppressor of cytokine signaling-1) expression in [T.sub.H]1 cells. The study reveals a unique, previously undescribed role of IL-7-IL-7R in [T.sub.H]17 cell survival and expansion and has implications in the treatment of autoimmune disease. Interleukin-7 receptor (IL-7R) is genetically associated with susceptibility to multiple sclerosis. Here we describe that IL-7 is essential for survival and expansion of pathogenic T helper type 17 (T(H)17) cells in experimental autoimmune encephalomyelitis (EAE). IL-7 directly expanded effector T(H)17 cells in EAE and human T(H)17 cells from subjects with multiple sclerosis, whereas it was not required for T(H)17 differentiation. IL-7R antagonism rendered differentiated T(H)17 cells susceptible to apoptosis through the inhibition of Janus kinase-signal transducer and activator of transcription-5 (JAK-STAT5) pathway and altered expression of the prosurvival protein Bcl-2 and the proapoptotic protein Bax, leading to decreased severity of EAE. In contrast, T(H)1 and regulatory T (T(reg)) cells were less susceptible to or not affected by IL-7R antagonism in vivo. The selectivity was attributable to minimal expression of IL-7Ralpha in T(reg) cells and correlated with a high level of Socs1 (encoding suppressor of cytokine signaling-1) expression in T(H)1 cells. The study reveals a unique, previously undescribed role of IL-7-IL-7R in T(H)17 cell survival and expansion and has implications in the treatment of autoimmune disease. Variation in the IL-7 receptor is associated with susceptibility to multiple sclerosis. Jingwu Zhang and his colleagues provide an explanation. They show that the cytokine IL-7 regulates the surival and proliferation of T helper type 17 cells--a cell type known to be involved in the pathogenesis of multiple sclerosis. The findings suggest that IL-7 antagonism could be useful in individuals with autoimmune diseases such as multiple sclerosis (( Interleukin-7 receptor (IL-7R) is genetically associated with susceptibility to multiple sclerosis. Here we describe that IL-7 is essential for survival and expansion of pathogenic T helper type 17 (T.sub.H17) cells in experimental autoimmune encephalomyelitis (EAE). IL-7 directly expanded effector T.sub.H17 cells in EAE and human T.sub.H17 cells from subjects with multiple sclerosis, whereas it was not required for T.sub.H17 differentiation. IL-7R antagonism rendered differentiated T.sub.H17 cells susceptible to apoptosis through the inhibition of Janus kinase-signal transducer and activator of transcription-5 (JAK-STAT5) pathway and altered expression of the prosurvival protein Bcl-2 and the proapoptotic protein Bax, leading to decreased severity of EAE. In contrast, T.sub.H1 and regulatory T (T.sub.reg) cells were less susceptible to or not affected by IL-7R antagonism in vivo. The selectivity was attributable to minimal expression of IL-7R[alpha] in T.sub.reg cells and correlated with a high level of Socs1 (encoding suppressor of cytokine signaling-1) expression in T.sub.H1 cells. The study reveals a unique, previously undescribed role of IL-7-IL-7R in T.sub.H17 cell survival and expansion and has implications in the treatment of autoimmune disease. Interleukin-7 receptor (IL-7R) is genetically associated with susceptibility to multiple sclerosis. Here we describe that IL-7 is essential for survival and expansion of pathogenic T helper type 17 (TH17) cells in experimental autoimmune encephalomyelitis (EAE). IL-7 directly expanded effector TH17 cells in EAE and human TH17 cells from subjects with multiple sclerosis, whereas it was not required for TH17 differentiation. IL-7R antagonism rendered differentiated TH17 cells susceptible to apoptosis through the inhibition of Janus kinase–signal transducer and activator of transcription-5 (JAK-STAT5) pathway and altered expression of the prosurvival protein Bcl-2 and the proapoptotic protein Bax, leading to decreased severity of EAE. In contrast, TH1 and regulatory T (Treg) cells were less susceptible to or not affected by IL-7R antagonism in vivo. The selectivity was attributable to minimal expression of IL-7Rα in Treg cells and correlated with a high level of Socs1 (encoding suppressor of cytokine signaling-1) expression in TH1 cells. The study reveals a unique, previously undescribed role of IL-7–IL-7R in TH17 cell survival and expansion and has implications in the treatment of autoimmune disease. Interleukin-7 receptor (IL-7R) is genetically associated with susceptibility to multiple sclerosis. Here we describe that IL-7 is essential for survival and expansion of pathogenic T helper type 17 (T sub(H)17) cells in experimental autoimmune encephalomyelitis (EAE). IL-7 directly expanded effector T sub(H)17 cells in EAE and human T sub(H)17 cells from subjects with multiple sclerosis, whereas it was not required for T sub(H)17 differentiation. IL-7R antagonism rendered differentiated T sub(H)17 cells susceptible to apoptosis through the inhibition of Janus kinase-signal transducer and activator of transcription-5 (JAK-STAT5) pathway and altered expression of the prosurvival protein Bcl-2 and the proapoptotic protein Bax, leading to decreased severity of EAE. In contrast, T sub(H)1 and regulatory T (T sub(reg)) cells were less susceptible to or not affected by IL-7R antagonism in vivo. The selectivity was attributable to minimal expression of IL-7Ra in T sub(reg) cells and correlated with a high level of Socs1 (encoding suppressor of cytokine signaling-1) expression in T sub(H)1 cells. The study reveals a unique, previously undescribed role of IL-7-IL-7R in T sub(H)17 cell survival and expansion and has implications in the treatment of autoimmune disease. Variation in the IL-7 receptor is associated with susceptibility to multiple sclerosis. Jingwu Zhang and his colleagues provide an explanation. They show that the cytokine IL-7 regulates the surival and proliferation of T helper type 17 cells—a cell type known to be involved in the pathogenesis of multiple sclerosis. The findings suggest that IL-7 antagonism could be useful in individuals with autoimmune diseases such as multiple sclerosis ( pages 166–168 ). Interleukin-7 receptor (IL-7R) is genetically associated with susceptibility to multiple sclerosis. Here we describe that IL-7 is essential for survival and expansion of pathogenic T helper type 17 (T H 17) cells in experimental autoimmune encephalomyelitis (EAE). IL-7 directly expanded effector T H 17 cells in EAE and human T H 17 cells from subjects with multiple sclerosis, whereas it was not required for T H 17 differentiation. IL-7R antagonism rendered differentiated T H 17 cells susceptible to apoptosis through the inhibition of Janus kinase–signal transducer and activator of transcription-5 (JAK-STAT5) pathway and altered expression of the prosurvival protein Bcl-2 and the proapoptotic protein Bax, leading to decreased severity of EAE. In contrast, T H 1 and regulatory T (T reg ) cells were less susceptible to or not affected by IL-7R antagonism in vivo . The selectivity was attributable to minimal expression of IL-7Rα in T reg cells and correlated with a high level of Socs1 (encoding suppressor of cytokine signaling-1) expression in T H 1 cells. The study reveals a unique, previously undescribed role of IL-7–IL-7R in T H 17 cell survival and expansion and has implications in the treatment of autoimmune disease. Interleukin-7 receptor (IL-7R) is genetically associated with susceptibility to multiple sclerosis. Here we describe that IL-7 is essential for survival and expansion of pathogenic T helper type 17 (T(H)17) cells in experimental autoimmune encephalomyelitis (EAE). IL-7 directly expanded effector T(H)17 cells in EAE and human T(H)17 cells from subjects with multiple sclerosis, whereas it was not required for T(H)17 differentiation. IL-7R antagonism rendered differentiated T(H)17 cells susceptible to apoptosis through the inhibition of Janus kinase-signal transducer and activator of transcription-5 (JAK-STAT5) pathway and altered expression of the prosurvival protein Bcl-2 and the proapoptotic protein Bax, leading to decreased severity of EAE. In contrast, T(H)1 and regulatory T (T(reg)) cells were less susceptible to or not affected by IL-7R antagonism in vivo. The selectivity was attributable to minimal expression of IL-7Ralpha in T(reg) cells and correlated with a high level of Socs1 (encoding suppressor of cytokine signaling-1) expression in T(H)1 cells. The study reveals a unique, previously undescribed role of IL-7-IL-7R in T(H)17 cell survival and expansion and has implications in the treatment of autoimmune disease. [PUBLICATION ABSTRACT] Variation in the IL-7 receptor is associated with susceptibility to multiple sclerosis. Jingwu Zhang and his colleagues provide an explanation. They show that the cytokine IL-7 regulates the surival and proliferation of T helper type 17 cells--a cell type known to be involved in the pathogenesis of multiple sclerosis. The findings suggest that IL-7 antagonism could be useful in individuals with autoimmune diseases such as multiple sclerosis ((https://www.nature.com/articles/nm0210-166)). Interleukin-7 receptor (IL-7R) is genetically associated with susceptibility to multiple sclerosis. Here we describe that IL-7 is essential for survival and expansion of pathogenic T helper type 17 (T(H)17) cells in experimental autoimmune encephalomyelitis (EAE). IL-7 directly expanded effector T(H)17 cells in EAE and human T(H)17 cells from subjects with multiple sclerosis, whereas it was not required for T(H)17 differentiation. IL-7R antagonism rendered differentiated T(H)17 cells susceptible to apoptosis through the inhibition of Janus kinase-signal transducer and activator of transcription-5 (JAK-STAT5) pathway and altered expression of the prosurvival protein Bcl-2 and the proapoptotic protein Bax, leading to decreased severity of EAE. In contrast, T(H)1 and regulatory T (T(reg)) cells were less susceptible to or not affected by IL-7R antagonism in vivo. The selectivity was attributable to minimal expression of IL-7Ralpha in T(reg) cells and correlated with a high level of Socs1 (encoding suppressor of cytokine signaling-1) expression in T(H)1 cells. The study reveals a unique, previously undescribed role of IL-7-IL-7R in T(H)17 cell survival and expansion and has implications in the treatment of autoimmune disease.Interleukin-7 receptor (IL-7R) is genetically associated with susceptibility to multiple sclerosis. Here we describe that IL-7 is essential for survival and expansion of pathogenic T helper type 17 (T(H)17) cells in experimental autoimmune encephalomyelitis (EAE). IL-7 directly expanded effector T(H)17 cells in EAE and human T(H)17 cells from subjects with multiple sclerosis, whereas it was not required for T(H)17 differentiation. IL-7R antagonism rendered differentiated T(H)17 cells susceptible to apoptosis through the inhibition of Janus kinase-signal transducer and activator of transcription-5 (JAK-STAT5) pathway and altered expression of the prosurvival protein Bcl-2 and the proapoptotic protein Bax, leading to decreased severity of EAE. In contrast, T(H)1 and regulatory T (T(reg)) cells were less susceptible to or not affected by IL-7R antagonism in vivo. The selectivity was attributable to minimal expression of IL-7Ralpha in T(reg) cells and correlated with a high level of Socs1 (encoding suppressor of cytokine signaling-1) expression in T(H)1 cells. The study reveals a unique, previously undescribed role of IL-7-IL-7R in T(H)17 cell survival and expansion and has implications in the treatment of autoimmune disease.
Audience	Academic
Author	Wan, Bing Wang, Ji Tan, Zhu Lu, Hongtao Li, Runsheng Guo, Taylor B Song, Mingjuan Lu, Limin Hong, Jian Leung, Stewart Wang, Chunxia Zhao, Yonggang Liu, Ailian Zhang, Jingwu Z Qin, Xia Liu, Xuebin Pan, Heng Fang, Lei
Author_xml	– sequence: 1 givenname: Xuebin surname: Liu fullname: Liu, Xuebin organization: Department of Neuroimmunology, GlaxoSmithKline Research and Development Center – sequence: 2 givenname: Stewart surname: Leung fullname: Leung, Stewart organization: Department of Neuroimmunology, GlaxoSmithKline Research and Development Center – sequence: 3 givenname: Chunxia surname: Wang fullname: Wang, Chunxia organization: Department of Neuroimmunology, GlaxoSmithKline Research and Development Center – sequence: 4 givenname: Zhu surname: Tan fullname: Tan, Zhu organization: Department of Neuroimmunology, GlaxoSmithKline Research and Development Center – sequence: 5 givenname: Ji surname: Wang fullname: Wang, Ji organization: Department of Neuroimmunology, GlaxoSmithKline Research and Development Center – sequence: 6 givenname: Taylor B surname: Guo fullname: Guo, Taylor B organization: Department of Neuroimmunology, GlaxoSmithKline Research and Development Center – sequence: 7 givenname: Lei surname: Fang fullname: Fang, Lei organization: Department of Neuroimmunology, GlaxoSmithKline Research and Development Center – sequence: 8 givenname: Yonggang surname: Zhao fullname: Zhao, Yonggang organization: Department of Neuroimmunology, GlaxoSmithKline Research and Development Center – sequence: 9 givenname: Bing surname: Wan fullname: Wan, Bing organization: Department of Neuroimmunology, GlaxoSmithKline Research and Development Center – sequence: 10 givenname: Xia surname: Qin fullname: Qin, Xia organization: Department of Neuroimmunology, GlaxoSmithKline Research and Development Center – sequence: 11 givenname: Limin surname: Lu fullname: Lu, Limin organization: Department of Neuroimmunology, GlaxoSmithKline Research and Development Center – sequence: 12 givenname: Runsheng surname: Li fullname: Li, Runsheng organization: Department of Neuroimmunology, GlaxoSmithKline Research and Development Center – sequence: 13 givenname: Heng surname: Pan fullname: Pan, Heng organization: Department of Neuroimmunology, GlaxoSmithKline Research and Development Center – sequence: 14 givenname: Mingjuan surname: Song fullname: Song, Mingjuan organization: Department of Neuroimmunology, GlaxoSmithKline Research and Development Center – sequence: 15 givenname: Ailian surname: Liu fullname: Liu, Ailian organization: Department of Neuroimmunology, GlaxoSmithKline Research and Development Center – sequence: 16 givenname: Jian surname: Hong fullname: Hong, Jian organization: Department of Neurology, Baylor College of Medicine – sequence: 17 givenname: Hongtao surname: Lu fullname: Lu, Hongtao organization: Department of Neuroimmunology, GlaxoSmithKline Research and Development Center – sequence: 18 givenname: Jingwu Z surname: Zhang fullname: Zhang, Jingwu Z email: jingwu.z.zang@gsk.com organization: Department of Neuroimmunology, GlaxoSmithKline Research and Development Center
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Snippet	Variation in the IL-7 receptor is associated with susceptibility to multiple sclerosis. Jingwu Zhang and his colleagues provide an explanation. They show that... Interleukin-7 receptor (IL-7R) is genetically associated with susceptibility to multiple sclerosis. Here we describe that IL-7 is essential for survival and...
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SubjectTerms	631/250/127/1213 631/250/1619/554/1898/1273 631/80/86 692/699/249/1313/1666 Animals Apoptosis Autoimmune diseases BAX protein Bcl-2 protein Biomedical and Life Sciences Biomedical research Biomedicine Cancer Research Care and treatment Cell Differentiation Cell survival Cytokines Development and progression Effector cells Encephalomyelitis Encephalomyelitis, Autoimmune, Experimental - immunology Experimental allergic encephalomyelitis Gene expression Health aspects Helper cells Infectious Diseases Interleukin 7 Interleukin-7 - immunology Interleukins Janus kinase Janus Kinases - metabolism Kinases Lymphocytes Lymphocytes T Medical schools Metabolic Diseases Mice Mice, Transgenic Molecular Medicine Multiple sclerosis Neurosciences Prevention Proteins Selectivity Signal transduction SOCS-1 protein Stat5 protein STAT5 Transcription Factor - metabolism Survival T-Lymphocytes, Helper-Inducer - cytology Transcription
Title	Crucial role of interleukin-7 in T helper type 17 survival and expansion in autoimmune disease
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