Galectin-9 suppresses the generation of Th17, promotes the induction of regulatory T cells, and regulates experimental autoimmune arthritis
Abstract The effects of galectin-9 on a mouse collagen-induced arthritis (CIA) model were assessed to clarify whether galectin-9 suppresses CIA by regulating T cell immune responses. Galectin-9 suppressed CIA in a dose-dependent manner, and such suppression was observed even when treatment was start...
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| Veröffentlicht in: | Clinical immunology (Orlando, Fla.) Fla.), 2008-04, Vol.127 (1), p.78-88 |
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| creator | Seki, Masako Oomizu, Souichi Sakata, Ken-mei Sakata, Atsuko Arikawa, Tomohiro Watanabe, Kota Ito, Kanako Takeshita, Keisuke Niki, Toshiro Saita, Naoki Nishi, Nozomu Yamauchi, Akira Katoh, Shigeki Matsukawa, Akihiro Kuchroo, Vijay Hirashima, Mitsuomi |
| description | Abstract The effects of galectin-9 on a mouse collagen-induced arthritis (CIA) model were assessed to clarify whether galectin-9 suppresses CIA by regulating T cell immune responses. Galectin-9 suppressed CIA in a dose-dependent manner, and such suppression was observed even when treatment was started on 7 days after the booster, indicating its preventive and therapeutic effects. Galectin-9 induced the decreased levels of pro-inflammatory cytokines, IL-17, IL-12, and IFNγ in the joint. Galectin-9 induced the decreased number of CD4+ TIM-3+ T cells in peripheral blood. Galectin-9-deficient mice became susceptible to CIA may be by increased number of CD4+ TIM-3+ T cells and decreased number of Treg cells. We further found that galectin-9 induces differentiation of naive T cells to Treg cells, and it suppresses differentiation to Th17 cells in vitro . The present results suggested that galectin-9 ameliorates CIA by suppressing the generation of Th17, promoting the induction of regulatory T cells. |
| doi_str_mv | 10.1016/j.clim.2008.01.006 |
| format | Article |
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Galectin-9 suppressed CIA in a dose-dependent manner, and such suppression was observed even when treatment was started on 7 days after the booster, indicating its preventive and therapeutic effects. Galectin-9 induced the decreased levels of pro-inflammatory cytokines, IL-17, IL-12, and IFNγ in the joint. Galectin-9 induced the decreased number of CD4+ TIM-3+ T cells in peripheral blood. Galectin-9-deficient mice became susceptible to CIA may be by increased number of CD4+ TIM-3+ T cells and decreased number of Treg cells. We further found that galectin-9 induces differentiation of naive T cells to Treg cells, and it suppresses differentiation to Th17 cells in vitro . The present results suggested that galectin-9 ameliorates CIA by suppressing the generation of Th17, promoting the induction of regulatory T cells.</description><identifier>ISSN: 1521-6616</identifier><identifier>EISSN: 1521-7035</identifier><identifier>DOI: 10.1016/j.clim.2008.01.006</identifier><identifier>PMID: 18282810</identifier><identifier>CODEN: CLIIFY</identifier><language>eng</language><publisher>San Diego, CA: Elsevier Inc</publisher><subject>Allergy and Immunology ; Animals ; Arthritis, Experimental - immunology ; Arthritis, Experimental - metabolism ; Autoantigens - immunology ; Autoimmune Diseases - immunology ; Autoimmune Diseases - metabolism ; Biological and medical sciences ; Cell Differentiation - immunology ; Collagen - immunology ; Collagen-induced arthritis ; Diseases of the osteoarticular system ; Flow Cytometry ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; Galectin-9 ; Galectins - genetics ; Galectins - immunology ; Galectins - metabolism ; Humans ; Inflammatory joint diseases ; Interferon-gamma - metabolism ; Interleukin-12 - metabolism ; Interleukin-17 - metabolism ; Male ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Mice, Knockout ; Miscellaneous. Osteoarticular involvement in other diseases ; Pro-inflammatory cytokines ; Regulatory T cells ; Reverse Transcriptase Polymerase Chain Reaction ; Rodent ; T cell immunoglobulin- and mucin domain-containing molecule 3 ; T-Lymphocyte Subsets - cytology ; T-Lymphocyte Subsets - immunology ; T-Lymphocytes, Helper-Inducer - cytology ; T-Lymphocytes, Helper-Inducer - immunology ; T-Lymphocytes, Regulatory - cytology ; T-Lymphocytes, Regulatory - immunology ; Th1 ; Th17</subject><ispartof>Clinical immunology (Orlando, Fla.), 2008-04, Vol.127 (1), p.78-88</ispartof><rights>Elsevier Inc.</rights><rights>2008 Elsevier Inc.</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-d36fbd4d70d0b3613513a6ab2868ad1637599170bfeeea1aabb1900269074e203</citedby><cites>FETCH-LOGICAL-c470t-d36fbd4d70d0b3613513a6ab2868ad1637599170bfeeea1aabb1900269074e203</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1521661608000089$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20267382$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18282810$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Seki, Masako</creatorcontrib><creatorcontrib>Oomizu, Souichi</creatorcontrib><creatorcontrib>Sakata, Ken-mei</creatorcontrib><creatorcontrib>Sakata, Atsuko</creatorcontrib><creatorcontrib>Arikawa, Tomohiro</creatorcontrib><creatorcontrib>Watanabe, Kota</creatorcontrib><creatorcontrib>Ito, Kanako</creatorcontrib><creatorcontrib>Takeshita, Keisuke</creatorcontrib><creatorcontrib>Niki, Toshiro</creatorcontrib><creatorcontrib>Saita, Naoki</creatorcontrib><creatorcontrib>Nishi, Nozomu</creatorcontrib><creatorcontrib>Yamauchi, Akira</creatorcontrib><creatorcontrib>Katoh, Shigeki</creatorcontrib><creatorcontrib>Matsukawa, Akihiro</creatorcontrib><creatorcontrib>Kuchroo, Vijay</creatorcontrib><creatorcontrib>Hirashima, Mitsuomi</creatorcontrib><title>Galectin-9 suppresses the generation of Th17, promotes the induction of regulatory T cells, and regulates experimental autoimmune arthritis</title><title>Clinical immunology (Orlando, Fla.)</title><addtitle>Clin Immunol</addtitle><description>Abstract The effects of galectin-9 on a mouse collagen-induced arthritis (CIA) model were assessed to clarify whether galectin-9 suppresses CIA by regulating T cell immune responses. Galectin-9 suppressed CIA in a dose-dependent manner, and such suppression was observed even when treatment was started on 7 days after the booster, indicating its preventive and therapeutic effects. Galectin-9 induced the decreased levels of pro-inflammatory cytokines, IL-17, IL-12, and IFNγ in the joint. Galectin-9 induced the decreased number of CD4+ TIM-3+ T cells in peripheral blood. Galectin-9-deficient mice became susceptible to CIA may be by increased number of CD4+ TIM-3+ T cells and decreased number of Treg cells. We further found that galectin-9 induces differentiation of naive T cells to Treg cells, and it suppresses differentiation to Th17 cells in vitro . The present results suggested that galectin-9 ameliorates CIA by suppressing the generation of Th17, promoting the induction of regulatory T cells.</description><subject>Allergy and Immunology</subject><subject>Animals</subject><subject>Arthritis, Experimental - immunology</subject><subject>Arthritis, Experimental - metabolism</subject><subject>Autoantigens - immunology</subject><subject>Autoimmune Diseases - immunology</subject><subject>Autoimmune Diseases - metabolism</subject><subject>Biological and medical sciences</subject><subject>Cell Differentiation - immunology</subject><subject>Collagen - immunology</subject><subject>Collagen-induced arthritis</subject><subject>Diseases of the osteoarticular system</subject><subject>Flow Cytometry</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fundamental immunology</subject><subject>Galectin-9</subject><subject>Galectins - genetics</subject><subject>Galectins - immunology</subject><subject>Galectins - metabolism</subject><subject>Humans</subject><subject>Inflammatory joint diseases</subject><subject>Interferon-gamma - metabolism</subject><subject>Interleukin-12 - metabolism</subject><subject>Interleukin-17 - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Inbred DBA</subject><subject>Mice, Knockout</subject><subject>Miscellaneous. Osteoarticular involvement in other diseases</subject><subject>Pro-inflammatory cytokines</subject><subject>Regulatory T cells</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Rodent</subject><subject>T cell immunoglobulin- and mucin domain-containing molecule 3</subject><subject>T-Lymphocyte Subsets - cytology</subject><subject>T-Lymphocyte Subsets - immunology</subject><subject>T-Lymphocytes, Helper-Inducer - cytology</subject><subject>T-Lymphocytes, Helper-Inducer - immunology</subject><subject>T-Lymphocytes, Regulatory - cytology</subject><subject>T-Lymphocytes, Regulatory - immunology</subject><subject>Th1</subject><subject>Th17</subject><issn>1521-6616</issn><issn>1521-7035</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFks-K1TAUxosozjj6Ai4kG11N60naJi3IgAw6CgMuvK5Dmp7OzbVNapKK9xl8aVNuR8GFkkVC8vvOn3wny55TKChQ_vpQ6NFMBQNoCqAFAH-QndOa0VxAWT_czpxTfpY9CeEAADVj_HF2RhuWFoXz7OeNGlFHY_OWhGWePYaAgcQ9kju06FU0zhI3kN2eiksyeze5uAHG9ou-f_d4t4wqOn8kO6JxHMMlUba_v08S_DGjNxPaqEailujMNC0WifJx70004Wn2aFBjwGfbfpF9ef9ud_0hv_108_H67W2uKwEx70s-dH3VC-ihKzkta1oqrjrW8Eb1lJeiblsqoBsQUVGluo62AIy3ICpkUF5kr05xUzffFgxRTiasJSuLbglSQAU1rer_ggxEysN5AtkJ1N6F4HGQc-pU-aOkIFev5EGuXsnVKwlUJq-S6MUWfekm7P9INnMS8HIDVNBqHLyy2oTfHEstibJhiXtz4jB92neDXgZt0GrsjU_eyt6Zf9dx9Zc8IdakjF_xiOHgFm-THZLKwCTIz-tUrUMFTRooaNryFy93yK4</recordid><startdate>20080401</startdate><enddate>20080401</enddate><creator>Seki, Masako</creator><creator>Oomizu, Souichi</creator><creator>Sakata, Ken-mei</creator><creator>Sakata, Atsuko</creator><creator>Arikawa, Tomohiro</creator><creator>Watanabe, Kota</creator><creator>Ito, Kanako</creator><creator>Takeshita, Keisuke</creator><creator>Niki, Toshiro</creator><creator>Saita, Naoki</creator><creator>Nishi, Nozomu</creator><creator>Yamauchi, Akira</creator><creator>Katoh, Shigeki</creator><creator>Matsukawa, Akihiro</creator><creator>Kuchroo, Vijay</creator><creator>Hirashima, Mitsuomi</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20080401</creationdate><title>Galectin-9 suppresses the generation of Th17, promotes the induction of regulatory T cells, and regulates experimental autoimmune arthritis</title><author>Seki, Masako ; Oomizu, Souichi ; Sakata, Ken-mei ; Sakata, Atsuko ; Arikawa, Tomohiro ; Watanabe, Kota ; Ito, Kanako ; Takeshita, Keisuke ; Niki, Toshiro ; Saita, Naoki ; Nishi, Nozomu ; Yamauchi, Akira ; Katoh, Shigeki ; Matsukawa, Akihiro ; Kuchroo, Vijay ; Hirashima, Mitsuomi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-d36fbd4d70d0b3613513a6ab2868ad1637599170bfeeea1aabb1900269074e203</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Allergy and Immunology</topic><topic>Animals</topic><topic>Arthritis, Experimental - immunology</topic><topic>Arthritis, Experimental - metabolism</topic><topic>Autoantigens - immunology</topic><topic>Autoimmune Diseases - immunology</topic><topic>Autoimmune Diseases - metabolism</topic><topic>Biological and medical sciences</topic><topic>Cell Differentiation - immunology</topic><topic>Collagen - immunology</topic><topic>Collagen-induced arthritis</topic><topic>Diseases of the osteoarticular system</topic><topic>Flow Cytometry</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Fundamental immunology</topic><topic>Galectin-9</topic><topic>Galectins - genetics</topic><topic>Galectins - immunology</topic><topic>Galectins - metabolism</topic><topic>Humans</topic><topic>Inflammatory joint diseases</topic><topic>Interferon-gamma - metabolism</topic><topic>Interleukin-12 - metabolism</topic><topic>Interleukin-17 - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Inbred DBA</topic><topic>Mice, Knockout</topic><topic>Miscellaneous. 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Galectin-9 suppressed CIA in a dose-dependent manner, and such suppression was observed even when treatment was started on 7 days after the booster, indicating its preventive and therapeutic effects. Galectin-9 induced the decreased levels of pro-inflammatory cytokines, IL-17, IL-12, and IFNγ in the joint. Galectin-9 induced the decreased number of CD4+ TIM-3+ T cells in peripheral blood. Galectin-9-deficient mice became susceptible to CIA may be by increased number of CD4+ TIM-3+ T cells and decreased number of Treg cells. We further found that galectin-9 induces differentiation of naive T cells to Treg cells, and it suppresses differentiation to Th17 cells in vitro . The present results suggested that galectin-9 ameliorates CIA by suppressing the generation of Th17, promoting the induction of regulatory T cells.</abstract><cop>San Diego, CA</cop><pub>Elsevier Inc</pub><pmid>18282810</pmid><doi>10.1016/j.clim.2008.01.006</doi><tpages>11</tpages></addata></record> |
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| subjects | Allergy and Immunology Animals Arthritis, Experimental - immunology Arthritis, Experimental - metabolism Autoantigens - immunology Autoimmune Diseases - immunology Autoimmune Diseases - metabolism Biological and medical sciences Cell Differentiation - immunology Collagen - immunology Collagen-induced arthritis Diseases of the osteoarticular system Flow Cytometry Fundamental and applied biological sciences. Psychology Fundamental immunology Galectin-9 Galectins - genetics Galectins - immunology Galectins - metabolism Humans Inflammatory joint diseases Interferon-gamma - metabolism Interleukin-12 - metabolism Interleukin-17 - metabolism Male Medical sciences Mice Mice, Inbred C57BL Mice, Inbred DBA Mice, Knockout Miscellaneous. Osteoarticular involvement in other diseases Pro-inflammatory cytokines Regulatory T cells Reverse Transcriptase Polymerase Chain Reaction Rodent T cell immunoglobulin- and mucin domain-containing molecule 3 T-Lymphocyte Subsets - cytology T-Lymphocyte Subsets - immunology T-Lymphocytes, Helper-Inducer - cytology T-Lymphocytes, Helper-Inducer - immunology T-Lymphocytes, Regulatory - cytology T-Lymphocytes, Regulatory - immunology Th1 Th17 |
| title | Galectin-9 suppresses the generation of Th17, promotes the induction of regulatory T cells, and regulates experimental autoimmune arthritis |
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