Myeloid-derived suppressor cells play crucial roles in the regulation of mouse collagen-induced arthritis
Myeloid-derived suppressor cells (MDSCs) are of myeloid origin and are able to suppress T cell responses. The role of MDSCs in autoimmune diseases remains controversial, and little is known about the function of MDSCs in autoimmune arthritis. In this study, we clarify that MDSCs play crucial roles i...
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| Veröffentlicht in: | The Journal of immunology (1950) 2013-08, Vol.191 (3), p.1073-1081 |
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| container_title | The Journal of immunology (1950) |
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| creator | Fujii, Wataru Ashihara, Eishi Hirai, Hideyo Nagahara, Hidetake Kajitani, Naoko Fujioka, Kazuki Murakami, Ken Seno, Takahiro Yamamoto, Aihiro Ishino, Hidetaka Kohno, Masataka Maekawa, Taira Kawahito, Yutaka |
| description | Myeloid-derived suppressor cells (MDSCs) are of myeloid origin and are able to suppress T cell responses. The role of MDSCs in autoimmune diseases remains controversial, and little is known about the function of MDSCs in autoimmune arthritis. In this study, we clarify that MDSCs play crucial roles in the regulation of proinflammatory immune response in a collagen-induced arthritis (CIA) mouse model. MDSCs accumulated in the spleens of mice with CIA when arthritis severity peaked. These MDSCs inhibited the proliferation of CD4(+) T cells and their differentiation into Th17 cells in vitro. Moreover, MDSCs inhibited the production of IFN-γ, IL-2, TNF-α, and IL-6 by CD4(+) T cells in vitro, whereas they promoted the production of IL-10. Adoptive transfer of MDSCs reduced the severity of CIA in vivo, which was accompanied by a decrease in the number of CD4(+) T cells and Th17 cells in the draining lymph nodes. However, depletion of MDSCs abrogated the spontaneous improvement of CIA. In conclusion, MDSCs in CIA suppress the progression of CIA by inhibiting the proinflammatory immune response of CD4(+) T cells. These observations suggest that MDSCs play crucial roles in the regulation of autoimmune arthritis, which could be exploited in new cell-based therapies for human rheumatoid arthritis. |
| doi_str_mv | 10.4049/jimmunol.1203535 |
| format | Article |
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The role of MDSCs in autoimmune diseases remains controversial, and little is known about the function of MDSCs in autoimmune arthritis. In this study, we clarify that MDSCs play crucial roles in the regulation of proinflammatory immune response in a collagen-induced arthritis (CIA) mouse model. MDSCs accumulated in the spleens of mice with CIA when arthritis severity peaked. These MDSCs inhibited the proliferation of CD4(+) T cells and their differentiation into Th17 cells in vitro. Moreover, MDSCs inhibited the production of IFN-γ, IL-2, TNF-α, and IL-6 by CD4(+) T cells in vitro, whereas they promoted the production of IL-10. Adoptive transfer of MDSCs reduced the severity of CIA in vivo, which was accompanied by a decrease in the number of CD4(+) T cells and Th17 cells in the draining lymph nodes. However, depletion of MDSCs abrogated the spontaneous improvement of CIA. In conclusion, MDSCs in CIA suppress the progression of CIA by inhibiting the proinflammatory immune response of CD4(+) T cells. These observations suggest that MDSCs play crucial roles in the regulation of autoimmune arthritis, which could be exploited in new cell-based therapies for human rheumatoid arthritis.</description><identifier>ISSN: 0022-1767</identifier><identifier>EISSN: 1550-6606</identifier><identifier>DOI: 10.4049/jimmunol.1203535</identifier><identifier>PMID: 23804709</identifier><language>eng</language><publisher>United States</publisher><subject>Adoptive Transfer ; Animals ; Arthritis, Experimental - immunology ; Arthritis, Experimental - therapy ; CD4-Positive T-Lymphocytes - immunology ; CD4-Positive T-Lymphocytes - metabolism ; Cell Differentiation ; Cell Proliferation ; Collagen ; Inflammation - immunology ; Interferon-gamma - biosynthesis ; Interleukin-1 - biosynthesis ; Interleukin-2 - biosynthesis ; Interleukin-6 - biosynthesis ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred DBA ; Myeloid Cells - immunology ; Myeloid Cells - metabolism ; Th17 Cells - immunology ; Tumor Necrosis Factor-alpha - biosynthesis</subject><ispartof>The Journal of immunology (1950), 2013-08, Vol.191 (3), p.1073-1081</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c523t-c7947626f44996386a7cb512f8b5f08bce0b91b2f4a0f21d854c074ae047df3</citedby><cites>FETCH-LOGICAL-c523t-c7947626f44996386a7cb512f8b5f08bce0b91b2f4a0f21d854c074ae047df3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23804709$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fujii, Wataru</creatorcontrib><creatorcontrib>Ashihara, Eishi</creatorcontrib><creatorcontrib>Hirai, Hideyo</creatorcontrib><creatorcontrib>Nagahara, Hidetake</creatorcontrib><creatorcontrib>Kajitani, Naoko</creatorcontrib><creatorcontrib>Fujioka, Kazuki</creatorcontrib><creatorcontrib>Murakami, Ken</creatorcontrib><creatorcontrib>Seno, Takahiro</creatorcontrib><creatorcontrib>Yamamoto, Aihiro</creatorcontrib><creatorcontrib>Ishino, Hidetaka</creatorcontrib><creatorcontrib>Kohno, Masataka</creatorcontrib><creatorcontrib>Maekawa, Taira</creatorcontrib><creatorcontrib>Kawahito, Yutaka</creatorcontrib><title>Myeloid-derived suppressor cells play crucial roles in the regulation of mouse collagen-induced arthritis</title><title>The Journal of immunology (1950)</title><addtitle>J Immunol</addtitle><description>Myeloid-derived suppressor cells (MDSCs) are of myeloid origin and are able to suppress T cell responses. The role of MDSCs in autoimmune diseases remains controversial, and little is known about the function of MDSCs in autoimmune arthritis. In this study, we clarify that MDSCs play crucial roles in the regulation of proinflammatory immune response in a collagen-induced arthritis (CIA) mouse model. MDSCs accumulated in the spleens of mice with CIA when arthritis severity peaked. These MDSCs inhibited the proliferation of CD4(+) T cells and their differentiation into Th17 cells in vitro. Moreover, MDSCs inhibited the production of IFN-γ, IL-2, TNF-α, and IL-6 by CD4(+) T cells in vitro, whereas they promoted the production of IL-10. Adoptive transfer of MDSCs reduced the severity of CIA in vivo, which was accompanied by a decrease in the number of CD4(+) T cells and Th17 cells in the draining lymph nodes. However, depletion of MDSCs abrogated the spontaneous improvement of CIA. In conclusion, MDSCs in CIA suppress the progression of CIA by inhibiting the proinflammatory immune response of CD4(+) T cells. These observations suggest that MDSCs play crucial roles in the regulation of autoimmune arthritis, which could be exploited in new cell-based therapies for human rheumatoid arthritis.</description><subject>Adoptive Transfer</subject><subject>Animals</subject><subject>Arthritis, Experimental - immunology</subject><subject>Arthritis, Experimental - therapy</subject><subject>CD4-Positive T-Lymphocytes - immunology</subject><subject>CD4-Positive T-Lymphocytes - metabolism</subject><subject>Cell Differentiation</subject><subject>Cell Proliferation</subject><subject>Collagen</subject><subject>Inflammation - immunology</subject><subject>Interferon-gamma - biosynthesis</subject><subject>Interleukin-1 - biosynthesis</subject><subject>Interleukin-2 - biosynthesis</subject><subject>Interleukin-6 - biosynthesis</subject><subject>Lymphocyte Activation</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred DBA</subject><subject>Myeloid Cells - immunology</subject><subject>Myeloid Cells - metabolism</subject><subject>Th17 Cells - immunology</subject><subject>Tumor Necrosis Factor-alpha - biosynthesis</subject><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkb1PwzAUxC0EoqWwMyGPLCnPjuMkI6r4kooYYI8c57kYOXGwE6T-96Rqy8r0lruf3t0Rcs1gKUCUd1-2bcfOuyXjkGZpdkLmLMsgkRLkKZkDcJ6wXOYzchHjFwBI4OKczHhagMihnBP7ukXnbZM0GOwPNjSOfR8wRh-oRuci7Z3aUh1GbZWjwTuM1HZ0-EQacDM6NVjfUW9o68eIVHvn1Aa7xHbNqCeeCsNnsIONl-TMKBfx6nAX5P3x4WP1nKzfnl5W9-tEZzwdEp2XIpdcGiHKUqaFVLmuM8ZNUWcGiloj1CWruREKDGdNkQkNuVA4BWpMuiC3e2of_PeIcahaG3dBVIfTg9VUD5M8B8H_lwrGZAqiKCYp7KU6-BgDmqoPtlVhWzGodktUxyWqwxKT5eZAH-sWmz_Dsfr0F_GFh7M</recordid><startdate>20130801</startdate><enddate>20130801</enddate><creator>Fujii, Wataru</creator><creator>Ashihara, Eishi</creator><creator>Hirai, Hideyo</creator><creator>Nagahara, Hidetake</creator><creator>Kajitani, Naoko</creator><creator>Fujioka, Kazuki</creator><creator>Murakami, Ken</creator><creator>Seno, Takahiro</creator><creator>Yamamoto, Aihiro</creator><creator>Ishino, Hidetaka</creator><creator>Kohno, Masataka</creator><creator>Maekawa, Taira</creator><creator>Kawahito, Yutaka</creator><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>7X8</scope><scope>7T5</scope><scope>H94</scope></search><sort><creationdate>20130801</creationdate><title>Myeloid-derived suppressor cells play crucial roles in the regulation of mouse collagen-induced arthritis</title><author>Fujii, Wataru ; Ashihara, Eishi ; Hirai, Hideyo ; Nagahara, Hidetake ; Kajitani, Naoko ; Fujioka, Kazuki ; Murakami, Ken ; Seno, Takahiro ; Yamamoto, Aihiro ; Ishino, Hidetaka ; Kohno, Masataka ; Maekawa, Taira ; Kawahito, Yutaka</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c523t-c7947626f44996386a7cb512f8b5f08bce0b91b2f4a0f21d854c074ae047df3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adoptive Transfer</topic><topic>Animals</topic><topic>Arthritis, Experimental - immunology</topic><topic>Arthritis, Experimental - therapy</topic><topic>CD4-Positive T-Lymphocytes - immunology</topic><topic>CD4-Positive T-Lymphocytes - metabolism</topic><topic>Cell Differentiation</topic><topic>Cell Proliferation</topic><topic>Collagen</topic><topic>Inflammation - immunology</topic><topic>Interferon-gamma - biosynthesis</topic><topic>Interleukin-1 - biosynthesis</topic><topic>Interleukin-2 - biosynthesis</topic><topic>Interleukin-6 - biosynthesis</topic><topic>Lymphocyte Activation</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred DBA</topic><topic>Myeloid Cells - immunology</topic><topic>Myeloid Cells - metabolism</topic><topic>Th17 Cells - immunology</topic><topic>Tumor Necrosis Factor-alpha - biosynthesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fujii, Wataru</creatorcontrib><creatorcontrib>Ashihara, Eishi</creatorcontrib><creatorcontrib>Hirai, Hideyo</creatorcontrib><creatorcontrib>Nagahara, Hidetake</creatorcontrib><creatorcontrib>Kajitani, Naoko</creatorcontrib><creatorcontrib>Fujioka, Kazuki</creatorcontrib><creatorcontrib>Murakami, Ken</creatorcontrib><creatorcontrib>Seno, Takahiro</creatorcontrib><creatorcontrib>Yamamoto, Aihiro</creatorcontrib><creatorcontrib>Ishino, Hidetaka</creatorcontrib><creatorcontrib>Kohno, Masataka</creatorcontrib><creatorcontrib>Maekawa, Taira</creatorcontrib><creatorcontrib>Kawahito, Yutaka</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>The Journal of immunology (1950)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fujii, Wataru</au><au>Ashihara, Eishi</au><au>Hirai, Hideyo</au><au>Nagahara, Hidetake</au><au>Kajitani, Naoko</au><au>Fujioka, Kazuki</au><au>Murakami, Ken</au><au>Seno, Takahiro</au><au>Yamamoto, Aihiro</au><au>Ishino, Hidetaka</au><au>Kohno, Masataka</au><au>Maekawa, Taira</au><au>Kawahito, Yutaka</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Myeloid-derived suppressor cells play crucial roles in the regulation of mouse collagen-induced arthritis</atitle><jtitle>The Journal of immunology (1950)</jtitle><addtitle>J Immunol</addtitle><date>2013-08-01</date><risdate>2013</risdate><volume>191</volume><issue>3</issue><spage>1073</spage><epage>1081</epage><pages>1073-1081</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><abstract>Myeloid-derived suppressor cells (MDSCs) are of myeloid origin and are able to suppress T cell responses. The role of MDSCs in autoimmune diseases remains controversial, and little is known about the function of MDSCs in autoimmune arthritis. In this study, we clarify that MDSCs play crucial roles in the regulation of proinflammatory immune response in a collagen-induced arthritis (CIA) mouse model. MDSCs accumulated in the spleens of mice with CIA when arthritis severity peaked. These MDSCs inhibited the proliferation of CD4(+) T cells and their differentiation into Th17 cells in vitro. Moreover, MDSCs inhibited the production of IFN-γ, IL-2, TNF-α, and IL-6 by CD4(+) T cells in vitro, whereas they promoted the production of IL-10. Adoptive transfer of MDSCs reduced the severity of CIA in vivo, which was accompanied by a decrease in the number of CD4(+) T cells and Th17 cells in the draining lymph nodes. However, depletion of MDSCs abrogated the spontaneous improvement of CIA. In conclusion, MDSCs in CIA suppress the progression of CIA by inhibiting the proinflammatory immune response of CD4(+) T cells. These observations suggest that MDSCs play crucial roles in the regulation of autoimmune arthritis, which could be exploited in new cell-based therapies for human rheumatoid arthritis.</abstract><cop>United States</cop><pmid>23804709</pmid><doi>10.4049/jimmunol.1203535</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | The Journal of immunology (1950), 2013-08, Vol.191 (3), p.1073-1081 |
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| subjects | Adoptive Transfer Animals Arthritis, Experimental - immunology Arthritis, Experimental - therapy CD4-Positive T-Lymphocytes - immunology CD4-Positive T-Lymphocytes - metabolism Cell Differentiation Cell Proliferation Collagen Inflammation - immunology Interferon-gamma - biosynthesis Interleukin-1 - biosynthesis Interleukin-2 - biosynthesis Interleukin-6 - biosynthesis Lymphocyte Activation Male Mice Mice, Inbred DBA Myeloid Cells - immunology Myeloid Cells - metabolism Th17 Cells - immunology Tumor Necrosis Factor-alpha - biosynthesis |
| title | Myeloid-derived suppressor cells play crucial roles in the regulation of mouse collagen-induced arthritis |
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