TH17 cells contribute to uveitis and scleritis and are expanded by IL-2 and inhibited by IL-27/STAT1
T-helper type 17 cells (T H 17) are implicated in rodent models of immune-mediated diseases. Here we report their involvement in human uveitis and scleritis, and validate our findings in experimental autoimmune uveoretinitis (EAU), a model of uveitis. T H 17 cells were present in human peripheral bl...
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| Veröffentlicht in: | Nature medicine 2007-06, Vol.13 (6), p.711-718 |
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| creator | Amadi-Obi, Ahjoku Yu, Cheng-Rong Liu, Xuebin Mahdi, Rashid M Clarke, Grace Levy Nussenblatt, Robert B Gery, Igal Lee, Yun Sang Egwuagu, Charles E |
| description | T-helper type 17 cells (T
H
17) are implicated in rodent models of immune-mediated diseases. Here we report their involvement in human uveitis and scleritis, and validate our findings in experimental autoimmune uveoretinitis (EAU), a model of uveitis. T
H
17 cells were present in human peripheral blood mononuclear cells (PBMC), and were expanded by interleukin (IL)-2 and inhibited by interferon (IFN)-γ. Their numbers increased during active uveitis and scleritis and decreased following treatment. IL-17 was elevated in EAU and upregulated tumor necrosis factor (TNF)-α in retinal cells, suggesting a mechanism by which T
H
17 may contribute to ocular pathology. Furthermore, IL-27 was constitutively expressed in retinal ganglion and photoreceptor cells, was upregulated by IFN-γ and inhibited proliferation of T
H
17. These findings suggest that T
H
1 cells may mitigate uveitis by antagonizing the T
H
17 phenotype through the IFN-γ–mediated induction of IL-27 in target tissue. The finding that IL-2 promotes T
H
17 expansion provides explanations for the efficacy of IL-2R antibody therapy in uveitis, and suggests that antagonism of T
H
17 by IFN-γ and/or IL-27 could be used for the treatment of chronic inflammation. |
| doi_str_mv | 10.1038/nm1585 |
| format | Article |
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H
17) are implicated in rodent models of immune-mediated diseases. Here we report their involvement in human uveitis and scleritis, and validate our findings in experimental autoimmune uveoretinitis (EAU), a model of uveitis. T
H
17 cells were present in human peripheral blood mononuclear cells (PBMC), and were expanded by interleukin (IL)-2 and inhibited by interferon (IFN)-γ. Their numbers increased during active uveitis and scleritis and decreased following treatment. IL-17 was elevated in EAU and upregulated tumor necrosis factor (TNF)-α in retinal cells, suggesting a mechanism by which T
H
17 may contribute to ocular pathology. Furthermore, IL-27 was constitutively expressed in retinal ganglion and photoreceptor cells, was upregulated by IFN-γ and inhibited proliferation of T
H
17. These findings suggest that T
H
1 cells may mitigate uveitis by antagonizing the T
H
17 phenotype through the IFN-γ–mediated induction of IL-27 in target tissue. The finding that IL-2 promotes T
H
17 expansion provides explanations for the efficacy of IL-2R antibody therapy in uveitis, and suggests that antagonism of T
H
17 by IFN-γ and/or IL-27 could be used for the treatment of chronic inflammation.</description><identifier>ISSN: 1078-8956</identifier><identifier>EISSN: 1546-170X</identifier><identifier>DOI: 10.1038/nm1585</identifier><identifier>PMID: 17496900</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>Animals ; Autoimmune diseases ; Autoimmune Diseases - immunology ; Autoimmune Diseases - metabolism ; Autoimmune Diseases - pathology ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Cell Proliferation ; Cells, Cultured ; Coculture Techniques ; Eye diseases ; Growth Inhibitors - physiology ; Humans ; Infectious Diseases ; Inflammatory diseases ; Interleukin-2 - physiology ; Interleukins - biosynthesis ; Interleukins - genetics ; Interleukins - physiology ; Metabolic Diseases ; Mice ; Mice, Inbred C57BL ; Molecular Medicine ; Neurosciences ; Organ Culture Techniques ; Pathology ; Rodents ; Scleritis - immunology ; Scleritis - metabolism ; Scleritis - pathology ; STAT1 Transcription Factor - physiology ; T-Lymphocytes, Helper-Inducer - cytology ; T-Lymphocytes, Helper-Inducer - immunology ; T-Lymphocytes, Helper-Inducer - metabolism ; Tumors ; Uveitis - immunology ; Uveitis - metabolism ; Uveitis - pathology</subject><ispartof>Nature medicine, 2007-06, Vol.13 (6), p.711-718</ispartof><rights>Springer Nature America, Inc. 2007</rights><rights>COPYRIGHT 2007 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jun 2007</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4935-eb6c7474ebd7df9dc03d4981ce7ae993ca7446b49181286125618c433dfc9b3e3</citedby><cites>FETCH-LOGICAL-c4935-eb6c7474ebd7df9dc03d4981ce7ae993ca7446b49181286125618c433dfc9b3e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/nm1585$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/nm1585$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17496900$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Amadi-Obi, Ahjoku</creatorcontrib><creatorcontrib>Yu, Cheng-Rong</creatorcontrib><creatorcontrib>Liu, Xuebin</creatorcontrib><creatorcontrib>Mahdi, Rashid M</creatorcontrib><creatorcontrib>Clarke, Grace Levy</creatorcontrib><creatorcontrib>Nussenblatt, Robert B</creatorcontrib><creatorcontrib>Gery, Igal</creatorcontrib><creatorcontrib>Lee, Yun Sang</creatorcontrib><creatorcontrib>Egwuagu, Charles E</creatorcontrib><title>TH17 cells contribute to uveitis and scleritis and are expanded by IL-2 and inhibited by IL-27/STAT1</title><title>Nature medicine</title><addtitle>Nat Med</addtitle><addtitle>Nat Med</addtitle><description>T-helper type 17 cells (T
H
17) are implicated in rodent models of immune-mediated diseases. Here we report their involvement in human uveitis and scleritis, and validate our findings in experimental autoimmune uveoretinitis (EAU), a model of uveitis. T
H
17 cells were present in human peripheral blood mononuclear cells (PBMC), and were expanded by interleukin (IL)-2 and inhibited by interferon (IFN)-γ. Their numbers increased during active uveitis and scleritis and decreased following treatment. IL-17 was elevated in EAU and upregulated tumor necrosis factor (TNF)-α in retinal cells, suggesting a mechanism by which T
H
17 may contribute to ocular pathology. Furthermore, IL-27 was constitutively expressed in retinal ganglion and photoreceptor cells, was upregulated by IFN-γ and inhibited proliferation of T
H
17. These findings suggest that T
H
1 cells may mitigate uveitis by antagonizing the T
H
17 phenotype through the IFN-γ–mediated induction of IL-27 in target tissue. The finding that IL-2 promotes T
H
17 expansion provides explanations for the efficacy of IL-2R antibody therapy in uveitis, and suggests that antagonism of T
H
17 by IFN-γ and/or IL-27 could be used for the treatment of chronic inflammation.</description><subject>Animals</subject><subject>Autoimmune diseases</subject><subject>Autoimmune Diseases - immunology</subject><subject>Autoimmune Diseases - metabolism</subject><subject>Autoimmune Diseases - pathology</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Cell Proliferation</subject><subject>Cells, Cultured</subject><subject>Coculture Techniques</subject><subject>Eye diseases</subject><subject>Growth Inhibitors - physiology</subject><subject>Humans</subject><subject>Infectious Diseases</subject><subject>Inflammatory diseases</subject><subject>Interleukin-2 - physiology</subject><subject>Interleukins - biosynthesis</subject><subject>Interleukins - genetics</subject><subject>Interleukins - physiology</subject><subject>Metabolic Diseases</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Molecular Medicine</subject><subject>Neurosciences</subject><subject>Organ Culture Techniques</subject><subject>Pathology</subject><subject>Rodents</subject><subject>Scleritis - 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Academic</collection><jtitle>Nature medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Amadi-Obi, Ahjoku</au><au>Yu, Cheng-Rong</au><au>Liu, Xuebin</au><au>Mahdi, Rashid M</au><au>Clarke, Grace Levy</au><au>Nussenblatt, Robert B</au><au>Gery, Igal</au><au>Lee, Yun Sang</au><au>Egwuagu, Charles E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TH17 cells contribute to uveitis and scleritis and are expanded by IL-2 and inhibited by IL-27/STAT1</atitle><jtitle>Nature medicine</jtitle><stitle>Nat Med</stitle><addtitle>Nat Med</addtitle><date>2007-06</date><risdate>2007</risdate><volume>13</volume><issue>6</issue><spage>711</spage><epage>718</epage><pages>711-718</pages><issn>1078-8956</issn><eissn>1546-170X</eissn><abstract>T-helper type 17 cells (T
H
17) are implicated in rodent models of immune-mediated diseases. Here we report their involvement in human uveitis and scleritis, and validate our findings in experimental autoimmune uveoretinitis (EAU), a model of uveitis. T
H
17 cells were present in human peripheral blood mononuclear cells (PBMC), and were expanded by interleukin (IL)-2 and inhibited by interferon (IFN)-γ. Their numbers increased during active uveitis and scleritis and decreased following treatment. IL-17 was elevated in EAU and upregulated tumor necrosis factor (TNF)-α in retinal cells, suggesting a mechanism by which T
H
17 may contribute to ocular pathology. Furthermore, IL-27 was constitutively expressed in retinal ganglion and photoreceptor cells, was upregulated by IFN-γ and inhibited proliferation of T
H
17. These findings suggest that T
H
1 cells may mitigate uveitis by antagonizing the T
H
17 phenotype through the IFN-γ–mediated induction of IL-27 in target tissue. The finding that IL-2 promotes T
H
17 expansion provides explanations for the efficacy of IL-2R antibody therapy in uveitis, and suggests that antagonism of T
H
17 by IFN-γ and/or IL-27 could be used for the treatment of chronic inflammation.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>17496900</pmid><doi>10.1038/nm1585</doi><tpages>8</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1078-8956 |
| ispartof | Nature medicine, 2007-06, Vol.13 (6), p.711-718 |
| issn | 1078-8956 1546-170X |
| language | eng |
| recordid | cdi_proquest_miscellaneous_70597867 |
| source | MEDLINE; Springer Nature - Complete Springer Journals; Nature |
| subjects | Animals Autoimmune diseases Autoimmune Diseases - immunology Autoimmune Diseases - metabolism Autoimmune Diseases - pathology Biomedical and Life Sciences Biomedicine Cancer Research Cell Proliferation Cells, Cultured Coculture Techniques Eye diseases Growth Inhibitors - physiology Humans Infectious Diseases Inflammatory diseases Interleukin-2 - physiology Interleukins - biosynthesis Interleukins - genetics Interleukins - physiology Metabolic Diseases Mice Mice, Inbred C57BL Molecular Medicine Neurosciences Organ Culture Techniques Pathology Rodents Scleritis - immunology Scleritis - metabolism Scleritis - pathology STAT1 Transcription Factor - physiology T-Lymphocytes, Helper-Inducer - cytology T-Lymphocytes, Helper-Inducer - immunology T-Lymphocytes, Helper-Inducer - metabolism Tumors Uveitis - immunology Uveitis - metabolism Uveitis - pathology |
| title | TH17 cells contribute to uveitis and scleritis and are expanded by IL-2 and inhibited by IL-27/STAT1 |
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