Soluble IL-2Rα (sCD25) exacerbates autoimmunity and enhances the development of Th17 responses in mice
A strong association exists between mutations at the IL2 receptor alpha chain (CD25) gene locus and susceptibility to a number of T cell driven autoimmune diseases. Interestingly, the presence of certain CD25 susceptibility alleles has been correlated with significantly increased levels of the solub...
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| description | A strong association exists between mutations at the IL2 receptor alpha chain (CD25) gene locus and susceptibility to a number of T cell driven autoimmune diseases. Interestingly, the presence of certain CD25 susceptibility alleles has been correlated with significantly increased levels of the soluble form of CD25 (sCD25) in the serum of patients. However, the functional consequences, if any, of this observation are unknown. We have demonstrated that elevated levels of sCD25 in vivo resulted in exacerbated experimental autoimmune encephalomyelitis (EAE) and enhanced antigen-specific Th17 responses in the periphery. sCD25 exerted its effects early during the Th17 developmental programme in vitro, through inhibiting signalling downstream of the IL-2R. Although, sCD25 did not interact with the T cell surface, it specifically bound to secreted IL-2 demonstrating its ability to act as a decoy receptor for IL-2 in the T cell microenvironment. These data identify the ability of sCD25 to promote autoimmune disease pathogenesis and enhance Th17 responses through its ability to sequester local IL-2. |
| doi_str_mv | 10.1371/journal.pone.0047748 |
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Interestingly, the presence of certain CD25 susceptibility alleles has been correlated with significantly increased levels of the soluble form of CD25 (sCD25) in the serum of patients. However, the functional consequences, if any, of this observation are unknown. We have demonstrated that elevated levels of sCD25 in vivo resulted in exacerbated experimental autoimmune encephalomyelitis (EAE) and enhanced antigen-specific Th17 responses in the periphery. sCD25 exerted its effects early during the Th17 developmental programme in vitro, through inhibiting signalling downstream of the IL-2R. Although, sCD25 did not interact with the T cell surface, it specifically bound to secreted IL-2 demonstrating its ability to act as a decoy receptor for IL-2 in the T cell microenvironment. These data identify the ability of sCD25 to promote autoimmune disease pathogenesis and enhance Th17 responses through its ability to sequester local IL-2.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0047748</identifier><identifier>PMID: 23077668</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Autoimmune diseases ; Autoimmune Diseases - immunology ; Autoimmune Diseases - metabolism ; Autoimmune Diseases - pathology ; Autoimmunity ; Biology ; CD25 antigen ; Cell Differentiation ; Cell surface ; Children & youth ; Clinical medicine ; Cytokines ; Disease ; Encephalomyelitis, Autoimmune, Experimental - immunology ; Encephalomyelitis, Autoimmune, Experimental - metabolism ; Encephalomyelitis, Autoimmune, Experimental - pathology ; Experimental allergic encephalomyelitis ; Helper cells ; Hospitals ; Humans ; Immunity, Cellular ; Interleukin 2 ; Interleukin 2 receptors ; Interleukin-2 - immunology ; Interleukin-2 - metabolism ; Interleukin-2 Receptor alpha Subunit - blood ; Interleukin-2 Receptor alpha Subunit - immunology ; Lymphocytes ; Lymphocytes T ; Medicine ; Mice ; Mutation ; Pathogenesis ; Proteins ; R&D ; Research & development ; Rheumatoid arthritis ; Signal Transduction ; Signaling ; Th17 Cells - immunology ; Th17 Cells - metabolism</subject><ispartof>PloS one, 2012-10, Vol.7 (10), p.e47748-e47748</ispartof><rights>Russell et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 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Interestingly, the presence of certain CD25 susceptibility alleles has been correlated with significantly increased levels of the soluble form of CD25 (sCD25) in the serum of patients. However, the functional consequences, if any, of this observation are unknown. We have demonstrated that elevated levels of sCD25 in vivo resulted in exacerbated experimental autoimmune encephalomyelitis (EAE) and enhanced antigen-specific Th17 responses in the periphery. sCD25 exerted its effects early during the Th17 developmental programme in vitro, through inhibiting signalling downstream of the IL-2R. Although, sCD25 did not interact with the T cell surface, it specifically bound to secreted IL-2 demonstrating its ability to act as a decoy receptor for IL-2 in the T cell microenvironment. These data identify the ability of sCD25 to promote autoimmune disease pathogenesis and enhance Th17 responses through its ability to sequester local IL-2.</description><subject>Animals</subject><subject>Autoimmune diseases</subject><subject>Autoimmune Diseases - immunology</subject><subject>Autoimmune Diseases - metabolism</subject><subject>Autoimmune Diseases - pathology</subject><subject>Autoimmunity</subject><subject>Biology</subject><subject>CD25 antigen</subject><subject>Cell Differentiation</subject><subject>Cell surface</subject><subject>Children & youth</subject><subject>Clinical medicine</subject><subject>Cytokines</subject><subject>Disease</subject><subject>Encephalomyelitis, Autoimmune, Experimental - immunology</subject><subject>Encephalomyelitis, Autoimmune, Experimental - metabolism</subject><subject>Encephalomyelitis, Autoimmune, Experimental - pathology</subject><subject>Experimental allergic encephalomyelitis</subject><subject>Helper cells</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Immunity, Cellular</subject><subject>Interleukin 2</subject><subject>Interleukin 2 receptors</subject><subject>Interleukin-2 - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Russell, Shane E</au><au>Moore, Anne C</au><au>Fallon, Padraic G</au><au>Walsh, Patrick T</au><au>Pietropaolo, Massimo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Soluble IL-2Rα (sCD25) exacerbates autoimmunity and enhances the development of Th17 responses in mice</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2012-10-15</date><risdate>2012</risdate><volume>7</volume><issue>10</issue><spage>e47748</spage><epage>e47748</epage><pages>e47748-e47748</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>A strong association exists between mutations at the IL2 receptor alpha chain (CD25) gene locus and susceptibility to a number of T cell driven autoimmune diseases. Interestingly, the presence of certain CD25 susceptibility alleles has been correlated with significantly increased levels of the soluble form of CD25 (sCD25) in the serum of patients. However, the functional consequences, if any, of this observation are unknown. We have demonstrated that elevated levels of sCD25 in vivo resulted in exacerbated experimental autoimmune encephalomyelitis (EAE) and enhanced antigen-specific Th17 responses in the periphery. sCD25 exerted its effects early during the Th17 developmental programme in vitro, through inhibiting signalling downstream of the IL-2R. Although, sCD25 did not interact with the T cell surface, it specifically bound to secreted IL-2 demonstrating its ability to act as a decoy receptor for IL-2 in the T cell microenvironment. These data identify the ability of sCD25 to promote autoimmune disease pathogenesis and enhance Th17 responses through its ability to sequester local IL-2.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23077668</pmid><doi>10.1371/journal.pone.0047748</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Autoimmune diseases Autoimmune Diseases - immunology Autoimmune Diseases - metabolism Autoimmune Diseases - pathology Autoimmunity Biology CD25 antigen Cell Differentiation Cell surface Children & youth Clinical medicine Cytokines Disease Encephalomyelitis, Autoimmune, Experimental - immunology Encephalomyelitis, Autoimmune, Experimental - metabolism Encephalomyelitis, Autoimmune, Experimental - pathology Experimental allergic encephalomyelitis Helper cells Hospitals Humans Immunity, Cellular Interleukin 2 Interleukin 2 receptors Interleukin-2 - immunology Interleukin-2 - metabolism Interleukin-2 Receptor alpha Subunit - blood Interleukin-2 Receptor alpha Subunit - immunology Lymphocytes Lymphocytes T Medicine Mice Mutation Pathogenesis Proteins R&D Research & development Rheumatoid arthritis Signal Transduction Signaling Th17 Cells - immunology Th17 Cells - metabolism |
| title | Soluble IL-2Rα (sCD25) exacerbates autoimmunity and enhances the development of Th17 responses in mice |
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