IL-3 Is a Marker of Encephalitogenic T Cells, but Not Essential for CNS Autoimmunity
Identifying molecules that are differentially expressed in encephalitogenic T cells is critical to the development of novel and specific therapies for multiple sclerosis (MS). In this study, IL-3 was identified as a molecule highly expressed in encephalitogenic Th1 and Th17 cells, but not in myelin-...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2018-06-01
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| Series: | Frontiers in Immunology |
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| Online Access: | https://www.frontiersin.org/article/10.3389/fimmu.2018.01255/full |
| _version_ | 1828849895561232384 |
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| author | Priscilla W. Lee Matthew K. Xin Wei Pei Yuhong Yang Amy E. Lovett-Racke |
| author_facet | Priscilla W. Lee Matthew K. Xin Wei Pei Yuhong Yang Amy E. Lovett-Racke |
| author_sort | Priscilla W. Lee |
| collection | DOAJ |
| description | Identifying molecules that are differentially expressed in encephalitogenic T cells is critical to the development of novel and specific therapies for multiple sclerosis (MS). In this study, IL-3 was identified as a molecule highly expressed in encephalitogenic Th1 and Th17 cells, but not in myelin-specific non-encephalitogenic Th1 and Th17 cells. However, B10.PL IL-3-deficient mice remained susceptible to experimental autoimmune encephalomyelitis (EAE), a mouse model of MS. Furthermore, B10.PL myelin-specific T cell receptor transgenic IL-3−/− Th1 and Th17 cells were capable of transferring EAE to wild-type mice. Antibody neutralization of IL-3 produced by encephalitogenic Th1 and Th17 cells failed to alter their ability to transfer EAE. Thus, IL-3 is highly expressed in myelin-specific T cells capable of inducing EAE compared to activated, non-encephalitogenic myelin-specific T cells. However, loss of IL-3 in encephalitogenic T cells does not reduce their pathogenicity, indicating that IL-3 is a marker of encephalitogenic T cells, but not a critical element in their pathogenic capacity. |
| first_indexed | 2024-12-12T23:00:49Z |
| format | Article |
| id | doaj.art-baf61627f3bc425881c70fd432aa1ec7 |
| institution | Directory Open Access Journal |
| issn | 1664-3224 |
| language | English |
| last_indexed | 2024-12-12T23:00:49Z |
| publishDate | 2018-06-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Immunology |
| spelling | doaj.art-baf61627f3bc425881c70fd432aa1ec72022-12-22T00:08:49ZengFrontiers Media S.A.Frontiers in Immunology1664-32242018-06-01910.3389/fimmu.2018.01255370415IL-3 Is a Marker of Encephalitogenic T Cells, but Not Essential for CNS AutoimmunityPriscilla W. Lee0Matthew K. Xin1Wei Pei2Yuhong Yang3Amy E. Lovett-Racke4Department of Microbial Infection and Immunity, The Ohio State University, Columbus, OH, United StatesDepartment of Microbial Infection and Immunity, The Ohio State University, Columbus, OH, United StatesDepartment of Neurology, The Ohio State University, Columbus, OH, United StatesDepartment of Neurology, The Ohio State University, Columbus, OH, United StatesDepartment of Microbial Infection and Immunity, The Ohio State University, Columbus, OH, United StatesIdentifying molecules that are differentially expressed in encephalitogenic T cells is critical to the development of novel and specific therapies for multiple sclerosis (MS). In this study, IL-3 was identified as a molecule highly expressed in encephalitogenic Th1 and Th17 cells, but not in myelin-specific non-encephalitogenic Th1 and Th17 cells. However, B10.PL IL-3-deficient mice remained susceptible to experimental autoimmune encephalomyelitis (EAE), a mouse model of MS. Furthermore, B10.PL myelin-specific T cell receptor transgenic IL-3−/− Th1 and Th17 cells were capable of transferring EAE to wild-type mice. Antibody neutralization of IL-3 produced by encephalitogenic Th1 and Th17 cells failed to alter their ability to transfer EAE. Thus, IL-3 is highly expressed in myelin-specific T cells capable of inducing EAE compared to activated, non-encephalitogenic myelin-specific T cells. However, loss of IL-3 in encephalitogenic T cells does not reduce their pathogenicity, indicating that IL-3 is a marker of encephalitogenic T cells, but not a critical element in their pathogenic capacity.https://www.frontiersin.org/article/10.3389/fimmu.2018.01255/fullmultiple sclerosisexperimental autoimmune encephalomyelitisIL-3GM-CSFTh1 cellsTh17 cells |
| spellingShingle | Priscilla W. Lee Matthew K. Xin Wei Pei Yuhong Yang Amy E. Lovett-Racke IL-3 Is a Marker of Encephalitogenic T Cells, but Not Essential for CNS Autoimmunity Frontiers in Immunology multiple sclerosis experimental autoimmune encephalomyelitis IL-3 GM-CSF Th1 cells Th17 cells |
| title | IL-3 Is a Marker of Encephalitogenic T Cells, but Not Essential for CNS Autoimmunity |
| title_full | IL-3 Is a Marker of Encephalitogenic T Cells, but Not Essential for CNS Autoimmunity |
| title_fullStr | IL-3 Is a Marker of Encephalitogenic T Cells, but Not Essential for CNS Autoimmunity |
| title_full_unstemmed | IL-3 Is a Marker of Encephalitogenic T Cells, but Not Essential for CNS Autoimmunity |
| title_short | IL-3 Is a Marker of Encephalitogenic T Cells, but Not Essential for CNS Autoimmunity |
| title_sort | il 3 is a marker of encephalitogenic t cells but not essential for cns autoimmunity |
| topic | multiple sclerosis experimental autoimmune encephalomyelitis IL-3 GM-CSF Th1 cells Th17 cells |
| url | https://www.frontiersin.org/article/10.3389/fimmu.2018.01255/full |
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