A modified superantigen rescues Ly6G−CD11b+blood monocyte suppressor function and suppresses antigen-specific inflammation in EAE
| العنوان: | A modified superantigen rescues Ly6G−CD11b+blood monocyte suppressor function and suppresses antigen-specific inflammation in EAE |
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| المؤلفون: | Aras Toker, Clare Y Slaney, John D. Fraser, Jacquie L. Harper, B Thomas Bäckström |
| المصدر: | Autoimmunity. 46:269-278 |
| بيانات النشر: | Informa UK Limited, 2013. |
| سنة النشر: | 2013 |
| مصطلحات موضوعية: | Adoptive cell transfer, Encephalomyelitis, Autoimmune, Experimental, T cell, Encephalomyelitis, Bacterial Toxins, Immunology, Exotoxins, Lymphocyte Activation, Monocytes, Myelin oligodendrocyte glycoprotein, Epitopes, Mice, Immune system, T-Lymphocyte Subsets, immune system diseases, Superantigen, medicine, Animals, Antigens, Ly, Immunology and Allergy, CD11b Antigen, Superantigens, biology, Monocyte, Experimental autoimmune encephalomyelitis, medicine.disease, Adoptive Transfer, Peptide Fragments, nervous system diseases, medicine.anatomical_structure, biology.protein, Myelin-Oligodendrocyte Glycoprotein |
| الوصف: | In a previous study, we showed that the Ly6G(-)CD11b(+) blood monocytes residing in naïve mice are intrinsically immunosuppressive and that loss of this suppressive function may contribute to the development of autoimmunity in experimental autoimmune encephalomyelitis (EAE), a murine model of human multiple sclerosis. Here we report that mice treated with a modified superantigen coupled to myelin oligodendrocyte glycoprotein 35-55 (MOG(35-55)) peptide (DM-MOG(35-55)) suppressed the development of EAE. The treatment was associated with impaired MOG(35-55)-specific T cell proliferation and a decrease in IL-17 and IFNγ production in the draining lymph nodes. Analysis of circulating blood immune cells showed that the suppressor function of Ly6G(-)CD11b(+) blood monocytes was reduced in EAE mice, but was restored in mice treated with DM-MOG(35-55). Importantly, adoptive transfer of blood CD11b(+)Ly6G(-) cells isolated from DM-MOG(35-55)-treated mice protected recipient mice from developing EAE. Together, these results show that DM coupled to the auto-antigen MOG(35-55): 1) suppresses EAE via antigen-specific suppression of T cell responses, and 2) re-establishes suppressor function of Ly6G(-)CD11b(+) blood monocytes. Auto-antigens coupled to DM could therefore represent a new therapeutic approach for controlling inappropriate inflammation in autoimmune diseases such as multiple sclerosis by inducing antigen-specific T cell suppression. |
| تدمد: | 1607-842X 0891-6934 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::05cbc31a5b90ef2600a64f75229a029e https://doi.org/10.3109/08916934.2013.767893 |
| رقم الأكسشن: | edsair.doi.dedup.....05cbc31a5b90ef2600a64f75229a029e |
| قاعدة البيانات: | OpenAIRE |
PDF full text from Publisher | تدمد: | 1607842X 08916934 |
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