Caerulomycin A suppresses the differentiation of naïve T cells and alleviates the symptoms of experimental autoimmune encephalomyelitis

Kujur, Weshely and Gurram, Rama Krishna and Maurya, Sudeep K. and Nadeem, Sajid and Chodisetti, Sathi Babu and Khan, Nargis and Agrewala, J N (2017) Caerulomycin A suppresses the differentiation of naïve T cells and alleviates the symptoms of experimental autoimmune encephalomyelitis. Autoimmunity, 50 (5). pp. 317-328. ISSN 0891-6934

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Official URL: http://dx.doi.org/10.1080/08916934.2017.1332185

Abstract

Multiple sclerosis (MS) is a highly detrimental autoimmune disease of the central nervous system. There is no cure for it but the treatment typically focuses on subsiding severity and recurrence of the disease. Experimental autoimmune encephalomyelitis (EAE) is an animal model of MS. It is characterized by frequent relapses due to the generation of memory T cells. Caerulomycin A (CaeA) is known to suppress the Th1 cells, Th2 cells, and Th17 cells. Interestingly, it enhances the generation of regulatory T cells (Tregs). Th1 cells and Th17 cells are known to aggravate EAE, whereas Tregs suppress the disease symptoms. Consequently, in the current study we evaluated the influence of CaeA on EAE. Intriguingly, we observed by whole body imaging that CaeA regressed the clinical symptoms of EAE. Further, there was reduction in the pool of Th1 cells, Th17 cells, and CD8 T cells. The mechanism involved in suppressing the EAE symptoms was due to the inhibition in the generation of effector and central memory T cells and induction of the expansion of Tregs. In essence, these findings implicate that CaeA may be considered as a potent future immunosuppressive drug.

Item Type: Article
Additional Information: Copyright of this article belongs to Taylor & Francis.
Uncontrolled Keywords: CaeA; EAE; Immunosuppression; Th1 cells; Th17; Tregs
Subjects: Q Science > QR Microbiology
Depositing User: Dr. K.P.S.Sengar
Date Deposited: 27 Mar 2018 10:19
Last Modified: 27 Mar 2018 10:19
URI: http://crdd.osdd.net/open/id/eprint/2026

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