Beta-interferons in multiple sclerosis

Aggarwal, Sourabh; Sharma, Vishal; Mathew, Jesna

doi:10.4103/0972-2327.74189

Cited by 1 publication

(1 citation statement)

References 5 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition to their antiviral functions, types I IFNs are capable of exerting immunomodulatory effects on both innate and adaptive immune cells. IFNα and IFNβ have been used to treat patients with cancer or autoimmune diseases, particularly multiple sclerosis [35] , [45] , [46] , [47] , [48] , [49] , [50] , [51] . Our previous study shows that that type I IFN is required for LPS-induced IL-10 upregulation in macrophages [9] .…”

Section: Introductionmentioning

confidence: 99%

Type I IFN Promotes IL-10 Production from T Cells to Suppress Th17 Cells and Th17-Associated Autoimmune Inflammation

et al. 2011

View full text Add to dashboard Cite

Whereas the immune system is essential for host defense against pathogen infection or endogenous danger signals, dysregulated innate and adaptive immune cells may facilitate harmful inflammatory or autoimmune responses. In the CNS, chronic inflammation plays an important role in the pathogenesis of neurodegenerative diseases such as multiple sclerosis (MS). Our previous study has demonstrated a critical role for the type I IFN induction and signaling pathways in constraining Th17-mediated experimental autoimmune encephalomyelitis (EAE), an animal model of human MS. However, it remains unknown if self-reactive Th17 cells can be reprogrammed to have less encephalitogenic activities or even have regulatory effects through modulation of innate pathways. In this study, we investigated the direct effects of type I IFN on Th17 cells. Our data show that IFNβ treatment of T cells cultured under Th17 polarizing conditions resulted in reduced production of IL-17, but increased production of IL-10. We also found that IFNβ induced IL-10 production by antigen specific T cells derived from immunized mice. Furthermore, IFNβ treatment could suppress the encephalitogenic activity of myelin-specific T cells, and ameliorate clinical symptoms of EAE in an adoptive transfer model. Together, results from this study suggest that IFNβ may induce antigen-specific T cells to produce IL-10, which in turn negatively regulate Th17-mediate inflammatory and autoimmune response.

show abstract