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Neuropharmacology. 2009 May-Jun;56(6-7):929-36. doi: 10.1016/j.neuropharm.2009.02.007. Epub 2009 Mar 11.

TGF-beta as a promising option in the treatment of multiple sclerosis.

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1
Departmant of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran-14155, Box 6446, Iran. mirshafiey@tums.ac.ir

Abstract

Transforming growth factor-beta (TGF-beta) is a potent regulatory cytokine with diverse effects on hemopoietic cells. The pivotal function of TGF-beta in the immune system is to maintain tolerance via the regulation of lymphocyte proliferation, differentiation, and survival. Among T cells, CD4+CD25+FOXP3+ T regs contain the main source of TGF-beta that suppresses immune responses in inflammatory sites. Defects in TGF-beta1 expression or its signaling in T cells correlate with the onset of several autoimmune diseases. Thus, understanding the function and regulation of TGF-beta during immune responses offers therapeutic promise for the control of autoimmune diseases such as multiple sclerosis. However, the main mechanism by which TGF-beta exerts its protective effects on the experimental model of multiple sclerosis remains to be elucidated. Paradoxically, TGF-beta1 also acts as a pro-inflammatory cytokine and induces interleukin 17-producing pathogenic T helper cells (Th IL-17 cells) synergistically during an inflammatory response in which interleukin 6 is produced. In this review, we will describe the regulatory and therapeutic effects of TGF-beta in multiple sclerosis.

[Indexed for MEDLINE]

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