Safavi F, Li H, Gonnella P, Mari ER, Rasouli J, Zhang GX, Rostami A.c-kit plays a critical role in induction of intravenous tolerance in experimental autoimmune encephalomyelitis.
Immunol Res. 2015 Jan 15. [Epub ahead of print]
c-kit (CD117) is a tyrosine kinase receptor found in various types of immune cells. We examined the role of c-kit in autoantigen-induced i.v. tolerance in experimental autoimmune encephalomyelitis (EAE), an animal model of MS. Our results show that induction of intravenous tolerance against EAE in B6 mice is characterized by increased numbers of CD117+ cells and altered mast cell-associated molecules in the periphery and in the CNS. W-sh (c-kit-deficient) mice were resistant to i.v autoantigen-induced tolerance, with increased proinflammatory cytokine production in the periphery. I.v. autoantigen in WT mice suppressed the production of proinflammatory cytokines IFN-γ and IL-6 and up-regulated the expression of FoxP3, a transcription factor of Tregs; however, in W-sh mice, IFN-γ and IL-6 were increased with a failure of FoxP3 induction upon i.v. autoantigen injection and is thus a mechanism for resistance to i.v. tolerance induction in these mice. We conclude that c-kit signaling has a regulatory role in i.v. tolerance and could be a target for potential immunotherapy in autoimmune disorders.
Not sure, what to say here, you can all read, if you can induce immune tolerance you can get rid of the problem with minimal effect on the rest of the immune system