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Intervention of PKC-θ as an immunosuppressive regimen

By Zuoming eSun

Abstract

PKC-θ is selectively enriched in T cells and specifically translocates to immunological synapse where it mediates critical T cell receptor signals required for T cell activation, differentiation and survival. T cells deficient in PKC-θ are defective in their ability to differentiate into inflammatory effector cells that mediate actual immune responses whereas, their differentiation into regulatory T cells (Treg) that inhibits the inflammatory T cells is enhanced. Therefore, the manipulation of PKC-θ activity can shift the ratio between inflammatory effector T cells and inhibitory Tregs, to control T cell-mediated immune responses that are responsible for autoimmunity and allograft rejection. Indeed, PKC-θ deficient mice are resistant to the development of several Th2 and Th17-dependent autoimmune diseases and are defective in mounting alloimmune responses required for rejection of transplanted allografts and graft-versus-host disease (GVHD). Selective inhibition of PKC-θ is therefore considered as a potential treatment for prevention of autoimmune diseases and allograft rejection

Topics: Autoimmunity, T cells, T cell activation, T cell differentiation, allograft rejection, PKC-θ, Immunologic diseases. Allergy, RC581-607
Publisher: Frontiers Media S.A.
Year: 2012
DOI identifier: 10.3389/fimmu.2012.00225
OAI identifier: oai:doaj.org/article:a98953f77cc943f5a8c56a2b2d8c5210
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