Modulation of the postischemic immune response to improve stroke outcome

Abstract

Recent advances in understanding how the poststroke immune response may contribute to ischemic brain injury are discussed in this article. In particular, the potential of modulating the postischemic immune response to improve stroke outcome is explored.

Figure 1

Following stroke there is ample opportunity for the immune system to come into contact with CNS antigens, either in the brain or in the periphery. The type of immune response/effector cell that results from lymphocyte engagement with the antigen (red dot) depends upon the microenvironment/cytokine milieu at the site of antigen encounter. Treg responses are associated with better outcome from stroke, while Th1 responses are associated with worse outcome. Nothing is known about the Th17 response after stroke; based on what is known about the role of Th17 cells in autoimmunity, however, it is likely that Th17 responses would be similarly detrimental. Neuroprotective strategies could either serve to enhance the Treg response after stroke or prevent the Th1 (and Th17?) response. lymph = lymphocyte, APC = antigen presenting cell, TCR = T cell receptor, MHC II = major histocompatibility complex II, IFN = interferon, IL = interleukin, TGF = transforming growth factor, LTA = lymphotoxin