Autoimmune responses to brain following stroke.

This review provides a synthesis of the work done by our laboratory that demonstrates the presence of cellular immune responses directed towards brain antigens in animals following experimental stroke as well as in patients following ischemic stroke. These responses include both antigen-specific TH1(+) responses, which are associated with worse stroke outcome, and antigen-specific TREG responses, which are associated with better stroke outcome. The likelihood of developing a detrimental TH1(+) response to brain antigens is increased by administration of a systemic inflammatory stimulus in experimental stroke and by systemic infection in patients with stroke. We propose that the microenvironment within the lymph nodes and brain is altered by systemic inflammation and allows for bystander activation of lymphocytes and the development of autoimmune responses to brain antigens following cerebral ischemic injury.