Table 2.

Selected evidence for and against the involvement of adaptive immunity in ischemic brain injury

A. In favor of adaptive immunity causing tissue damage
Evidence	Findings	References
CNS antigens and associated humoral response are present after stroke	MBP, NSE, S100beta, GFAP, NMDA receptor, neurofilament	134–138
T-cell response to CNS antigens after stroke	Lymphocyte sensitization to CNS antigens	139
APC increase in the human and rodent brain after stroke	DC and macrophages found in perivascular space and brain parenchyma after stroke	35–38,118
γδT cells and Treg are involved in experimental stroke	γδT cells contribute to brain damage through IL-17; Treg are protective in the late phase of cerebral ischemia	41,42
T cells sensitized against CNS antigens mediate damage in stroke	RTL targeted to myelin-specific T cells reduces ischemic brain injury	49
Tolerization to CNS antigens is protective in experimental stroke	Mucosal administration of MBP or MOG reduces damage in focal ischemia	44

B. Against adaptive immunity causing damage
Evidence	Findings	References
Temporal dissociation between adaptive response and tissue damage	T cells mediated damage occurs early (<24hrs) after stroke, not consistent with antigen presentation and clonal expansion	39,52
T-cell mediated ischemic damage is antigen independent	T-cell reactive against CNS or non-CNS antigens are equally damaging	40
Absence of co-stimulatory molecules necessary for antigen presentation does not effect stroke outcome	Mice lacking CD28 or B7 are not protected from focal ischemia	40
Unlike other models of autoimmunity, both CD4+ and CD8+ T cells are involved in the injury	CD4+ and CD8+ null mice are equally protected	41,52