10 September 2014. Vol.5 No.5
The immune response to focal cerebral ischemia: 1) Focal cerebral ischemia secondary to thrombotic or embolic event. 2) Injury to neurovascular unit resulting in either death or injury to endothelial cells, neurons, microglia etc. 3) Release of DAMPs from injured and dead neurovascular unit components resulting in innate immune activation via TLRs, RAGE and purinergic receptors on microglia and other APCs. 4) Innate immune activation leading to inflammasome activation; Signal 1= expression of pro-IL-1β and pro-IL-18. 5) Inflammasome activation; Signal 2= activation of caspase 1 and production of mature IL-1β and IL-18. 6) Production of other cytokine via NF-kB activation leading to endothelial cell and macrophage activation as well as activation of other transitional immune effector such as γδ T cells. 7) Activation of other transitional immune effectors such as immature DC, via DAMPs, and surface TLRs and migration of these immature DCs to regional lymph nodes resulting in activation of the adaptive immune response 8) Activation and differentiation of B cells. 9) Activation and differentiation of T cells. 10) Models of stroke-induced immunodepression via beta adrenergic or Th1-mediated mechanisms. BBB, Blood brain barrier; CD200R, CD200 receptor; DAMP, Danger associated molecular pattern; HMGB1, High mobility group box 1; RAGE, Receptor for advanced glycation end products; MyD88, Myeloid differentiation primary response gene 88; ASC, Apoptosis-associate speck-like protein containing a CARD (Caspase activation and recruitment domain); IL, Interleukin; DC, Dendritic cell; TCR, T cell receptor; MHC, Major histocompatibility complex, CD, Cell differentiation; Treg, T regulatory; Th, T helper; TGF, Transforming growth factor; TR1, Type 1 regulatory T cell; CNS, Central nervous system; NK, Natural killer; MBP, Myelin basic protein.