Stroke and T-Cells
- 1 January 2005
- journal article
- review article
- Published by Springer Science and Business Media LLC in NeuroMolecular Medicine
- Vol. 7 (3), 229-242
- https://doi.org/10.1385/nmm:7:3:229
Abstract
The microvasculature of the brain region affected by a stroke assumes an inflammatory phenotype that is characterized by endothelial cell activation and barrier dysfunction and the recruitment of adherent leukocytes. Although most attention has been devoted to the possible role of neutrophils in the tissue responses to ischemic stroke there is evidence that T-lymphocytes also accumulate in the postischemic brain. Although comparable detailed analyses of lymphocyte involvement in ischemic brain injury have not been performed, emerging findings suggest a role for T-cells in the pathogenesis of ischemic stroke. The recruitment of T-cells to the site of brain injury is critically dependent on the coordinated expression of adhesion molecules on the activated capillary endothelium. Whether the recruited lymphocytes are acting directly on brain tissue or indirectly through activation of other circulating blood cells and/or extravascular cells remain unclear. Cytotoxic CD8+ T-cells may induce brain injury through molecules released from their cytotoxic granules. CD4+ T-helper 1 (TH1) cells, which secrete proinflammatory cytokines, including interleukin-2 (IL-2), IL-12, interferon-γ, and tumor necrosis factor-α, may play a key role in the pathogenesis of stroke, whereas CD4+ TH2 cells may play a protective role through anti-inflammatory cytokines such as IL-4, IL-5, IL-10, and IL-13. T-cells should be considered as therapeutic targets for ischemic stroke. However, because infection is a leading cause of mortality in the postacute phase of ischemic stroke, and considering anti-inflammatory role of CD4+ TH2, treatment targeting T-cells should be carefully designed to reduce deleterious and enhance protective actions of T-cells.Keywords
This publication has 97 references indexed in Scilit:
- Molecular Determinants of the Prothrombogenic and Inflammatory Phenotype Assumed by the Postischemic Cerebral MicrocirculationStroke, 2003
- Upregulation of CD40-CD40 Ligand (CD154) in Patients With Acute Cerebral IschemiaStroke, 2003
- An Improved Synthesis of Chiral α-(4-Bromobenzyl)alanine Ethyl Ester and Its Application to the Synthesis of LFA-1 Antagonist BIRT-377The Journal of Organic Chemistry, 2001
- Increased IL-1β, IL-8, and IL-17 mRNA Expression in Blood Mononuclear Cells Observed in a Prospective Ischemic Stroke StudyStroke, 1999
- CD18-Mediated Neutrophil Recruitment Contributes to the Pathogenesis of Reperfused but Not Nonreperfused StrokeStroke, 1999
- Mice Deficient in Mac-1 (CD11b/CD18) Are Less Susceptible to Cerebral Ischemia/Reperfusion InjuryStroke, 1999
- Tumor Necrosis Factor-αStroke, 1997
- Leukocyte Activation Detected by Increased Plasma Levels of Inflammatory Mediators in Patients With Ischemic Cerebrovascular DiseasesStroke, 1996
- TGF-β1 Protects Hippocampal Neurons Against Degeneration Caused by Transient Global IschemiaStroke, 1996
- Interleukin-1 beta mRNA expression in ischemic rat cortex.Stroke, 1993