CD11b (Mac-1): a marker for CD8+ cytotoxic T cell activation and memory in virus infection.

摘要: We have found that CD11b, a cell surface integrin of macrophages, granulocytes, and NK cells, is expressed by subset CD8+ T cells include both the active virus-specific CTL memory populations. CD8+CD11b+ comprise less than 3% naive mouse splenocytes, but after lymphocytic choriomeningitis virus (LCMV) infection increase 9- to 12-fold peak (day 8) response. Depletion day-8 splenocytes with anti-Mac-1 C' or enrichment sorting for CD11b+ spleen demonstrated LCMV-specific are CD11b+. The subpopulation also contained bulk IL-2-responsive cells. MEL-14, homing marker down-regulated on activated was majority became Less 1% LCMV-immune splenic lymphocytes CD11b. Antibody depletion this population severely impaired ability immune respond in vitro secondary stimulation LCMV-infected peritoneal did not affect generation primary allospecific response MLC. Mixing CD8-depleted CD11b-depleted failed restore these mount response, indicating coexpressing CD8 CD11b essential As determined limiting dilution analysis, precursors were enriched splenocytes. stained far fewer from mice CD44 (Pgp-1), among it identified small CD44hi may be best single available discriminating between