The in situ cellular immune response in acute herpes simplex encephalitis.
To characterize the in situ cellular immune response in acute herpes simplex encephalitis (HSE), the authors stained frozen brain specimens from 19 patients with HSE and 8 controls with a panel of monoclonal antibodies, which allowed them to identify inflammatory cell subsets and expression of activation markers and major histocompatibility complex (MHC) molecules. Parenchymal and meningeal inflammatory infiltrates were composed of T cells, with fewer natural killer and B cells, and variable numbers of granulocytes and macrophages. T4+ and T8+ cells were present in equal numbers. Inflammatory cells expressed interleukin-2 receptor, MHC Class I (HLA-alpha chain, beta-2 microglobulin), and MHC Class II (HLA-DR, HLA-DQ) molecules. There was increased MHC molecule expression in HSE on resident cells, including neurons and vascular endothelium, and vascular expression of HLA-DR was greater than that of HLA-DQ (P less than 0.01). No correlations between immune parameters with amount of corticosteroid therapy or duration of illness before biopsy was performed or outcome were found. T cell-mediated cytotoxic and delayed hypersensitivity mechanisms may contribute to tissue injury in HSE.
D000917:Antibody Formation; D002540:Cerebral Cortex / Q000276:immunology / Q000473:pathology; D004660:Encephalitis / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D006680:HLA Antigens / Q000032:analysis; D006561:Herpes Simplex / Q000276:immunology* / Q000473:pathology; D006801:Humans; D008285:Major Histocompatibility Complex
D006680:HLA Antigens