Zinkernagel R M, Planz O, Ehl S, Battegay M, Odermatt B, Klenerman P, Hengartner H
Department of Pathology, University of Zurich, Switzerland.
Immunol Rev. 1999 Apr;168:305-15. doi: 10.1111/j.1600-065x.1999.tb01300.x.
Immunosuppression caused by the non-cytopathic lymphocytic choriomeningitis virus (LCMV) (an RNA virus) is mediated by antiviral cytotoxic T cells that destroy LCMV-infected cells, also of the immune system. While this immunopathological destruction of antigen-presenting cells, macrophages and follicular dendritic cells and of some CD4+ T cells causes general immunosuppression and impairs immune response to third party antigens, it also enhances exhaustion/deletion of LCMV-specific CD8+ T-cell responses. LCMV seems in addition to infect neutralizing antibody-producing B cells via the specific receptor; immunopathological LCMV specific CD8+ T-cell-mediated elimination of these infected B cells (but not of uninfected internal virus antigen-specific B cells) causes a highly specific immunosuppression that delays neutralizing antibody responses and thereby enhances virus persistence. Both generalized and specific immunosuppression by CD8+ T-cell-mediated immunopathology may be involved in human infections with HIV, hepatitis B virus or hepatitis C virus.
由非细胞病变性淋巴细胞性脉络丛脑膜炎病毒(LCMV,一种RNA病毒)引起的免疫抑制是由抗病毒细胞毒性T细胞介导的,这些细胞会破坏LCMV感染的细胞,免疫系统的细胞也会被破坏。虽然抗原呈递细胞、巨噬细胞、滤泡树突状细胞以及一些CD4+ T细胞的这种免疫病理破坏会导致全身免疫抑制并损害对第三方抗原的免疫反应,但它也会增强LCMV特异性CD8+ T细胞反应的耗竭/缺失。此外,LCMV似乎通过特定受体感染产生中和抗体的B细胞;免疫病理的LCMV特异性CD8+ T细胞介导的这些受感染B细胞(而非未感染的内部病毒抗原特异性B细胞)的清除会导致高度特异性的免疫抑制,从而延迟中和抗体反应,进而增强病毒持续性。CD8+ T细胞介导的免疫病理导致的全身和特异性免疫抑制可能都与人类感染HIV、乙型肝炎病毒或丙型肝炎病毒有关。