β2-微球蛋白缺陷小鼠中针对淋巴细胞脉络丛脑膜炎病毒（LCMV）的、受Ⅱ类分子限制的细胞毒性T细胞

LCMV-specific, class II-restricted cytotoxic T cells in beta 2-microglobulin-deficient mice.

作者信息

Muller D, Koller B H, Whitton J L, LaPan K E, Brigman K K, Frelinger J A

机构信息

Department of Microbiology and Immunology, University of North Carolina, Chapel Hill 27599.

出版信息

Science. 1992 Mar 20;255(5051):1576-8. doi: 10.1126/science.1347959.

DOI:10.1126/science.1347959

PMID:1347959

Abstract

Intracranial infection of normal mice with lymphocytic choriomeningitis virus (LCMV) causes meningitis and death mediated by CD8+ major histocompatibility complex (MHC) class I-restricted cytotoxic T lymphocytes (CTLs). beta 2-Microglobulin-deficient mice (beta 2M-/-) do not express functional MHC class I proteins and do not produce significant numbers of CD8+ T cells. When beta 2M-/- mice were infected with LCMV, many died from LCMV disease and produced a specific response to LCMV mediated by CD4+ CTLs that were class II-restricted. In these mice, CD4+ CTLs may compensate for the lack of CD8+ CTLs.

摘要

正常小鼠感染淋巴细胞性脉络丛脑膜炎病毒（LCMV）后发生的颅内感染会导致脑膜炎，并由CD8⁺主要组织相容性复合体（MHC）I类限制性细胞毒性T淋巴细胞（CTL）介导死亡。β2微球蛋白缺陷小鼠（β2M⁻/⁻）不表达功能性MHC I类蛋白，也不产生大量CD8⁺T细胞。当β2M⁻/⁻小鼠感染LCMV时，许多小鼠死于LCMV疾病，并产生由II类限制性CD4⁺CTL介导的针对LCMV的特异性反应。在这些小鼠中，CD4⁺CTL可能弥补了CD8⁺CTL的缺失。