Sha Z, Compans R W
Department of Microbiology and Immunology, Emory University, Atlanta, Georgia 30322, USA.
J Virol. 2000 Jun;74(11):4999-5005. doi: 10.1128/jvi.74.11.4999-5005.2000.
Through cognate interaction between antigen-specific B-cell and CD4(+) alphabeta T cells, the CD4(+) alphabeta T cells secrete cytokines that initiate immunoglobulin (Ig) class switching from IgM to IgG. In this study, we show that formalin-inactivated influenza PR8 virus induces virus-specific IgM and IgG responses in the absence of CD4(+) T cells and that all four subclasses of IgG are produced. The immunized CD4-deficient mice were also found to be completely protected against lethal infection with live, pathogenic influenza virus. The ability of CD4(+) T-cell-deficient mice to generate these IgG responses was not found to be impaired when these mice were depleted of CD8(+) T cells with an anti-CD8 monoclonal antibody. In contrast, alphabeta T-cell-deficient mice (TCRbeta(-/-)) were not found to produce significant amounts of IgG upon immunization with formalin-inactivated PR8 virus. These results suggest that CD4(-) CD8(-) double-negative alphabeta T cells are playing a role in regulating Ig class switching in the absence of CD4(+) T cells.
通过抗原特异性B细胞与CD4(+)αβ T细胞之间的同源相互作用,CD4(+)αβ T细胞分泌细胞因子,启动免疫球蛋白(Ig)从IgM到IgG的类别转换。在本研究中,我们发现福尔马林灭活的流感PR8病毒在缺乏CD4(+) T细胞的情况下可诱导病毒特异性IgM和IgG反应,并且能产生所有四种IgG亚类。还发现免疫的CD4缺陷小鼠对致病性活流感病毒的致死性感染具有完全的抵抗力。当用抗CD8单克隆抗体清除CD8(+) T细胞时,未发现CD4(+) T细胞缺陷小鼠产生这些IgG反应的能力受损。相反,在用福尔马林灭活的PR8病毒免疫后,未发现αβ T细胞缺陷小鼠(TCRβ(-/-))产生大量的IgG。这些结果表明,在缺乏CD4(+) T细胞的情况下,CD4(-) CD8(-)双阴性αβ T细胞在调节Ig类别转换中发挥作用。