Kopf M, Ruedl C, Schmitz N, Gallimore A, Lefrang K, Ecabert B, Odermatt B, Bachmann M F
Basel Institute for Immunology, Basel, Switzerland.
Immunity. 1999 Dec;11(6):699-708. doi: 10.1016/s1074-7613(00)80144-2.
OX40, a member of the TNF receptor superfamily, is expressed on activated T cells and implicated in stimulation of T cells and T-dependent humoral responses. We generated OX40-/- mice and found that the formation of extrafollicular plasma cells, germinal centers, and antibody responses was independent of OX40. After infection with LCMV and influenza virus, OX40-/- mice retain primary and memory cytotoxic T cell responses with normal expansion and decline of specific CTL. In contrast, CD4+ T cell proliferation and the number of IFN-gamma-producing CD4+ T cells were reduced in OX40-/- mice. Moreover, the number of CD4+ T cells infiltrating the lungs of influenza virus-infected OX40-/- mice was reduced. These results define a unique role of OX40 in the generation of optimal CD4+ T cell responses in vivo.
OX40是肿瘤坏死因子受体超家族的成员之一，在活化的T细胞上表达，与T细胞刺激及T细胞依赖性体液反应有关。我们培育出了OX40基因敲除小鼠，并发现滤泡外浆细胞、生发中心的形成以及抗体反应均不依赖于OX40。感染淋巴细胞脉络丛脑膜炎病毒（LCMV）和流感病毒后，OX40基因敲除小鼠保留了初级和记忆性细胞毒性T细胞反应，特异性CTL正常扩增和衰退。相比之下，OX40基因敲除小鼠中CD4+ T细胞增殖以及产生γ干扰素的CD4+ T细胞数量减少。此外，感染流感病毒的OX40基因敲除小鼠肺部浸润的CD4+ T细胞数量减少。这些结果确定了OX40在体内产生最佳CD4+ T细胞反应中的独特作用。
