Mitchell T, Kappler J, Marrack P
Department of Medicine, National Jewish Medical and Research Center, Howard Hughes Medical Institute, Denver, CO 80206, USA.
J Immunol. 1999 Apr 15;162(8):4527-35.
In animals, T cells often die rapidly after activation, unless activation occurs in the presence of inflammatory factors. To understand how such activated cells survive to participate in immune responses, we studied the effects of viral infection on T cells responding to an unrelated superantigen. Normal T cells activated by superantigen in uninfected mice died as a result of their activation, whereas T cells that were activated during vaccinia infection survived longer in vivo and in culture. This bystander effect of viral infection on activated T cells was independent of effects on the magnitude of the initial T cell response, on induction of Bcl-2 and Bcl-x, on T cell proliferation, and on Fas killing. The failure of such effects to predict the fate of activated T cells in vivo indicates that virus infections shape T cell responses via mechanisms that differ from those described previously. These mechanisms may contribute to the ability of viral infections to induce autoimmunity.
在动物体内，T细胞激活后通常会迅速死亡，除非激活过程是在炎症因子存在的情况下发生。为了了解这些被激活的细胞如何存活以参与免疫反应，我们研究了病毒感染对响应无关超抗原的T细胞的影响。在未感染小鼠中被超抗原激活的正常T细胞因激活而死亡，而在痘苗病毒感染期间被激活的T细胞在体内和体外培养中存活时间更长。病毒感染对活化T细胞的这种旁观者效应与对初始T细胞反应强度、Bcl-2和Bcl-x诱导、T细胞增殖以及Fas杀伤的影响无关。这些效应无法预测体内活化T细胞命运，表明病毒感染通过与先前描述的机制不同的机制塑造T细胞反应。这些机制可能有助于病毒感染诱导自身免疫的能力。
