Guerder S, Eynon E E, Flavell R A
Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.
J Immunol. 1998 Sep 1;161(5):2128-40.
To define more clearly the roles of CD80 (RIP-CD80) and CD86 (RIP-CD86) in the activation of autoreactive T cells in vivo, we generated transgenic mice expressing either or both costimulatory molecules on the beta cells of the pancreas. While RIP-CD80 mice do not show any sign of autoimmunity, at the age of 7 mo RIP-CD86 transgenic mice develop a lymphoid infiltrate with both IFN-gamma- and IL-4-positive cells in the vicinity of the islets; these mice, however, never progress to diabetes. This fundamental difference in the ability of CD80 and CD86 to activate self-reactive T cells in vivo is, however, obliterated when the level of TCR signaling is increased by either TNF-alpha or transgenic MHC class II expression. These results support the suggestion that CD80 and CD86 mainly differ at the level of the intensity of the signals they deliver.
为了更清楚地界定CD80（RIP - CD80）和CD86（RIP - CD86）在体内自身反应性T细胞激活中的作用，我们构建了在胰腺β细胞上表达一种或两种共刺激分子的转基因小鼠。虽然RIP - CD80小鼠未表现出任何自身免疫迹象，但在7月龄时，RIP - CD86转基因小鼠在胰岛附近出现了同时含有γ干扰素阳性细胞和白细胞介素4阳性细胞的淋巴细胞浸润；然而，这些小鼠从未发展为糖尿病。然而，当通过肿瘤坏死因子α或转基因MHC II类分子表达增加TCR信号水平时，CD80和CD86在体内激活自身反应性T细胞能力上的这种根本差异就消失了。这些结果支持了这样一种观点，即CD80和CD86主要在它们传递信号的强度水平上存在差异。
