Wasik M A, Beller D I
Evans Memorial Department of Clinical Research, Boston University Medical Center, Massachusetts 02118.
Clin Immunol Immunopathol. 1989 Aug;52(2):331-40. doi: 10.1016/0090-1229(89)90184-0.
Here we report that cyclosporin A (CsA) inhibits the induction of membrane interleukin 1 (mIL-1) expression on murine peritoneal macrophages. The inhibition of mIL-1 expression was noted in response to both autoreactive T-cell lines specific for class I or class II MHC determinants as well as bacterial endotoxin. The macrophages were the direct target of this inhibition as shown by pretreating T cells and macrophages separately with CsA. The effective suppression by CsA of endotoxin-induced mIL-1 expression was dependent not only on the concentration of endotoxin employed, but also on the relative time of addition of CsA and endotoxin. Furthermore, CsA pretreatment of macrophages abrogated their ability to stimulate synthesis of IL-4 by a Th2 cell clone. These data suggest that inhibition of induction of accessory molecules such as mIL-1 may be a mechanism by which CsA abrogates the capacity of macrophages to present antigen.
在此我们报告，环孢菌素A（CsA）可抑制小鼠腹腔巨噬细胞上膜白细胞介素1（mIL-1）表达的诱导。在针对I类或II类MHC决定簇的自身反应性T细胞系以及细菌内毒素的刺激下，均观察到mIL-1表达受到抑制。通过分别用CsA预处理T细胞和巨噬细胞表明，巨噬细胞是这种抑制作用的直接靶点。CsA对内毒素诱导的mIL-1表达的有效抑制不仅取决于所用内毒素的浓度，还取决于CsA和内毒素添加的相对时间。此外，巨噬细胞经CsA预处理后，其刺激Th2细胞克隆合成IL-4的能力被消除。这些数据表明，抑制诸如mIL-1等辅助分子的诱导可能是CsA消除巨噬细胞提呈抗原能力的一种机制。
