Triozzi P L, Eicher D M, Rinehart J J
Department of Medicine, The Ohio State University, Columbus.
Cell Immunol. 1992 Apr;140(2):295-303. doi: 10.1016/0008-8749(92)90197-w.
The modulation of adhesion molecules on human large granular lymphocytes (LGL) by interleukin (IL)-2 was investigated both in vivo and in vitro. Intercellular adhesion molecule-1 (ICAM-1; CD54) expression increased on LGL of cancer patients receiving IL-2 adoptive immunotherapy. ICAM-1 expression on LGL isolated by Percoll gradient centrifugation, LGL purified, and expanded by adherence to plastic surfaces and LGL identified by Leu 19 (CD56) monoclonal antibody were increased significantly in response to IL-2 in vitro. Exposure of LGL to IL-1, interferon (IFN)-gamma, and tumor necrosis factor (TNF) in vitro did not induce ICAM-1. The expression of LFA-1 (CD11a/CD18), a receptor for ICAM-1, and other leukocyte adhesion molecules, including Mac-1 (CD11b/CD18) and p150,95 (CD11c/CD18), was only maintained by IL-2. IL-2 induction of ICAM-1 and the maintenance of CD18 complex expression on small lymphocytes separated by Percoll gradients were similar to that on LGL. We conclude that IL-2 enhances the expression of ICAM-1 on multiple human lymphocyte populations including LGL effectors. Expression of the CD18 complex on LGL does not appear to be highly regulated by IL-2. These findings may have implications relevant to the role of these adhesion molecules in the activities of LGL modulated by IL-2.
我们在体内和体外研究了白细胞介素（IL）-2对人大型颗粒淋巴细胞（LGL）上黏附分子的调节作用。接受IL-2过继性免疫治疗的癌症患者的LGL上细胞间黏附分子-1（ICAM-1；CD54）的表达增加。通过Percoll梯度离心分离的LGL、通过贴壁于塑料表面纯化并扩增的LGL以及用Leu 19（CD56）单克隆抗体鉴定的LGL，在体外对IL-2的反应中ICAM-1表达显著增加。体外将LGL暴露于IL-1、干扰素（IFN）-γ和肿瘤坏死因子（TNF）不会诱导ICAM-1。ICAM-1的受体LFA-1（CD11a/CD18）以及其他白细胞黏附分子，包括Mac-1（CD11b/CD18）和p150,95（CD11c/CD18），仅由IL-2维持表达。IL-2诱导ICAM-1以及维持通过Percoll梯度分离的小淋巴细胞上CD18复合物的表达与在LGL上相似。我们得出结论，IL-2增强了包括LGL效应细胞在内的多个人类淋巴细胞群体上ICAM-1的表达。LGL上CD18复合物的表达似乎不受IL-2的高度调节。这些发现可能与这些黏附分子在IL-2调节的LGL活性中的作用相关。
