Shingu M, Hashimoto M, Ezaki I, Nobunaga M
Department of Clinical Immunology, Kyushu University, Beppu, Japan.
Clin Exp Immunol. 1994 Oct;98(1):46-51. doi: 10.1111/j.1365-2249.1994.tb06605.x.
The present study was designed to establish (i) the effects of cytokines on soluble ICAM-1 (sICAM-1) production by human synovial cells (SC) and ICAM-1 expression on these cells, and (ii) the effects of sICAM-1 on lymphocyte-SC adhesion. sICAM-1 production was enhanced in parallel with ICAM-1 expression by IL-1 beta, TNF-alpha and IFN-gamma. IL-4 showed no effects on ICAM-1 expression. In contrast with the transient elevation of cell-associated ICAM-1 by IL-1 beta, which peaked 36 h after stimulation and declined thereafter, sICAM-1 continued to accumulate in culture supernatants even after 48 h. Purified sICAM-1 was obtained from a 48 h culture synovial cell supernatant by affinity chromatography using ICAM-1 monoclonal antibody. The purified sICAM-1 significantly inhibited adhesion of lymphocytes and monocytes to cytokine-stimulated synovial cells. These results suggest that sICAM-1 may modulate chronic synovitis by inhibiting ICAM-1-mediated cell-to-cell adhesion.
(i)细胞因子对人滑膜细胞(SC)可溶性细胞间黏附分子-1(sICAM-1)产生及这些细胞上ICAM-1表达的影响;(ii)sICAM-1对淋巴细胞与滑膜细胞黏附的影响。白细胞介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)和干扰素-γ(IFN-γ)可使sICAM-1的产生与ICAM-1的表达同时增强。白细胞介素-4(IL-4)对ICAM-1的表达无影响。与IL-1β引起的细胞相关ICAM-1短暂升高不同(刺激后36小时达到峰值,随后下降),即使在48小时后,sICAM-1仍继续在培养上清液中积累。使用ICAM-1单克隆抗体通过亲和层析从48小时培养的滑膜细胞上清液中获得纯化的sICAM-1。纯化的sICAM-1显著抑制淋巴细胞和单核细胞与细胞因子刺激的滑膜细胞的黏附。这些结果表明,sICAM-1可能通过抑制ICAM-1介导的细胞间黏附来调节慢性滑膜炎。