Kasinrerk W, Baumruker T, Majdic O, Knapp W, Stockinger H
Institute of Immunology-Vienna International Research Cooperation Center, University of Vienna, Austria.
J Immunol. 1993 Jan 15;150(2):579-84.
In this paper we demonstrate that granulocyte-macrophage CSF (GM-CSF) specifically induces the expression of CD1 molecules, CD1a, CD1b and CD1c, upon human monocytes. CD1 molecules appeared upon monocytes on day 1 of stimulation with rGM-CSF, and expression was up-regulated until day 3. Monocytes cultured in the presence of LPS, FMLP, PMA, recombinant granulocyte-CSF, rIFN-gamma, rTNF-alpha, rIL-1 alpha, rIL-1 beta, and rIL-6 remained negative. The induction of CD1 molecules by rGM-CSF was restricted to monocytes, since no such effect was observed upon peripheral blood granulocytes, PBL, and the myeloid cell lines Monomac1, Monomac6, MV4/11, HL60, U937, THP1, KG1, and KG1A. CD1a mRNA was detectable in rGM-CSF-induced monocytes but not in those freshly isolated. SDS-PAGE and immunoblotting analyses of CD1a mAb VIT6 immunoprecipitate from lysate of rGM-CSF-activated monocytes revealed an appropriate CD1a polypeptide band of 49 kDa associated with beta 2-microglobulin. Expression of CD1 molecules on monocytes complements the distribution of these structures on accessory cells, and their specific induction by GM-CSF strengthens the suggestion that CD1 is a family of crucial structures required for interaction between accessory cells and T cells.
在本文中，我们证明粒细胞巨噬细胞集落刺激因子（GM-CSF）可特异性诱导人单核细胞表达CD1分子，即CD1a、CD1b和CD1c。在用重组GM-CSF刺激的第1天，单核细胞上出现CD1分子，其表达在第3天之前上调。在脂多糖（LPS）、N-甲酰甲硫氨酸-亮氨酸-苯丙氨酸（FMLP）、佛波酯（PMA）、重组粒细胞集落刺激因子、重组干扰素-γ（rIFN-γ）、重组肿瘤坏死因子-α（rTNF-α）、重组白细胞介素-1α（rIL-1α）、重组白细胞介素-1β（rIL-1β）和重组白细胞介素-6存在的情况下培养的单核细胞仍为阴性。rGM-CSF对CD1分子的诱导仅限于单核细胞，因为在外周血粒细胞、外周血淋巴细胞（PBL）以及髓系细胞系Monomac1、Monomac6、MV4/11、HL60、U937、THP1、KG1和KG1A中未观察到这种效应。在rGM-CSF诱导的单核细胞中可检测到CD1a mRNA，但在新鲜分离的单核细胞中未检测到。对rGM-CSF激活的单核细胞裂解物进行SDS-聚丙烯酰胺凝胶电泳（SDS-PAGE）和免疫印迹分析，用CD1a单克隆抗体VIT6免疫沉淀，结果显示与β2-微球蛋白相关的49 kDa的适当CD1a多肽条带。单核细胞上CD1分子的表达补充了这些结构在辅助细胞上的分布，并且GM-CSF对它们的特异性诱导进一步表明CD1是辅助细胞与T细胞相互作用所需的关键结构家族。
