Huet S, Boumsell L, Dausset J, Degos L, Bernard A
Laboratoire d'Immunologie des Tumeurs de l'Enfant, Institut Gustave-Roussy, Villejuif, France.
Eur J Immunol. 1988 Aug;18(8):1187-94. doi: 10.1002/eji.1830180807.
Previously, we have shown that paraformaldehyde-fixed monocytes are able to fully complement, in terms of [3H]dThd incorporation, a primary stimulus delivered to purified T cells by monoclonal antibodies (mAb) reacting with CD3 or CD2 molecules. Here, we show that depending on the stimulus used (CD3 mAb or different pairs of CD2 mAb) HLA class I molecules from monocytes are directly involved in complementary signals provided to T cells. This was evidenced by the following observations: (a) mAb reacting with the heavy or light chain of class I molecules, or their Fab fragments, completely blocked proliferation of peripheral blood lymphocytes (PBL) activated by CD3 mAb; (b) mAb against the heavy chain of HLA class I but not against beta 2-microglobulin partially blocked (approximately equal to 50%) PBL activation by the CD2 "GT2 + T111" mAb pair but did not block activation by CD2 "D66 + T111" mAb; (c) this pattern of inhibition was observed when anti-class I mAb were used in the soluble phase or when they were bound to monocytes subsequently fixed with paraformaldehyde and cultivated with purified autologous T cells; (d) fixed monocytes are able to restore interleukin (IL) 2 receptor expression on purified T cells stimulated by CD3 mAb or CD2 "GT2 + T111", contrary to anti-HLA class I mAb-pretreated monocytes. The inhibitory effects of anti-HLA class I mAb bound to monocytes were not found to be reversed by recombinant IL2 or recombinant IL1. We assume that HLA class I would be involved in two or more signals delivered to T cells by monocytes, the requirement in those signals depending on the initial stimulus applied to T cells.(ABSTRACT TRUNCATED AT 250 WORDS)
此前,我们已经表明,就[3H]胸苷掺入而言,多聚甲醛固定的单核细胞能够完全补充由与CD3或CD2分子反应的单克隆抗体(mAb)传递给纯化T细胞的主要刺激。在此,我们表明,根据所使用的刺激(CD3 mAb或不同的CD2 mAb对),单核细胞的HLA I类分子直接参与提供给T细胞的互补信号。以下观察结果证明了这一点:(a)与I类分子的重链或轻链或其Fab片段反应的mAb完全阻断了由CD3 mAb激活的外周血淋巴细胞(PBL)的增殖;(b)针对HLA I类重链而非β2-微球蛋白的mAb部分阻断(约50%)由CD2“GT2 + T111”mAb对激活的PBL,但不阻断由CD2“D66 + T111”mAb激活的PBL;(c)当抗I类mAb在可溶性相中使用或与随后用多聚甲醛固定并与纯化的自体T细胞一起培养的单核细胞结合时,观察到这种抑制模式;(d)与抗HLA I类mAb预处理的单核细胞相反,固定的单核细胞能够恢复由CD3 mAb或CD2“GT2 + T111”刺激的纯化T细胞上的白细胞介素(IL)2受体表达。未发现与单核细胞结合的抗HLA I类mAb的抑制作用可被重组IL2或重组IL1逆转。我们假设HLA I类会参与单核细胞传递给T细胞的两个或更多信号,这些信号的需求取决于施加给T细胞的初始刺激。(摘要截断于250字)