LeMaoult Joël, Zafaranloo Kamélia, Le Danff Caroline, Carosella Edgardo D
Service de Recherches en Hémato-Immunologie, Commissariat à L'Energie Atomique-DRM-DSV, Institut Universitaire d'Hématologie, Hôpital Saint Louis, Paris, France.
FASEB J. 2005 Apr;19(6):662-4. doi: 10.1096/fj.04-1617fje. Epub 2005 Jan 24.
The nonclassical HLA class I antigen HLA-G is an inhibitory molecule involved in immune tolerance and immune escape. HLA-G exerts its inhibitory functions via interaction with inhibitory receptors ILT2, ILT4, and KIR2DL4, differentially expressed by NK, T, and antigen-presenting cells. Cells expressing HLA-G and cells expressing its receptors are often found in the vicinity of each other, but the mechanisms responsible for this colocalization are still unknown. We report that ILT2, ILT3, ILT4, and KIR2DL4 expression is up-regulated by HLA-G in antigen-presenting cells, NK cells, and T cells. Because this up-regulation seems not to require antigenic costimulation, it might precede an immune response. Functionally, up-regulation of inhibitory receptors in immune cells before stimulation might increase their activation thresholds and participate in immune escape mechanisms.
非经典的I类人类白细胞抗原（HLA）HLA-G是一种参与免疫耐受和免疫逃逸的抑制性分子。HLA-G通过与抑制性受体ILT2、ILT4和KIR2DL4相互作用发挥其抑制功能，这些受体在自然杀伤细胞（NK）、T细胞和抗原呈递细胞中差异表达。表达HLA-G的细胞与其受体表达细胞常彼此相邻，但导致这种共定位的机制仍不清楚。我们报告，在抗原呈递细胞、NK细胞和T细胞中，HLA-G可上调ILT2、ILT3、ILT4和KIR2DL4的表达。由于这种上调似乎不需要抗原共刺激，它可能先于免疫反应发生。在功能上，刺激前免疫细胞中抑制性受体的上调可能会提高其激活阈值，并参与免疫逃逸机制。
