Kimata H, Saxon A
Department of Medicine, University of California, School of Medicine, Los Angeles 90024.
J Clin Invest. 1988 Jul;82(1):160-7. doi: 10.1172/JCI113565.
Expression of Fc receptors for IgE (FcER) or IgA (FcAR) on purified natural killer (NK) cells was investigated. No FcER+ and a few FcAR+ NK cells were detectable on freshly separated NK (NKH-1+) cells from normal donors. Incubation of NK cells with IgE-anti-IgE immune complexes or IgA-anti-IgA immune complexes induced up to 10 and 20% FcER+ or FcAR+ cells, respectively. These FcR were induced on CD3- but not on CD3+ NKH-1+ cells. In contrast, NK cells from patients with various dysgammaglobulinemias could not be induced to express FcER or FcAR corresponding to their abnormal circulating IgE and/or IgA levels. Enriched FcER+ or FcAR+ induced NK cell supernatants from normals enhanced IgE or IgA synthesis from Ig secreting B cell lines in an isotype-specific fashion without increasing proliferation. Thus NK cells, after interaction with specific Ig isotypes in complexes, express FcR and produce differentiation factors for that isotype.
研究了纯化的自然杀伤(NK)细胞上IgE(FcεR)或IgA(FcαR)的Fc受体表达情况。在从正常供体新鲜分离的NK(NKH-1+)细胞上,未检测到FcεR+ NK细胞,仅检测到少数FcαR+ NK细胞。用IgE-抗IgE免疫复合物或IgA-抗IgA免疫复合物孵育NK细胞,分别诱导出高达10%和20%的FcεR+或FcαR+细胞。这些Fc受体在CD3- NKH-1+细胞上被诱导表达,但在CD3+ NKH-1+细胞上未被诱导表达。相反,各种异常球蛋白血症患者的NK细胞不能根据其异常循环IgE和/或IgA水平被诱导表达FcεR或FcαR。来自正常人的富集FcεR+或FcαR+诱导NK细胞上清液,以同型特异性方式增强Ig分泌B细胞系的IgE或IgA合成,而不增加增殖。因此,NK细胞在与复合物中的特异性Ig同型相互作用后,表达Fc受体并产生针对该同型的分化因子。