Coico R F, Tamma S L, Bessler M, Wei C F, Thorbecke G J
Department of Microbiology, City University of New York Medical School, NY 10031.
J Immunol. 1990 Dec 1;145(11):3556-61.
Studies with human myeloma-derived IgD have demonstrated the existence of IgD-R on peripheral blood T cells. These receptors, which are detected by rosetting with IgD-coated ox E (IgD-rosette-forming cells), are competitively inhibited by IgD, but not by IgM or IgG. Similar results were obtained with human T cell clones and T hybridomas derived from such clones either by rosetting assays or by staining with biotinylated-IgD. In agreement with studies of murine IgD-R+ cells, human IgD-R can be up-regulated by exposure of peripheral blood T cells, T cell clones, and hybridomas derived from such clones, to oligomeric IgD, but not monomeric IgD. Human IgD-R can also be induced by IL-2, IL-4, and IFN-gamma. In contrast with studies of murine IgD-R, which are expressed primarily by CD4+ cells, phenotyping studies show that both the CD4+ and CD8+ human T cell subsets are capable of expressing IgD-R.
对源自人类骨髓瘤的IgD进行的研究已证明外周血T细胞上存在IgD-R。这些受体可通过与IgD包被的氧化E(IgD花环形成细胞)进行花环试验检测到,可被IgD竞争性抑制,但不受IgM或IgG抑制。通过花环试验或用生物素化IgD染色,对源自此类克隆的人类T细胞克隆和T杂交瘤也得到了类似结果。与对鼠IgD-R+细胞的研究一致,人IgD-R可通过将外周血T细胞、T细胞克隆以及源自此类克隆的杂交瘤暴露于寡聚IgD而非单体IgD而上调。人IgD-R也可由IL-2、IL-4和IFN-γ诱导。与主要由CD4+细胞表达的鼠IgD-R研究不同,表型研究表明,CD4+和CD8+人类T细胞亚群均能够表达IgD-R。