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Human T cells express specific binding sites for C1q. Role in T cell activation and proliferation.

放射性配体 分子生物学 T细胞 细胞培养 细胞毒性T细胞 化学 受体 细胞内 T淋巴细胞 生物 生物化学 体外 免疫系统 免疫学 遗传学
作者
A. Chen,S. Gaddipati,Yongtaek Hong,David J. Volkman,Ellinor I.B. Peerschke,Berhane Ghebrehiwet
出处
期刊:Journal of Immunology [The American Association of Immunologists]
卷期号:153 (4): 1430-1440 被引量:97
标识
DOI:10.4049/jimmunol.153.4.1430
摘要

Abstract Although the receptor that binds to the collagen-like domain of human C1q (C1qR) is expressed on a wide variety of cell types, the presence or absence of this receptor on human T lymphocytes has been debatable. The current studies were undertaken to re-examine whether human T cells possess specific binding sites for C1q by using a combination of techniques, including radioligand binding studies, flow cytometric analysis, and epifluorescence imaging techniques. Radioligand binding studies indicate that both peripheral T cells and the cultured T cell line, MOLT4, bind 125I-labeled C1q in a specific and apparently saturable manner, reaching equilibrium within 30 min at 37 degrees C under conditions of subphysiologic (90 mM NaCl) ionic strength. Western blot analysis with anti-C1qR of membrane proteins derived from Raji and MOLT4 cells showed an apparent single band of approximately 60 kDa under nonreducing conditions. Furthermore, when peripheral blood T cells were stimulated with 12,-o-tetradecanoyl phorbol-13-ester acetate for 5 days at 37 degrees C and assessed by FACS for their ability to bind anti-C1qR, the mitogen-induced cells were found to bind 40 to 50% more than their unstimulated counterparts. In addition, both CD4+ and CD8+ T cells were found to bind anti-C1qR. When the cells were mitogen induced with either 12,-o-tetradecanoyl phorbol-13-ester acetate, Con A, or PWM for 48 h in the presence or absence of 50 micrograms/ml C1q then pulsed with 1 microCi [3H]thymidine for 16 h at 37 degrees C, proliferation was significantly inhibited (40 to 80%, n = 7) as assessed by reduced [3H]thymidine incorporation. Taken together, the data suggest that: 1) Human T cells express C1qR in which immunoblots reveal a 60-kDa single chain protein. 2) C1qR expression is up-regulated by mitogens that induce T cell proliferation. 3) The primary ligand, C1q, induces an antiproliferative signal, which suggests that the C1qR plays a role in T cell activation and proliferation. In addition, the data contribute to the characterization of C1qRs on cells in peripheral blood and indicate that all cells, with the exception of erythrocytes, bear functional C1q receptors.
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