首页> 美国政府科技报告 >Valency of CD3 Binding and Internalization of the CD3 Cell-Surface Complex Control T Cell Responses to Second Signals: Distinction between Effects on Protein in Kinase C, Cytoplasmic Free Calcium, and Proliferation
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Valency of CD3 Binding and Internalization of the CD3 Cell-Surface Complex Control T Cell Responses to Second Signals: Distinction between Effects on Protein in Kinase C, Cytoplasmic Free Calcium, and Proliferation

机译:CD3结合和内化CD3细胞表面复合物对照T细胞对第二信号的反应的价值:激酶C中蛋白质,细胞质游离钙和增殖之间的区别

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We have studied the relationship of valency of CD3 stimulation and modulation of the CD3 receptor complex with biochemical and proliferative responses of T cells. Anti-CD3 Fab, as well as F(ab)2 and whole antibody caused rapid modulation of the CD3 antigen, whereas anti-CD3 conjugated to Sepharose did not. In the absence of monocytes, T cells stimulated with anti-CD Fab, F(ab)2, or F(ab)2 Sepharose showed differences in their ability to respond to second signals given by PMA, IL 1, IL 2, or antibodies to Tp67 and Tp44. None of the anti-CD3 signals alone caused resting T cells to produce IL 2, and only the Sepharaose-bound anti-CD3 F(ab)2 caused T cells to express high levels of functional IL 2 receptrs. Anti CD3 F(ab)2-Sepharose-stimulated T cells to express high levels of functional IL 2 receptors. Anti-CD3 F(ab)2 Sepharose-stimulated T cells produced IL 2 and proliferated in response to each of the second signals. Because anti-CD3-Sepharose did not cause modulation of the CD3 antigen, the ability of the Sepharose-bound antibody to induce T cells to express IL 2 receptors and to response to individual second signals may be related to lack of modulation rather than valency of binding. Stimulations that resulted in modulation (i.e., anti-CD3 whole antibody, anti-CD3 F(ab)2, or anti-CD3 Fab fragments) caused an increase in cytoplasmic calcium levels in resting T cells by blocked proliferation of T cells in response to mitogenic lectins or CD2 stimulation.

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