Gutheil W G, Subramanyam M, Flentke G R, Sanford D G, Munoz E, Huber B T, Bachovchin W W
Department of Biochemistry, Tufts University School of Medicine, Boston, MA 02111.
Proc Natl Acad Sci U S A. 1994 Jul 5;91(14):6594-8. doi: 10.1073/pnas.91.14.6594.
The human immunodeficiency virus 1 (HIV-1) Tat protein suppresses antigen-induced, but not mitogen-induced, activation of human T cells when added to T-cell cultures [Viscidi, R. P., Mayur, K., Lederman, H. M. & Frankel, A. D. (1989) Science 246, 1606-1608]. This activity is potentially pertinent to the development of AIDS because lymphocytes from HIV-infected individuals exhibit a similar antigen-specific dysfunction. Here we report that Tat binds with high affinity to the T-cell activation molecule dipeptidyl aminopeptidase IV (DP IV), also known as CD26. This molecule occurs on the surface of CD4+ cells responsible for the recall antigen response and appears to play an essential role in this response. Tat binds to both the cell surface and soluble forms of DP IV at physiological salt concentrations without inhibiting the protease activity of DP IV against small chromogenic substrates used to assay activity, but Tat markedly inhibits the activity of DP IV at lower salt concentrations. The kinetics of inhibition indicate the affinity of Tat for DP IV varies from 20 pM to 11 nM, and the activity of the Tat-DP IV complex varies from 13% to 100%, as the NaCl concentration varies from 0 to 140 mM. Cytofluorometry experiments demonstrate that Tat competes with anti-Ta1, a monoclonal antibody (mAb) specific for DP IV, for binding to cell surface DP IV, thus indicating that Tat binds DP IV at or near the Ta1 epitope. Moreover, the anti-Ta1 mAb blocks the immunosuppressive activity of Tat. The high affinity of Tat for DP IV, previous evidence implicating DP IV in antigen-specific T-cell activation events, and the ability of anti-Ta1 mAb to block the immunosuppressive effect of Tat make DP IV a plausible receptor for Tat's immunosuppressive activity.
人类免疫缺陷病毒1型(HIV-1)的Tat蛋白添加到T细胞培养物中时,可抑制抗原诱导而非丝裂原诱导的人类T细胞活化[维斯迪,R.P.,马尤尔,K.,莱德曼,H.M.和弗兰克尔,A.D.(1989年)《科学》246,1606 - 1608]。该活性可能与艾滋病的发展相关,因为来自HIV感染个体的淋巴细胞表现出类似的抗原特异性功能障碍。在此我们报告,Tat与T细胞活化分子二肽基氨基肽酶IV(DP IV),也称为CD26,具有高亲和力结合。该分子存在于负责回忆抗原反应的CD4 +细胞表面,并且似乎在该反应中起重要作用。在生理盐浓度下,Tat可与细胞表面形式和可溶性形式的DP IV结合,而不抑制DP IV对用于测定活性的小显色底物的蛋白酶活性,但在较低盐浓度下,Tat可显著抑制DP IV的活性。抑制动力学表明,随着NaCl浓度从0变化到140 mM,Tat对DP IV的亲和力从20 pM变化到11 nM,Tat-DP IV复合物的活性从13%变化到100%。细胞荧光测定实验表明,Tat与抗Ta1(一种对DP IV特异的单克隆抗体(mAb))竞争结合细胞表面DP IV,从而表明Tat在Ta1表位或其附近结合DP IV。此外,抗Ta1 mAb可阻断Tat的免疫抑制活性。Tat对DP IV的高亲和力、先前暗示DP IV参与抗原特异性T细胞活化事件的证据以及抗Ta1 mAb阻断Tat免疫抑制作用的能力使DP IV成为Tat免疫抑制活性的一个合理受体。