Effects of abnormalities of adhesion molecule on T-cell function in HIV-infected patients.

(1)粘附分子，即β 1（VLA-β 1）（CD29），α 4（VLA-alpha4）（CD49d），alpha6（VLA-alpha6）（CD49f），alphaL检测淋巴细胞和单核细胞的LFA-1 α（CD 11 a）、β 3（CD 61）、β 7、L-选择素（CD 62 L）、ICAM-1（CD 54）以及HLA-DR、CD 69、CD 30、CD 71、CD 45 RO、CD 26、β 2-微球蛋白在HIV感染的血友病患者中的作用。Thy1，2作为阴性对照。HIV感染者CD_4、CD_8 β_3（CD_（61））明显降低（P <0.01）。本研究未能阐明T淋巴细胞β 3（CD61）水平低下的原因及临床意义。(2)白血病细胞浸润皮肤的ATL细胞（3/6例）表达E-选择素的配体CLA抗原。来自白血病浸润至肠道的患者的ATL细胞（3例中的2例）表达整合素β 7。结果提示，白血病细胞表面粘附分子的表达对ATL细胞向组织浸润起决定作用。(3)ATL细胞的增殖可能是通过LFA-1/ICAM-1的同型和钙依赖性粘附、这些粘附分子的信号转导、细胞因子的产生和增殖等一系列过程进行的。

(1) The adhesion melecules, that is, beta1 (VLA-beta1) (CD29), alpha4 (VLA-alpha4) (CD49d), alpha6 (VLA-alpha6) (CD49f), alphaL (LFA-1alpha) (CD11a), beta3 (CD61), beta7, L-selectin (CD62L), ICAM-1 (CD54) of lymphocytes and monocytes were measured as well as HLA-DR,CD69, CD30, CD71, CD45RO,CD26, beta2-micro-globulin in HIV-infected patients with hemophilia. Thy1,2 was used as negative control. beta3 (CD61) of CD4 and CD8 were significantly lowered (p<0.01) in HIV-infected patients. In this study, the reason and clinical significance of low level of beta3 (CD61) of T lymphocytes could not clarified.(2) ATL cells (3 of 6 cases) from the patients with leukemic cell infiltration to skin expressed CLA antigen (legand of E-selectin). ATL cells (2 of 3 cases) from the patients with leukemic infiltration to gut expressed integrin beta7. The results suggested that the express of adhesion molecules on leukemic cells play a role in determination of ATL cells infiltration to tissure.(3) ATL cells may proliferate in the sequentioal manner, such as, homotypic and calcium-dependent adhesion through LFA-1/ICAM-1, the signal transduction throug hthese adhesion molecules, the production of cytokines and the proliferation.