ANALYSIS OF NATURAL-KILLER (NK) CELL SUBSETS DEFINED BY THE EXPRESSION OF 2 NOVEL SURFACE-ANTIGENS (EB6 AND GL183) IN AIDS AND AIDS-RELATED CONDITIONS

被引:35
作者
CAUDA, R
GOLETTI, D
LUCIA, MB
TUMBARELLO, M
RUMI, C
ORENGO, AM
MORETTA, A
机构
[1] UNIV CATTOLICA S CUORE, SERV EMATOL, I-00168 ROME, ITALY
[2] UNIV GENOA, IST ISTOL & EMBRIOL, GENOA, ITALY
来源
CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY | 1994年 / 70卷 / 03期
关键词
D O I
10.1006/clin.1994.1029
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
In this study we analyzed the expression of EB6 and GL183, which are part of P58 molecular family that represents the putative NK receptor for MHC class I molecules, in peripheral blood lymphocytes of 60 patients with HIV infection (20 asymptomatic HIV-seropositive individuals, 20 patients with constitutional symptoms, and 20 AIDS patients) and correlated it with the level of CD4(+), CD56(+) cells, and the NK cell activity in order to determine a possible relation with disease progression. The absolute number (but not the percentage) of CD56(+), EB6(+), and GL183(+) cells was significantly reduced only in AIDS patients but not in the other AIDS-related clinical conditions. On the contrary, NK cell activity was reduced in all HIV-infected patients. In a g-month follow-up, patients with constant clinical conditions and stable CD4(+) cells level showed no significant difference, either in the percentage or absolute number of EB6(+) and GL183(+) cells. Interestingly, dual-color fluorescence indicates that GL183 and EB6 molecules (that in normal individuals are virtually absent on CD3(-) NK cells) are expressed in HIV-infected individuals not only in CD56(+) cells but also in CD3(+) cells. This may reflect a depletion of other T cell subsets or alternatively (less likely) a specific immune response. Our data indicate that the expression of EB6 and GL183 in T and NK cells from HIV-infected patients might be relevant in the course of the disease and for the disease-associated functional defect of NK cell activity (C) 1994 Academic Press, Inc.
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页码:198 / 205
页数:8
相关论文
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