CHANGE IN EXPRESSION OF FC-GAMMA-RIII (CD16) ON NEUTROPHILS FROM HUMAN IMMUNODEFICIENCY VIRUS-INFECTED INDIVIDUALS

被引：33

作者：

BOROS, P ^{[1
]}

GARDOS, E ^{[1
]}

BEKESI, GJ ^{[1
]}

UNKELESS, JC ^{[1
]}

机构：

[1] CUNY MT SINAI SCH MED,DEPT NEOPLAST DIS,NEW YORK,NY 10029

来源：

CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY | 1990年 / 54卷 / 02期

关键词：

D O I：

10.1016/0090-1229(90)90089-9

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 [免疫学];

摘要：

FcγRIII on neutrophils is a phosphatidyl inositol glycan (PIG)-anchored protein that can be released from the cells by activation with chemotactic peptides. We have examined the expression of FcγRIII (CD16), CD11b, and FcγRII (CD32) on neutrophils from human immunodeficiency virus (HIV)-I-infected individuals by two-color FACS. In patients with AIDS and AIDS-related complex and in HIV-I positive intravenous drug abusers we observed a substantial population (25%) of neutrophils that were autofluorescent, and did not stain with the anti-FcγRIII mAb 3G8. This population was largely absent (3%) in HIV-I negative control individuals. No changes in the expression of FcγRII, CD11b, or another PIG-anchored protein, decay accelerating factor (CD55) on neutrophils, were found. The presence of the FcγRIII negative neutrophil population may be related to altered functions leading to common bacterial infections in advanced AIDS. © 1990.

引用

页码：281 / 289

页数：9

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