TY - JOUR
T1 - Change in expression of FcγRIII (CD16) on neutrophils from human immunodeficiency virus-infected individuals
AU - Boros, Peter
AU - Gardos, Eva
AU - Bekesi, George J.
AU - Unkeless, Jay C.
N1 - Funding Information:
We thank Dr. Clark Anderson for providing mAbs IV.3 and 32.2, and Dr. Michael Davitz for mAb IAIO. We acknowledge the assistance of Ms. Julia Roboz and the excellent technical assistance of Ms. Joyce Caraffa. This work was supported by PHS Grant AI24322 and AI24671 (J.C.U.) and by NIH Grant 5PC-30CA 23012, NIAID Contract NO1 52572 and 72660, and the T. J. Martell Foundation for Leukemia and Cancer Research (J.G.B.).
PY - 1990/2
Y1 - 1990/2
N2 - 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.
AB - 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.
UR - https://www.scopus.com/pages/publications/0025177301
U2 - 10.1016/0090-1229(90)90089-9
DO - 10.1016/0090-1229(90)90089-9
M3 - Article
C2 - 2136822
AN - SCOPUS:0025177301
SN - 0090-1229
VL - 54
SP - 281
EP - 289
JO - Clinical Immunology and Immunopathology
JF - Clinical Immunology and Immunopathology
IS - 2
ER -