Autoantibodies to leukocyte alphaMbeta2 integrin glycoproteins in HIV infection
Copyright 1999 Academic Press.
Veröffentlicht in: | Clinical immunology (Orlando, Fla.). - 1999. - 90(1999), 3 vom: 01. März, Seite 352-9 |
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1. Verfasser: | |
Weitere Verfasser: | , , , |
Format: | Aufsatz |
Sprache: | English |
Veröffentlicht: |
1999
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Zugriff auf das übergeordnete Werk: | Clinical immunology (Orlando, Fla.) |
Schlagworte: | Journal Article Autoantibodies Glycoproteins Macrophage-1 Antigen |
Zusammenfassung: | Copyright 1999 Academic Press. HIV infection is often associated with polyclonal B-cell activation, autoantibodies, and clinically evident autoimmune disease. Because neutropenia and anti-neutrophil autoantibodies are common clinical features of HIV disease, we studied a series of HIV+ patients to determine whether anti-alphaMbeta2 integrin (MAC-1) specific anti-neutrophil autoantibodies occur in HIV disease, as we have shown to occur in patients with immune neutropenia not associated with HIV. Two new assays specific for anti-alphaMbeta2 IgG were developed to carry out these studies: an ELISA method using affinity-purified alphaMbeta2 integrin protein, and a flow cytometry method using subclones of the 293 human fetal kidney cell line, stably transfected with cDNAs for the alphaM and/or beta2 integrin subunits. In studies of the sera of 20 untreated HIV+ individuals, anti-alphaMbeta2 activity was detected in 9 (45%) by one or the other of these assays and in 5 (25%) by both assays. Seven of the 20 HIV+ study subjects had unexplained neutropenia, and of these, 6 (86%) were positive for anti-alphaMbeta2 autoantibodies. Our findings indicate that anti-alphaMbeta2 integrin autoantibodies are frequent in HIV+ individuals, particularly when unexplained neutropenia is also present, and raise the possibility that these autoantibodies may have a role in the acquired neutrophil dysfunction and increased risk of nonopportunistic bacterial infections observed in HIV disease |
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Beschreibung: | Date Completed 13.04.1999 Date Revised 17.11.2004 published: Print Citation Status MEDLINE |
ISSN: | 1521-7035 |