Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
|
| pubmed:dateCreated |
1992-2-20
|
| pubmed:abstractText |
We investigated monocyte-derived macrophage function in 25 HIV-positive patients, 19 in the CDC class III and 6 class IV; 17 were intravenous drug abusers (IVDA) and 8 were homosexual men. Macrophages from HIV-positive patients behaved normally in assays of superoxide anion (O2-) production and candidacidal activity. After 3 days' treatment with 200 U/ml recombinant interferon-gamma (rIFN-gamma) or 250 U/ml recombinant granulocyte/macrophage-colony stimulating factor (rGM-CSF), both control and HIV-positive patients' phagocytes expressed the activated state, as indicated by the increased O2- production in response to phagocytable or soluble stimuli; however, these cytokines did not enhance candidacidal activity. Compared to appropriate HIV-negative controls (18 healthy heterosexuals, 4 homosexuals and 4 IVDA), macrophages from 19 of the 25 HIV-positive patients presented a significant defect in their Fc receptor (FcR)-dependent phagocytosis, independently from the CDC stage, AZT therapy, or life style. Treatment of macrophages with rIFN-gamma impaired their capacity to ingest IgG-coated erythrocytes, both in controls and HIV-positive subjects. Treatment of phagocytes with rGM-CSF significantly increased their FcR-dependent phagocytosis in controls, whereas in HIV-positive patients and in HIV-negative homosexuals and IVDA only an upward tendency was observed. Although the mechanism of the impaired FcR-dependent phagocytosis in HIV-positive patients remain to be clarified, our results suggest that this functional defect may be secondary to phagocyte priming by circulating IFN-gamma in vivo. This macrophage alteration may be implicated in the immunodeficiency of HIV-positive patients. However, considering the potential role of FcRs in HIV infection enhancement, the defective FcR function might even be a protective mechanism against FcR-mediated HIV dissemination. In the light of these findings, the immunotherapeutic potential of IFN-gamma and GM-CSF in HIV infection merits further investigation.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Feb
|
| pubmed:issn |
0090-1229
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
62
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
176-82
|
| pubmed:dateRevised |
2011-11-17
|
| pubmed:meshHeading |
pubmed-meshheading:1730155-Acquired Immunodeficiency Syndrome,
pubmed-meshheading:1730155-Adult,
pubmed-meshheading:1730155-Blood Physiological Phenomena,
pubmed-meshheading:1730155-Candida,
pubmed-meshheading:1730155-Female,
pubmed-meshheading:1730155-Granulocyte-Macrophage Colony-Stimulating Factor,
pubmed-meshheading:1730155-HIV Infections,
pubmed-meshheading:1730155-HIV Seropositivity,
pubmed-meshheading:1730155-Humans,
pubmed-meshheading:1730155-Interferon-gamma,
pubmed-meshheading:1730155-Macrophages,
pubmed-meshheading:1730155-Male,
pubmed-meshheading:1730155-Phagocytosis,
pubmed-meshheading:1730155-Receptors, Fc,
pubmed-meshheading:1730155-Recombinant Proteins,
pubmed-meshheading:1730155-Respiratory Burst
|
| pubmed:year |
1992
|
| pubmed:articleTitle |
Monocyte-derived macrophage function in HIV-infected subjects: in vitro modulation by rIFN-gamma and rGM-CSF.
|
| pubmed:affiliation |
Instituto di Medicina Interna, Malattie Infettive e Immunopatologia, University of Milan, Italy.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|