Assessment of in Vitro Cytikine Response to Human Immunodeficiency Virus Antigens
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Date
1992-12
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Addis Abeba Universty
Abstract
The study of mononuclear cell responses after human
immunodeficiency virus type-l (HIV-l ) activation may help in
providing some insight into the understanding of the pathogenic
mechanisms of HIV infection or acquired immunodeficiency syndrome
(AIDS)-related disorders. The secretion of three cytokines,
interleukin-6 (IL-6) , tumor necrosis factor (TNF)-alpha, and
interferon(IFN)-gamma by peripheral blood mononuclear cells(PBMC)
was determined after in vitro stimulation with heat -inactivated
HIV-I antigens, using cytokine-specific monoclonal antibodies and
an indirect immunofluorescence technique. HIV-l antigen
stimulation of PBMC from healthy donors did not induce the
intracellular accumulation of IL-6, TNF-alpha, or IFN-gamma.
Similarly, cells from asymptomatic HIV-infected subjects did not
result in cytokine production either spontaneously or f ollowing
stimulation with HIV antigen. After activation with mitogen o r
antigen,cells from HIV-infected persons produced amounts of IL-6,
TNF-alpha and IFN-gamma comparable to that of cells from healthy
individuals. Furthermore, co-st imulation o f normal PBMC with HIVantigen
plus L.donovani resulted in intracellular accumulation
of IL-6 and TNF-alpha comparab~ e to that of cells that were
activated with Leishmania antigen alone. Heat-inactivated HIV-l
antigen does n o t appear to induce or modulate cytokine production
by PBMC. A defect in cytokine production is also accompanied by
i nh ibition of PPD-induced lymphoproliferative responses . Elevated
levels o f serum cytokines have been demonstrated in patients with
HIV infection indicating their role in the pathogenesis of
HIV-associated infections. Theref ore, data from our results may
partly support the idea that t he cause o f the abnormal l y
increased cycokine levels in t he sera o f HIV-infected subjects
x
might be jue to a variety of opportunistic pathogens that these
patients contract. As cytokines have been shown t o up-regulate
HIV repl ication, our data addit i onally demonstrate a role f o r
opportunistic infections in cytokine induced transactivation of
HIV-l and disease progression.
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Assessment of in Vitro Cytikine Response