D. Wolday et al., HIV-1 INHIBITS LEISHMANIA-INDUCED CELL-PROLIFERATION BUT NOT PRODUCTION OF INTERLEUKIN-6 AND TUMOR-NECROSIS-FACTOR-ALPHA, Scandinavian journal of immunology, 39(4), 1994, pp. 380-386
The immune response of normal human peripheral blood mononuclear cells
(PBMC) after stimulation with human immunodeficiency virus-1 (HIV-1)
antigens plus Leishmania donovani promastigotes in vitro was investiga
ted. HIV-1-antigen stimulation of PBMC did not induce the intracellula
r accumulation of interleukin-6 (IL-6), tumour necrosis factor-alpha (
TNF-alpha), or interferon-gamma (IFN-gamma). However, cells stimulated
with L. donovani antigens exhibited the production of IL-6 and TNF-al
pha, but not IFN-gamma. Furthermore, co-stimulation of PBMC with HIV-I
antigen plus L. donovani resulted in the intracellular accumulation o
f IL-6 and TNF-alpha comparable to that of cells that were activated w
ith L. donovani antigen alone. Heat-inactivated HIV-1 antigen did not
appear to induce or suppress cytokine production by PBMC. However, the
same HIV antigens did suppress L. donovani-induced proliferation as w
ell as PPD-induced proliferation in a dose-dependent fashion. Elevated
levels of serum cytokines have been demonstrated in patients with HIV
infection indicating their role in the pathogenesis of HIV-associated
immunosuppression. The results may partially support the idea that th
e abnormally increased cytokine levels in the sera of HIV-infected sub
jects is due to the various opportunistic pathogens that these patient
s contract, rather than a response to HIV antigens. As cytokines have
been shown to up-regulate HIV replication, the data suggest a role for
opportunistic infections in cytokine-induced transactivation of HIV-1
and disease progression.