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Effects of the Th1 and Th2 stimulatory cytokines interleukin-12 and
interleukin-4 on human immunodeficiency virus replication
A Foli, MW Saville, MW Baseler and R Yarchoan
Medicine Branch, National Cancer Institute, National Institutes of Health,
Bethesda, MD 20892, USA.
The cytokines interleukin-12 (IL-12) and IL-4 play important roles in the
development of Th1-like (type-1) and Th2-like (type-2) T-cell responses,
respectively, and there is evidence that type-1/type-2 T helper imbalances
are important in the pathogenesis of human immunodeficiency virus (HIV)
disease. With this background, we examined the effects of these cytokines
on HIV replication. Neither stimulated HIV replication in fresh peripheral
blood mononuclear cells (PBMC). However, in prestimulated PBMC, IL-12, and
to a greater extent, IL-4 as well as IL-2, induced production of HIV p24
antigen over 7 days of culture (no cytokine 3,900 x/divided by 1.31 [GM
x/divided by SEM] pg/mL; IL-12, 34,300 x/divided by 1.39 pg/mL; IL-4,
283,000 x/divided by 1.14 pg/mL; and IL-2, 328,000 x/divided by 1.31
pg/mL). Neither IL- 12- nor IL-4-induced HIV replication was attributable
to induction of IL-1, IL-2, tumor necrosis factor (TNF)-alpha, or TNF-beta.
Both IL-12- and IL-4-induced HIV replication was associated with selective
loss of the CD4+ subset in stimulated cultures. IL-4 stimulated HIV
replication in monocyte/macrophages, while IL-12 had little or no effect in
these cells. Finally, HIV replication stimulated by IL-12 or IL-4 was
inhibited by dideoxynucleosides. Thus, IL-12 and IL-4 enhance HIV
replication and HIV-induced cell death in prestimulated PBMC. Through
killing of the CD4+ T cells stimulated by these cytokines, this may result
in inappropriate type-1/type-2 responses in HIV-infected patients and
contribute to their Th1 immunodeficiency.
Volume 85,
Issue 8,
pp. 2114-2123,
04/15/1995
Copyright © 1995 by The American Society of Hematology
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