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Clinical and Diagnostic Laboratory Immunology, 11 1995, 712-718, Vol 2, No. 6
MP Daftarian, F Diaz-Mitoma, WD Creery, W Cameron and A Kumar
The loss of immune function following infection with human immunodeficiency
virus (HIV) may result from altered production of immunoregulatory
cytokines such as interleukin-10 (IL-10) and IL-12. In this study, we
analyzed IL-10 and IL-12 production by mitogen- stimulated peripheral blood
mononuclear cells (PBMC) from HIV+ individuals and correlated their levels
with proliferative responses to the recall antigens HIV p25 and influenza
virus. We report two distinct groups of HIV+ patients. One group produced
small amounts of IL-10, had PBMC that proliferated in response to recall
antigens, and demonstrated enhanced recall antigen-induced proliferation
upon addition of anti-IL- 10 antibodies and/or IL-12. Conversely, the
second group produced high levels of IL-10, had PBMC that failed to
proliferate to recall antigens, and did not demonstrate enhanced
proliferation upon addition of anti-IL-10 antibodies and/or IL-12.
Mitogen-stimulated PBMC from both groups produced significantly lower
levels of IL-12 than did those from HIV- controls. Analysis of the source
of the IL-10-producing cell subset in PBMC demonstrated that in HIV+
individuals, IL-10 is produced by monocytes, while in HIV- controls, it is
produced by both T cells and monocytes. Taken together, our results suggest
that monocytes from HIV+ individuals secrete decreased amounts of IL-12, a
Th1-type cytokine, which may lead to the development of Th2-type responses
characterized by high IL-10 secretion and immune dysfunction.
Copyright © 1995 by the American Society for Microbiology. All rights reserved.
Dysregulated production of interleukin-10 (IL-10) and IL-12 by peripheral blood lymphocytes from human immunodeficiency virus-infected individuals is associated with altered proliferative responses to recall antigens
Department of Pediatrics, Children's Hospital of Eastern Ontario, University of Ottawa, Canada.
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