Abstract
The pathogenesis of HIV infection and the susceptibility to opportunistic infections has been associated with poor type 1 cytokine production. In severely immunodeficient HIV patients who achieved increased CD4 T-cell counts on longterm highly active antiretroviral therapy, we observed reduced expression of IL-23p19 and IFN-gamma messenger RNA. Impaired IL-23-induced IFN-gamma production by memory T cells might thus contribute to opportunistic infections in a minority of patients with substantial CD4 T-cell recovery.
MeSH terms
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Adult
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Antiretroviral Therapy, Highly Active
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CD4 Lymphocyte Count
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Case-Control Studies
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HIV Infections / drug therapy
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HIV Infections / immunology*
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Humans
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Interferon-gamma / deficiency*
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Interferon-gamma / genetics
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Interleukin-23
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Interleukin-23 Subunit p19
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Interleukins / deficiency*
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Interleukins / genetics
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Lymphocytes / immunology
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Male
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RNA, Messenger / analysis
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Reverse Transcriptase Inhibitors / therapeutic use
Substances
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IL23A protein, human
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Interleukin-23
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Interleukin-23 Subunit p19
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Interleukins
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RNA, Messenger
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Reverse Transcriptase Inhibitors
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Interferon-gamma