Interleukin-2 and human immunodeficiency virus infection: pathogenic mechanisms and potential for immunologic enhancement.
A hallmark of human immunodeficiency virus (HIV) infection is the progressive loss of CD4+ T lymphocytes; however, qualitative defects in immune responses occur prior to the precipitous drop CD4+ T cell numbers. One of the first immunologic defects to be described in HIV-infected individuals is a deficiency in interleukin (IL)-2 production. The addition of IL-2 in vitro to cultures of mononuclear cells from HIV-infected individuals partially or completely restored certain defective cellular immune responses. However, production of or addition of IL-2 has also been associated with increased viral replication in infected T cells. These observations underscore the pernicious correlation between immune activation and HIV replication. However, recent in vitro and in vivo studies have provided promising preliminary results suggesting that, at least at certain stages of disease, the benefits of IL-2 mediated immune enhancement may outweigh or override the inductive effects of this cytokine on HIV production.
Kinter
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Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Md, USA.
Fauci
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D000276:Adjuvants, Immunologic / Q000008:administration & dosage / Q000009:adverse effects; D018791:CD4 Lymphocyte Count; D006678:HIV / Q000276:immunology / Q000502:physiology; D015658:HIV Infections / Q000209:etiology* / Q000276:immunology / Q000628:therapy*; D006801:Humans; D007111:Immunity, Cellular; D007167:Immunotherapy; D066298:In Vitro Techniques; D007376:Interleukin-2 / Q000009:adverse effects / Q000096:biosynthesis / Q000627:therapeutic use*; D015375:Receptors, Interleukin-2 / Q000378:metabolism; D014779:Virus Replication / Q000187:drug effects
D000276:Adjuvants, Immunologic; D007376:Interleukin-2; D015375:Receptors, Interleukin-2