INTERLEUKIN-2 AND HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION - PATHOGENICMECHANISMS AND POTENTIAL FOR IMMUNOLOGICAL ENHANCEMENT

Authors
Citation
A. Kinter et As. Fauci, INTERLEUKIN-2 AND HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION - PATHOGENICMECHANISMS AND POTENTIAL FOR IMMUNOLOGICAL ENHANCEMENT, Immunologic research, 15(1), 1996, pp. 1-15
Citations number
136
Categorie Soggetti
Immunology
Journal title
ISSN journal
0257277X
Volume
15
Issue
1
Year of publication
1996
Pages
1 - 15
Database
ISI
SICI code
0257-277X(1996)15:1<1:IAHI-P>2.0.ZU;2-4
Abstract
A hallmark of human immunodeficiency virus (HIV) infection is the prog ressive loss of CD4+ T lymphocytes; however, qualitative defects in im mune 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 add ition of IL-2 in vitro to cultures of mononuclear cells from HIV-infec ted individuals partially or completely restored certain defective cel lular immune responses, However, production of or addition of IL-2 has also been associated with increased viral replication in infected T c ells. These observations underscore the pernicious correlation between immune activation and HIV replication. However, recent in vitro and i n vivo studies have provided promising preliminary results suggesting that, at least at certain stages of disease, the benefits of IL-2-medi ated immune enhancement may outweigh or override the inductive effects of this cytokine on HIV production.