TYPE-1 AND TYPE-2 CYTOKINES IN HIV-INFECTION - A POSSIBLE ROLE IN APOPTOSIS AND DISEASE PROGRESSION

Citation
M. Clerici et al., TYPE-1 AND TYPE-2 CYTOKINES IN HIV-INFECTION - A POSSIBLE ROLE IN APOPTOSIS AND DISEASE PROGRESSION, Annals of medicine, 29(3), 1997, pp. 185-188
Citations number
18
Language
INGLESE
art.tipo
Editorial Material
Categorie Soggetti
Medicine, General & Internal
Journal title
ISSN journal
0785-3890
Volume
29
Issue
3
Year of publication
1997
Pages
185 - 188
Database
ISI
SICI code
0785-3890(1997)29:3<185:TATCIH>2.0.ZU;2-B
Abstract
The progression of HIV-infected subjects to AIDS was recently postulat ed to be controlled by the balance between type 1 cytokines (mainly en hancing cell-mediated immunity) and type 2 cytokines (mainly augmentin g antibody production), Thus, progression of HIV infection was suggest ed to be accompanied by a decline of in vitro production of interleuki n-2 (IL-2), IL-12 and interferon gamma (IFN-gamma) (type 1 cytokines) and an increase in the production of IL-4, IL-5, IL-6 and IL-10 (type 2 cytokines) by peripheral blood mononuclear cells of HIV-seropositive patients, According to this hypothesis, clinical markers of progressi on would be considered the loss of the ability to elicit a delayed-typ e hypersensitivity reaction to ubiquitous antigens (secondary to defec tive IL-2 production), hyper-IgE (secondary to increased IL-4 producti on) and hypereosynophilia (secondary to increased IL-5 production). Th e type 1 to type 2 shift was suggested to be predictive for the follow ing events: (i) reduction in CD4 counts; (ii) time to AIDS diagnosis; (iii) time to death, Support for this hypothesis stems from the recent observation that a strong type 1/weak type 2 cytokine production prof ile was observed in HIV-seropositive patients with delayed or absent d isease progression, whereas progression of HIV infection was character ized by a weak type 1/strong type 2 cytokine production profile. PBMC of HIV-seropositive individuals are susceptible to antigen-induced cel l death (AICD) after antigen recognition via T-cell receptor (TcR), Wh ile TcR-induced AICD is seen in CD4(+) and CD8(+) cells programmed cel l death induced by recall antigens is preferentially observed in CD4() cells, a situation more closely resembling the CD4 depletion of HIV infection, Because type 1 cytokines reduce, whereas type 2 cytokines a ugment T-lymphocyte AICD, an increase in the concentration of type 2 c ytokines could result in the decline in CD4(+) cells seen in HIV infec tion.