KINETICS OF CYTOKINE PRODUCTION BY THYMOCYTES DURING MURINE AIDS CAUSED BY LP-BM5 RETROVIRUS INFECTION

Citation
J. Wang et al., KINETICS OF CYTOKINE PRODUCTION BY THYMOCYTES DURING MURINE AIDS CAUSED BY LP-BM5 RETROVIRUS INFECTION, Immunology letters, 47(3), 1995, pp. 187-192
Citations number
42
Categorie Soggetti
Immunology
Journal title
ISSN journal
01652478
Volume
47
Issue
3
Year of publication
1995
Pages
187 - 192
Database
ISI
SICI code
0165-2478(1995)47:3<187:KOCPBT>2.0.ZU;2-Q
Abstract
C57BL\6 mice inoculated with the murine leukemia retrovirus mixture, L P-BM5, rapidly produce murine AIDS with many functional similarities t o human AIDS, Human HIV infection has recently been shown to inhibit t hymocyte maturation, Therefore, the kinetics of the proliferation of t hymocytes induced by Concanavalin A (ConA) and levels of cytokines pro duced by in vitro ConA-stimulated thymocytes were examined during the progression of murine AIDS, The proliferation of thymocytes induced by ConA was significantly enhanced by retrovirus infection at 4 weeks po st-infection compared to control, but significantly inhibited during 8 -12 weeks post-infection, Release of IL-2 by ConA-stimulated thymocyte s was significantly increased by retrovirus infection during 2-5 weeks postinfection and 11-18 weeks post-infection compared to control, but significantly decreased during 7-9 weeks post-infection. Secretion of IL-4 by ConA-stimulated thymocytes was significantly enhanced by retr ovirus infection from 5 to 18 weeks post-infection compared to control . The level of IL-6 produced by ConA-stimulated thymocytes was signifi cantly inhibited by retrovirus infection at the beginning of retroviru s infection (2-9 weeks), but significantly elevated after 11 weeks pos tinfection compared to control, Release of IFNgamma by ConA-stimulated thymocytes, however, was significantly enhanced during the whole peri od of retrovirus infection compared to control, while it surged at 13 weeks post-infection. We conclude that retrovirus infection affects th e thymus, producing altered T-cell differentiation via the dysregulati on of thymocyte cytokine secretion.