INHIBITION OF T-CELL RESPONSIVENESS DURING EXPERIMENTAL INFECTIONS WITH TRYPANOSOMA-BRUCEI - ACTIVE INVOLVEMENT OF ENDOGENOUS GAMMA-INTERFERON

Citation
A. Darji et al., INHIBITION OF T-CELL RESPONSIVENESS DURING EXPERIMENTAL INFECTIONS WITH TRYPANOSOMA-BRUCEI - ACTIVE INVOLVEMENT OF ENDOGENOUS GAMMA-INTERFERON, Infection and immunity, 61(7), 1993, pp. 3098-3102
Citations number
21
Categorie Soggetti
Immunology,"Infectious Diseases
Journal title
ISSN journal
00199567
Volume
61
Issue
7
Year of publication
1993
Pages
3098 - 3102
Database
ISI
SICI code
0019-9567(1993)61:7<3098:IOTRDE>2.0.ZU;2-#
Abstract
Lymph node cells (LNC) from mice infected with Trypanosoma brucei cont ain macrophage-like cells that inhibit interleukin-2 receptor (IL-2R) expression (M. Sileghem, A. Darji, R. Hamers, M. Van De Winkel, and P. De Baetselier, Eur. J. Immunol. 19:829-835, 1989). Evidence that gamm a interferon (IFN-gamma) is actively involved in (i) the inhibition of IL-2R expression and (ii) the generation of suppressive cells during infections with T. brucei is presented. First, despite an impaired T-c ell mitogenic response, LNC from infected mice are hyperresponsive for IFN-gamma production. Second, addition of neutralizing anti-IFN-gamma antibodies to cocultures of normal LNC and suppressive LNC population s reduces the level of suppression and restores the level of IL-2R exp ression. Third, administration of anti-IFN-gamma to T. brucei-infected animals increases the blastogenic response and reduces the suppressiv e activity of LNC.