concanavalin-a has been researched along with Encephalitis--Viral* in 1 studies
1 other study(ies) available for concanavalin-a and Encephalitis--Viral
| Article | Year |
|---|---|
Selective role for the p55 Kd TNF-alpha receptor in immune unresponsiveness induced by an acute viral encephalitis.
Brain infection by the laboratory strain challenge virus standard (CVS), a highly neurotropic strain of rabies virus, causes splenocytes to become less responsive to in vitro stimulation with ConA. CVS-induced immune unresponsiveness is less severe in mice lacking the p55 Kd TNF-alpha receptor (p55TNFR(-/-)) than in C57BL/6 mice, despite a similar invasion of the brain. Comparison of CVS infection in these two strains of mice indicated that decreased immune responsiveness is associated with: (1) an in vivo reduction of the percentages of Th1 (IL-2, IFN-gamma and TNF-alpha) but not of Th2 (IL-4) cytokine-secreting T cells; and (2) an in vivo increase of the percentages of CD25 and CD69-expressing splenocytes. In contrast, CVS-induced immune unresponsiveness is not associated with abnormal percentage of T, B, NK cells or monocytes in vivo. The reductions of the CD4/CD8 ratio and of splenocyte expression of I-A(b) during CVS infection are similar in p55TNFR(-/-) and C57BL/6 mice indicating that these two parameters are not linked to the decreased responsiveness of splenocytes. These data suggest that CVS-induced immune unresponsiveness is under the control of the p55 Kd TNF-alpha receptor. We propose that T cell activation through this receptor, in an environment of poor antigen presentation, results in a state of T cells characterized by the reduced production of IL-2, TNF-alpha and IFN-gamma in vivo, the decreased responsiveness of splenocytes to ConA stimulation in vitro and the expression of the activation markers CD25 and CD69. Topics: Acute Disease; Animals; Antigens, CD; Antigens, Differentiation, T-Lymphocyte; CD3 Complex; CD4-CD8 Ratio; Concanavalin A; Encephalitis, Viral; Female; Immunophenotyping; Interferon-gamma; Interleukin-10; Interleukin-2; Interleukin-4; Interleukin-6; Lectins, C-Type; Lymphocyte Activation; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Rabies; Rabies virus; Receptors, Interleukin-2; Receptors, Tumor Necrosis Factor; Spleen; Th1 Cells; Th2 Cells; Tumor Necrosis Factor-alpha | 2001 |