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Unimpaired clearance of Mycobacterium bovis BCG infection in selectively T-cell anergic TCR-V beta 8.2 transgenic
Y Koide1, A Yoshida, M Uchijima
1Department of Microbiology and Immunology, Hamamatsu University School of Medicine, Japan.
The anergy induced in mice with staphylococcal enterotoxin B (SEB) has been shown to involve selective unresponsiveness in cytokine expression. While interleukin-2 (IL-2), IL-3 and IL-4 mRNA levels are substantially reduced in anergic T cells upon restimulation with SEB, mRNA for interferon-gamma (IFN-gamma) is expressed normally. On the other hand, infection with Nippostrongylus brasiliensis is known to break an established T-cell anergy. This knowledge prompted us to examine the effect of infection with an intracellular microbe, bacillus Calmett-Guérin (BCG), on the expression of anergy induced with SEB. We have demonstrated that while the SEB-induced anergy was not abrogated by BCG infection, the V beta 8.2 transgenic mice, in which almost all T cells were anergized with SEB, were capable of developing the effective acquired protective immunity, possibly through the preserved capacity to induce IFN-gamma leading to induction of nitric oxide synthase.
The anergy induced in mice with staphylococcal enterotoxin B (SEB) has been shown to involve selective unresponsiveness in cytokine expression. While interleukin-2 (IL-2), IL-3 and IL-4 mRNA levels are substantially reduced in anergic T cells upon restimulation with SEB, mRNA for interferon-gamma (IFN-gamma) is expressed normally. On the other hand, infection with Nippostrongylus brasiliensis is known to break an established T-cell anergy. This knowledge prompted us to examine the effect of infection with an intracellular microbe, bacillus Calmett-Guérin (BCG), on the expression of anergy induced with SEB. We have demonstrated that while the SEB-induced anergy was not abrogated by BCG infection, the V beta 8.2 transgenic mice, in which almost all T cells were anergized with SEB, were capable of developing the effective acquired protective immunity, possibly through the preserved capacity to induce IFN-gamma leading to induction of nitric oxide synthase.