Plasmodium chabaudi and Trypanosoma cruzi infections can reverse IgG2ab chronic suppression in mice.
The effects of infections with Plasmodium chabaudi or Trypanosoma cruzi on chronic CD8+ T cell dependent IgG2ab suppression were analyzed in homozygous Ighb/b adult mice. These parasites are known to induce a CD4+ T cell dependent polyclonal activation characterized in particular by a considerable increase in IgG2a expression. We report here that infection with either parasite reversed the IgG2ab suppression in 18 out of 32 mice. However, in mice treated with anti-CD4 mAb in parallel to the parasite infection, the polyclonal activation was largely reduced and the suppression of IgG2ab expression was always maintained. The parasite induced escape from suppression could result from increased helper T cell activation stimulating some of the Ig production. A weakening of the CD8+ T cell activity which is specific of IgG2ab could also contribute to the IgG2ab production. Both effects would shift the previous equilibrium which was in favour of suppression to a new balance allowing expression of the IgG2ab allotype.
Benaroch
P
P
Unité d'Immunophysiologie Moléculaire, Institut Pasteur, Paris, France.
Falanga
P B
PB
Spinella
S
S
Bordenave
G
G
D000818:Animals; D014355:Chagas Disease / Q000276:immunology*; D007108:Immune Tolerance; D007074:Immunoglobulin G / Q000096:biosynthesis*; D008213:Lymphocyte Activation; D016131:Lymphocyte Subsets / Q000276:immunology; D008288:Malaria / Q000276:immunology*; D051379:Mice; D008807:Mice, Inbred BALB C; D016788:Plasmodium chabaudi
D007074:Immunoglobulin G