Activation of diverse repertoires of autoreactive T cells enhances the loss of anti-dsDNA B cell tolerance
J. Clin. Invest. Brian W. Busser, et al. 112:1361 doi:10.1172/JCI18310 [Go to this article.]

Figure 4
Activation of every class II–reactive T cell repertoire induced IgM ANAs with anti-dsDNA B cell activation and migration into the follicle. (a) Seven days after cGVHD induction, host sera were examined for the presence of IgM anti-chromatin autoantibodies. Scatter plots show IgM anti-chromatin autoantibody responses of individual mice. Recipients of every class II–reactive T cell repertoire had significantly more IgM anti-chromatin autoantibodies than 3H9.KI recipients of B6 CD4⁺ T cells (P < 0.05). The IgM autoantibody production was statistically similar among all recipients of class II–reactive CD4⁺ T cells (P > 0.05). (b) Seven days after cGVHD induction, splenic anti-dsDNA B cells of B6.PL/3H9.KI hosts were identified with Ab’s against B220 and λ1. The expansion in numbers of anti-dsDNA B cells was similar among all class II–reactive T cell recipients and significantly different from the B6-injected negative control (P < 0.05 for all groups). Representative results from four independent experiments are shown (c) CD22 expression on anti-dsDNA B cells (B220⁺ and λ1⁺). Histograms show the levels of CD22 for either B6-injected negative control (black lines) or following interaction with the indicated cell type (red lines). (d) Anti-dsDNA B cells were localized by staining spleen sections with Ab’s against B220 (blue) and Igλ1 (brown). In B6 → B6.PL/3H9.KI mice, λ1⁺ B cells localize to the T-B interface. Seven days after cGVHD induction, all class II–reactive repertoires induced the migration of λ1⁺ B cells into the follicle. Representative results from four separate experiments are shown.