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. Author manuscript; available in PMC: 2011 Aug 1.
Published in final edited form as: J Immunol. 2010 Jul 2;185(3):1375–1378. doi: 10.4049/jimmunol.0903369

FIGURE 3.

FIGURE 3

Blocking CTLA-4–B7 interaction confers the susceptibility of autoimmune myocarditis to CD28−/− mice or exacerbates the disease in WT mice. A, CD28−/− mice (n = 10) were immunized with 100 μg MYHC-α peptide in CFA with rhIgG1-Fc or hCTLA-4-Ig in the presence or absence of a neutralizing anti–IL-17. WT BALB/c mice immunized with MYHC-α peptide (n = 10) were used as a positive control. All mice were sacrificed on day 22. H&E-stained sections of heart from immunized mice (original magnification ×200). a, WT mice; b, CD28−/− mice treated with rhIgG1-fc treatment; and c, CD28−/− mice receiving hCTLA-4-Ig treatment. d, CD28−/− mice receiving hCTLA-4-Ig treatment and anti–IL-17 neutralization. B, H&E-stained sections of heart (original magnification ×200) of WT BALB/c mice (n = 10) were immunized with MYHC-α peptide as in A and i.p. injected with hamster IgG (100 μg) or anti-CTLA-4 (100 μg). C, The prevalence and severity of MYHC-α–induced myocarditis.