| First Author | Penninger JM | Year | 1993 |
| Journal | J Exp Med | Volume | 178 |
| Issue | 5 | Pages | 1837-42 |
| PubMed ID | 8228830 | Mgi Jnum | J:15279 |
| Mgi Id | MGI:63407 | Doi | 10.1084/jem.178.5.1837 |
| Citation | Penninger JM, et al. (1993) The induction of experimental autoimmune myocarditis in mice lacking CD4 or CD8 molecules [corrected] [published erratum appears in J Exp Med 1994 Jan 1;179(1):371]. J Exp Med 178(5):1837-42 |
| abstractText | Experimental induction of most autoimmune diseases appears to depend on the activation of CD4+ T helper cells, while CD8+ lymphocytes may have a role in disease progression. To study the role of CD4+ and CD8+ T cell subsets in T cell-dependent autoimmunity, mice lacking CD4 or CD8 molecules after gene targeting were injected with cardiac myosin to induce organ specific autoimmune myocarditis. Mice homozygous for the CD8 mutation (CD8-/-) developed significantly more severe disease as compared to CD4+/-CD8+/- controls. Surprisingly, CD4-/- mice developed autoimmune myocarditis with infiltration of TCR alpha beta +CD4-CD8- T cells in the heart tissue and appearance of autoantibodies. These data demonstrate that the lack of CD4+ or CD8+ T cells has no significant influence on the initiation of autoimmune myocarditis. CD4+ and CD8+ cells regulate disease severity and these results may explain the occurrence of autoimmunity in CD4 immunodeficiencies. |
