The induction of experimental autoimmune myocarditis in mice lacking CD4 or CD8 molecules [corrected].

Abstract

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.

• Authors: J M Penninger, N Neu, E Timms, V A Wallace, D R Koh, K Kishihara, C Pummerer, T W Mak
• Journal: The Journal of experimental medicine (J Exp Med) Vol. 178 Issue 5 Pg. 1837-42 (Nov 01 1993) ISSN: 0022-1007 [Print] United States
• PMID: 8228830 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Autoantibodies
• CD3 Complex
• CD8 Antigens
• Immunoglobulin G
• Myosins

Topics

• Animals
• Autoantibodies (analysis)
• Autoimmune Diseases (immunology, pathology)
• CD3 Complex (genetics, immunology)
• CD8 Antigens (genetics, immunology)
• Crosses, Genetic
• Female
• Homozygote
• Immunoglobulin G (immunology)
• Male
• Mice
• Mice, Inbred Strains
• Myocarditis (immunology, pathology)
• Myocardium (immunology, pathology)
• Myosins (immunology)
• T-Lymphocyte Subsets (immunology)