| First Author | Malkiel S | Year | 1999 |
| Journal | J Immunol | Volume | 163 |
| Issue | 10 | Pages | 5265-8 |
| PubMed ID | 10553048 | Mgi Jnum | J:118448 |
| Mgi Id | MGI:3699586 | Doi | 10.4049/jimmunol.163.10.5265 |
| Citation | Malkiel S, et al. (1999) Autoimmune myocarditis does not require B cells for antigen presentation. J Immunol 163(10):5265-8 |
| abstractText | T cells constitute the pathogenic effector cell population in autoimmune myocarditis in BALB/c mice. Using mice rendered deficient for B cells by a targeted disruption to the IgM transmembrane domain or by treatment with anti-IgM Ab from birth, we asked whether B cells are a critical APC in the induction of autoimmune myocarditis. B cell-deficient mice immunized with cardiac myosin develop myocarditis comparable in incidence and severity to that in wild-type mice, suggesting that autoreactive T cells that cause myocarditis in BALB/c mice are activated by macrophages or dendritic cells. Since it does not appear that presentation of cryptic epitopes is critical for the breakdown of self tolerance, potentially pathogenic T cells recognizing dominant myosin epitopes must have escaped tolerization. Either anatomic sequestration of cardiac myosin peptide-MHC complexes or subthreshold presentation of cardiac myosin peptides by conventional APC can explain the survival of these autoreactive T cells. |
