| First Author | Erb U | Year | 2013 |
| Journal | J Leukoc Biol | Volume | 94 |
| Issue | 4 | Pages | 845-57 |
| PubMed ID | 23817565 | Mgi Jnum | J:205318 |
| Mgi Id | MGI:5544555 | Doi | 10.1189/jlb.0413196 |
| Citation | Erb U, et al. (2013) Tolerance induction by hair-specific keratins in murine alopecia areata. J Leukoc Biol 94(4):845-57 |
| abstractText | AA is a presumptive autoimmune disease, severely damaging the hair follicle. Hair- and nail-specific keratins are discussed as potential candidates, which we controlled in C3H/HeJ mice that develop AA spontaneously or after skin transplantation. From nine keratins, K71 and K31 peptides supported T cell activation when presented by DCs to syngeneic naive T cells, and young C3H/HeJ mice receiving s.c. injections of peptide-loaded DC developed AA. The frequency of K71- and K31-specific CD4(+) and CD8(+) T cells increased four- to fivefold by vaccination, which corresponds with the frequency seen in skin transplantation-induced AA mice. Also, accessory molecule expression, the cytokine profile with a dominance of IFN-gamma-expressing T cells, the proliferative response against AA lysate or peptide-loaded DCs, as well as peptide-specific cytotoxic T cells were similar in keratin peptide- and skin transplantation-induced AA. Instead, vaccination with soluble K71 or K31 peptides significantly retarded AA induction and prevented progression. Soluble peptide vaccination did not provoke immunosuppression but induced long-lasting T cell anergy with unresponsiveness to DC-presented K71 and K31 peptides. Thus, keratins K71 and K31 contribute to AA induction, and peptide application in a nonimmunogenic form serves as an efficient therapeutic. |
