| First Author | Walter W | Year | 1996 |
| Journal | Immunogenetics | Volume | 44 |
| Issue | 1 | Pages | 19-26 |
| PubMed ID | 8613139 | Mgi Jnum | J:33108 |
| Mgi Id | MGI:80589 | Citation | Walter W, et al. (1996) H2-M polymorphism in mice susceptible to collagen-induced arthritis involves the peptide binding groove. Immunogenetics 44(1):19-26 |
| abstractText | The ability to develop type II collagen (CII)-induced arthritis (CIA) in mice is associated with the major histocompatibility I-A gene and with as yet poorly defined regulatory molecules of the major histocompatibility complex (MHC) class II antigen processing and presentation pathway. H2-M molecules are thought to be involved in the loading of antigenic peptides into the MHC class II binding cleft. We sequenced H2-Ma, H2-Mb1, and H2-Mb2 genes from CIA-susceptible and -resistant mouse strains and identified four different Ma and Mb2 alleles and three different Mb1 alleles defined by polymorphic residues within the predicted peptide binding groove. Most CIA-resistant mouse strains share common Ma, Mb1, and Mb2 alleles. In contrast, H2-M alleles designated Ma-III, Ma-IV, Mb1-III, and Mb2-IV could be exclusively identified in the CIA-susceptible H2r and H2q haplotypes, suggesting that allelic H2-M molecules may modulate the composition of different CII peptides loaded into MHC class II molecules, presumably presenting arthritogenic epitopes to T lymphocytes. |
