| First Author | Pereira P | Year | 1989 |
| Journal | J Exp Med | Volume | 170 |
| Issue | 6 | Pages | 1825-35 |
| PubMed ID | 2584926 | Mgi Jnum | J:27066 |
| Mgi Id | MGI:74484 | Doi | 10.1084/jem.170.6.1825 |
| Citation | Pereira P, et al. (1989) I-E-linked control of spontaneous rheumatoid factor production in normal mice. J Exp Med 170(6):1825-35 |
| abstractText | The concentration of serum IgM molecules binding to IgG2a (rheumatoid factor [RF]) in solid phase assays is 10-100-fold higher in normal, unmanipulated C3H/HeJ (H-2k) than in C57BL/6 (H-2b) mice. Analysis of MHC-congenic mice with the prototype strains show that C3H SW (H-2b) are low, and B6.H-2k are high RF expressor strains, respectively. Furthermore, segregation of RF phenotypes in progenies from backcrosses to C3H/HeJ of (C3H/HeJ x C57BL/6)F1 hybrid mice shows MHC- and IgH-linked controls. RF phenotypes also segregate as if they are MHC linked in crosses between H-2-congenic strains (C3H/HeJ and C3H.SW). The study of intra-H-2 (k/b and k/s) recombinant mice suggested that RF phenotype control is linked to the I-E region. This was confirmed by the typing of C57BL/6 mice expressing a transgenic E alpha chain, and thus, I-E+, which, in contrast to nontransgenic littermates, are high expressors of RF. |
