| First Author | Russell HI | Year | 1999 |
| Journal | Eur J Immunol | Volume | 29 |
| Issue | 3 | Pages | 905-11 |
| PubMed ID | 10092094 | Mgi Jnum | J:53522 |
| Mgi Id | MGI:1332890 | Doi | 10.1002/(SICI)1521-4141(199903)29:03<905::AID-IMMU905>3.0.CO;2-8 |
| Citation | Russell HI, et al. (1999) Class II antigen processing defects in two H2d mouse cell lines are caused by point mutations in the H2-DMa gene. Eur J Immunol 29(3):905-11 |
| abstractText | The molecular nature of the defect in two mouse antigen processing-defective cell lines was examined. Both mutants were derived from the A20 (BALB/c, H2d) B cell line, and both were found to have defects in the H2-DMa gene. Mutant 3A5 exhibits severely reduced amounts of H2-DMa message, and no detectable DMalpha protein. cDNA sequence revealed a C-->T transition at nucleotide 118, introducing a premature stop codon in exon 2 of the H2-DMa gene. In contrast, mutant 2A2 exhibits reduced but detectable levels of H2-DMa message and DMalpha protein only after treatment with IL-4, which induces the expression of both the H2-DMa and the H2-DMb genes in B cells. In this mutant the cDNA sequence revealed a missense mutation in exon 3 resulting in the conversion of a conserved proline residue in the Ig-like domain to serine. Stable transfection with full-length H2-DMa cDNA reconstitutes the antigen processing capacity of both mutants, as demonstrated by the ability to present native antigen to T cell clones, and by restored class II SDS stability. |
