| First Author | Schuler W | Year | 1986 |
| Journal | Cell | Volume | 46 |
| Issue | 7 | Pages | 963-72 |
| PubMed ID | 3093081 | Mgi Jnum | J:8420 |
| Mgi Id | MGI:56887 | Doi | 10.1016/0092-8674(86)90695-1 |
| Citation | Schuler W, et al. (1986) Rearrangement of antigen receptor genes is defective in mice with severe combined immune deficiency. Cell 46(7):963-72 |
| abstractText | A process unique to lymphocyte differentiation is the rearrangement of genes encoding antigen-specific receptors on B and T cells. A mouse mutant (C.B-17scid) with severe combined immune deficiency, i.e., that lacks functional B and T cells, shows no evidence of such gene rearrangements. However, rearrangements were detected in Abelson murine leukemia virus-transformed bone marrow cells and in spontaneous thymic lymphomas from C.B-17scid mice. Most of these rearrangements were abnormal: approximately 80% of Igh rearrangements deleted the entire Jh region, and approximately 60% of TCR beta rearrangements deleted the entire J beta 2 region. The deletions appeared to result from faulty D-to-J recombination. No such abnormal rearrangements were detected in transformed tissues from control mice. The scid mutation may adversely affect the recombinase system catalyzing the assembly of antigen receptor genes in developing B and T lymphocytes. |
