| First Author | Riggs JE | Year | 1994 |
| Journal | Mol Immunol | Volume | 31 |
| Issue | 11 | Pages | 783-91 |
| PubMed ID | 8047070 | Mgi Jnum | J:19789 |
| Mgi Id | MGI:67919 | Doi | 10.1016/0161-5890(94)90016-7 |
| Citation | Riggs JE, et al. (1994) VH11 bias and normal V-D-J junctions in SCID B lymphocytes rescued by neonatal T cell transfer. Mol Immunol 31(11):783-91 |
| abstractText | The scid mutation interferes with normal rearrangement of antigen receptor genes, leading to an absence of T and B lymphocytes in most SCID mice. However, the SCID phenotype is leaky, with an age- and strain-dependent increase in the incidence of mice with small number of T and B cells and readily detectable serum immunoglobulin. Introduction of neonatal T cells into young SCID mice results in a 100% incidence of the leaky phenotype. We have identified the location of antibody secreting cells in T cell-induced leaky SCID mice as the spleen and peritoneal cavity, and we have sequenced 35 productively rearranged immunoglobulin genes from these sites to determine if normal V-D-J recombination was occurring. VH11 sequences with potential autoreactivity were observed frequently in both the peritoneal cavity and spleen of T cell-induced leaky SCID mice, and these sequences were indistinguishable from those recovered from peritoneal cavity B cells from normal C.B-17 mice. Non-VH11 SCID sequences showed fewer N nucleotides and slightly more P nucleotides than normal V-D-J sequences. Many SCID junctions occurred at the site of short sequence homologies. These results suggest that successful V-D-J recombination is occurring with low frequency in all SCID mice, and that neonatal T cell transfer plus autoantigen stimulation allows the long term survival of these B cells. |
