| First Author | Hardin JD | Year | 1996 |
| Journal | Cell Immunol | Volume | 172 |
| Issue | 1 | Pages | 100-7 |
| PubMed ID | 8806812 | Mgi Jnum | J:34903 |
| Mgi Id | MGI:82358 | Doi | 10.1006/cimm.1996.0220 |
| Citation | Hardin JD, et al. (1996) Abnormal peripheral lymphocyte function in c-abl mutant mice. Cell Immunol 172(1):100-7 |
| abstractText | The proto-oncogene c-abl encodes a tyrosine kinase that is hypothesized to function in proliferation-stimulatory signaling pathways. Previous work on mice homozygous for targeted mutations in the c-abl gene (ablml and abl2 mutant strains) has demonstrated multiple defects, including a susceptibility to infections that results in a high mortality rate after weaning. FACS analysis of the hemopoietic system of c-abl mutants demonstrated variable reductions in B and T lymphocytes in adult bone marrow, thymus, spleen, and peripheral blood. In addition, bone marrow from mutants showed a decreased ability to respond to interleukin-7. We further found that B cells from ablm1 mice had a reduced ability to respond to lipopolysaccharide (decreased to 10% of control response) that was dependent on the culture conditions and the tissue of origin of B cells. Peripheral blood from the mutants also had a reduced response to the T cell mitogen concanavalin A. Immune response in ablm1 mice as determined by the mixed lymphocyte response and the sheep red blood cell plaque-forming assay was grossly normal. These findings suggest that although specific signaling pathways in lymphocytes may involve c-Abl, the immune system can function in the absence of a normal c-abl gene product. |
