| First Author | Joliat MJ | Year | 2002 |
| Journal | J Autoimmun | Volume | 18 |
| Issue | 2 | Pages | 105-17 |
| PubMed ID | 11908943 | Mgi Jnum | J:76141 |
| Mgi Id | MGI:2178707 | Doi | 10.1006/jaut.2001.0570 |
| Citation | Joliat MJ, et al. (2002) Absence of CD5 Dramatically Reduces Progression of Pulmonary Inflammatory Lesions in SHP-1 Protein-Tyrosine Phosphatase-Deficient 'Viable Motheaten' Mice. J Autoimmun 18(2):105-17 |
| abstractText | Mice homozygous for the viable motheaten (Hcph(me-v)) mutation are deficient in SHP-1 protein-tyrosine phosphatase, resulting in severe systemic autoimmunity and immune dysfunction. A high percentage of B-cells in viable motheaten mice express the cell surface glycoprotein CD5, in contrast to wild type mice that express CD5 on only a small percentage of B-cells. CD5(+) B-cells have been associated with autoantibody production. To determine the role of CD5 in the development of the inflammatory disease in me(v)/ me(v) mice, we created a stock of CD5(null)me(v)/ me(v) mice. The longevity of CD5(null)me(v)/ me(v) mice was increased 69% in comparison to me(v)/ me(v) mice on a similar (B6;129) background. The increased lifespan was associated with a marked reduction in pulmonary inflammation. Flow cytometry analysis of spleen cells from CD5(null)me(v)/ me(v) mice at 9-12 weeks of age revealed significant decreases in percentages of IgM/B220 double positive B-cells, Mac-1/Gr-1 double positive cells and CD4(+) T-cells compared with me(v)/ me(v) mice. CD5(null)me(v)/ me(v) mice also had significantly lower serum IgM levels in comparison to me(v)/ me(v) mice. Study of CD5(null)me(v)/ me(v) mice may provide further insight into the role of CD5 in cell signaling and may help explain the observed association of CD5(+) B-cells with autoimmune disease. Copyright 2002 Elsevier Science Ltd. |
