| First Author | Burne-Taney MJ | Year | 2003 |
| Journal | J Immunol | Volume | 171 |
| Issue | 6 | Pages | 3210-5 |
| PubMed ID | 12960350 | Mgi Jnum | J:85388 |
| Mgi Id | MGI:2674213 | Doi | 10.4049/jimmunol.171.6.3210 |
| Citation | Burne-Taney MJ, et al. (2003) B cell deficiency confers protection from renal ischemia reperfusion injury. J Immunol 171(6):3210-5 |
| abstractText | Recent data have demonstrated a role for CD4(+) cells in the pathogenesis of renal ischemia reperfusion injury (IRI). Identifying engagement of adaptive immune cells in IRI suggests that the other major cell of the adaptive immune response, B cells, may also mediate renal IRI. An established model of renal IRI was used: 30 min of renal pedicle clamping was followed by reperfusion in B cell-deficient ( micro MT) and wild-type mice. Renal function was significantly improved in micro MT mice compared with wild-type mice at 24, 48, and 72 h postischemia. micro MT mice also had significantly reduced tubular injury. Both groups of mice had similar renal phagocyte infiltration postischemia assessed by myeloperoxidase levels and similar levels of CD4(+) T cell infiltration postischemia. Peritubular complement C3d staining was also similar in both groups. To identify the contribution of cellular vs soluble mechanism of action, serum transfer into micro MT mice partially restored ischemic phenotype, but B cell transfers did not. These data are the first demonstration of a pathogenic role for B cells in ischemic acute renal failure, with a serum factor as a potential underlying mechanism of action. |
