TY - JOUR
T1 - B cell deficiency confers protection from renal ischemia reperfusion injury
AU - Burne-Taney, Melissa J.
AU - Ascon, Dolores B.
AU - Daniels, Frank
AU - Racusen, Lorraine
AU - Baldwin, William
AU - Rabb, Hamid
N1 - Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 2003/9/15
Y1 - 2003/9/15
N2 - 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 (μMT) and wild-type mice. Renal function was significantly improved in μMT mice compared with wild-type mice at 24, 48, and 72 h postischemia. μMT 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 μMT 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.
AB - 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 (μMT) and wild-type mice. Renal function was significantly improved in μMT mice compared with wild-type mice at 24, 48, and 72 h postischemia. μMT 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 μMT 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.
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U2 - 10.4049/jimmunol.171.6.3210
DO - 10.4049/jimmunol.171.6.3210
M3 - Article
C2 - 12960350
AN - SCOPUS:0041832283
SN - 0022-1767
VL - 171
SP - 3210
EP - 3215
JO - Journal of Immunology
JF - Journal of Immunology
IS - 6
ER -