Injury in renal ischemia-reperfusion is independent from immunoglobulins and T lymphocytes.
Ischemia-reperfusion injury (IRI) is a complex and incompletely understood process involving a cascade of events that culminates in apoptotic and/or necrotic cell death. Natural IgM antibodies and complement have been implicated in the pathogenesis of IRI in a variety of organ systems as have T lymphocytes in renal IRI. To investigate the role of Ig and T lymphocytes in renal IRI, recombination-activating gene (RAG)-1-deficient mice were studied. RAG-1(-/-) mice were not protected from acute renal failure induced by 27.5 min of bilateral renal ischemia and subsequent reperfusion [serum urea nitrogen levels 30 h after reperfusion, 155.2 +/- 5.6 and 152.8 +/- 11.4 mg/dl in RAG-1(-/-) and wild-type mice, respectively; n = 13 each]. Histological examination showed acute tubular necrosis and neutrophilic infiltration with no significant differences between groups. In contrast with other organ systems, Igs were not found in kidneys at time points ranging from 1 min to 30 h after ischemia. Thus Igs and mature T lymphocytes do not appear to play a significant role in the pathogenesis of IRI in the kidney.[1]References
- Injury in renal ischemia-reperfusion is independent from immunoglobulins and T lymphocytes. Park, P., Haas, M., Cunningham, P.N., Bao, L., Alexander, J.J., Quigg, R.J. Am. J. Physiol. Renal Physiol. (2002) [Pubmed]
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