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Production and Renal Ischemia-Reperfusion Injury1
,
,,
* Department of Medicine,
Department of Microbiology,
The Carter Immunology Center, and
Cardiovascular Research Center, University of Virginia, Charlottesville, VA 22908
Previous work has shown that ischemia-reperfusion (IR) injury (IRI) is dependent on CD4+ T cells from naive mice acting within 24 h. We hypothesize that NKT cells are key participants in the early innate response in IRI. Kidneys from C57BL/6 mice were subjected to IRI (0.5, 1, 3, and 24 h of reperfusion). After 30 min of reperfusion, we observed a significant increase in CD4+ cells (145% of control) from single-cell kidney suspensions as measured by flow cytometry. A significant fraction of CD4+ T cells expressed the activation marker, CD69+, and adhesion molecule, LFA-1high. Three hours after reperfusion, kidney IFN-
-producing cells were comprised largely of GR-1+CD11b+ neutrophils, but also contained CD1d-restricted NKT cells. Kidney IRI in mice administered Abs to block CD1d, or deplete NKT cells or in mice deficient of NKT cells (J
18–/–), was markedly attenuated. These effects were associated with a significant decrease in renal infiltration and, in activation of NKT cells, and a decrease in IFN--producing neutrophils. The results support the essential role of NKT cells and neutrophils in the innate immune response of renal IRI by mediating neutrophil infiltration and production of IFN-.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported in part by funds from National Institutes of Health Grants R01 DK56223, R01 DK62324, R01 H2070065, R01 CA78400, and R21 AI059996.
2 Address correspondence and reprint requests to Dr. Mark D. Okusa, Division of Nephrology, Box 800133, University of Virginia Health System, Charlottesville, VA 22908. E-mail address: mdo7y{at}virginia.edu
3 Abbreviations used in this paper: IR, ischemia-reperfusion; IRI, IR injury; KO, knockout; 7-AAD, 7-aminoactinomycin D; -GalCer, -galactosyl ceramide; PMN, polymorphonuclear neutrophil; BF, bright field; WT, wild type; IP-10, IFN--inducing protein 10.
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