Nkt Cell Activation Mediates Neutrophil Ifn-gamma Production and Renal Ischemia-reperfusion Injury.
From: Department of Medicine, Cardiovascular Research Center, University of Virginia, Charlottesville, VA 22908, USA.
Journal of immunology (Baltimore, Md. : 1950)
- Publish Date: May 2007
- ISSN: 0022-1767
- Volume: 178
- Issue: 9
- Pages: 5899-911
- Medium: Print
- Language: English
- Citation (JAMA): Li Li, Huang Liping, Sung Sun-sang J, et al. Nkt Cell Activation Mediates Neutrophil Ifn-gamma Production and Renal Ischemia-reperfusion Injury.. J. Immunol. May 2007;178:5899-911
Abstract
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-1(high). Three hours after reperfusion, kidney IFN-gamma-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 (Jalpha18(-/-)), 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-gamma-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-gamma.
Mesh Headings (Keywords): Animals, Antigen Presentation, Antigens, CD, Antigens, CD11b, Antigens, Differentiation, T-Lymphocyte, CD4-Positive T-Lymphocytes, Interferon Type II, Kidney, Killer Cells, Natural, Lymphocyte Activation, Lymphocyte Depletion, Lymphocyte Function-Associated Antigen-1, Mice, Mice, Mutant Strains, Neutrophils, Receptors, Chemokine, Reperfusion Injury
Check for Full Text / PubMed Unique Identifier (PMID): 17442974
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