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      Upregulation of Fractalkine in Human Crescentic Glomerulonephritis

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          Abstract

          Background/Aim: To evaluate the importance of fractalkine, a novel member of the CX3C chemokine, and natural killer (NK) cells in human crescentic glomerulonephritis, we determined the presence of fractalkine in the diseased kidneys immunohistochemically, and the correlation among fractalkine, NK cells and the degree of renal damage. Methods: Twenty-three patients (13 males and 10 females) with primary or secondary crescentic glomerular disease were evaluated in this study. Fractalkine and CD16-positive cells including NK cells were detected immunohistochemically. Results: Fractalkine-positive cells were detected in the interstitium of 23 patients with crescentic glomerulonephritis, while they were not detected in the glomeruli. In addition, CD16-positive cells were detected in both the glomeruli (1.3 ± 0.2/glomerulus) and interstitium (1.3 ± 0.2/visual field). The number of fractalkine-positive cells in the interstitium correlated with the number of CD16-positive cells before glucocorticoid therapy (r = 0.43, p = 0.047, n = 23). The number of fractalkine-positive cells in the interstitium before glucocorticoid therapy (0.2 ± 0.1/visual field) decreased after therapy (0.1 ± 0.1/visual field, p = 0.050) in 11 cases tested. The number of CD16-positive cells in the diseased kidneys did not change after glucocorticoid therapy. Conclusion: These results suggest that the local production of fractalkine may explain the presence of CD16-positive cells including NK cells, which may participate in the interstitial lesions of human crescentic glomerulonephritis before corticoid therapy.

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          Most cited references 3

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          Fractalkine and CX3CR1 Mediate a Novel Mechanism of Leukocyte Capture, Firm Adhesion, and Activation under Physiologic Flow

          Leukocyte migration into sites of inflammation involves multiple molecular interactions between leukocytes and vascular endothelial cells, mediating sequential leukocyte capture, rolling, and firm adhesion. In this study, we tested the role of molecular interactions between fractalkine (FKN), a transmembrane mucin-chemokine hybrid molecule expressed on activated endothelium, and its receptor (CX3CR1) in leukocyte capture, firm adhesion, and activation under physiologic flow conditions. Immobilized FKN fusion proteins captured resting peripheral blood mononuclear cells at physiologic wall shear stresses and induced firm adhesion of resting monocytes, resting and interleukin (IL)-2–activated CD8+ T lymphocytes and IL-2–activated NK cells. FKN also induced cell shape change in firmly adherent monocytes and IL-2–activated lymphocytes. CX3CR1-transfected K562 cells, but not control K562 cells, firmly adhered to FKN-expressing ECV-304 cells (ECV-FKN) and tumor necrosis factor α–activated human umbilical vein endothelial cells. This firm adhesion was not inhibited by pertussis toxin, EDTA/EGTA, or antiintegrin antibodies, indicating that the firm adhesion was integrin independent. In summary, FKN mediated the rapid capture, integrin-independent firm adhesion, and activation of circulating leukocytes under flow. Thus, FKN and CX3CR1 mediate a novel pathway for leukocyte trafficking.
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            Th1 and Th2 T helper cell subsets affect patterns of injury and outcomes in glomerulonephritis.

            The recognition that human immune responses can be directed by two different subsets of T helper cells (Th1 and Th2) has been an important development in modern immunology. Immune responses polarized by either the Th1 or Th2 subset predominance result in different inflammatory effector pathways and disease outcomes. Many autoimmune diseases are associated with either Th1- or Th2- polarized immune responses. Although these different immune response patterns are relevant to glomerulonephritis (GN), little attention has been paid to the consequences of Th1 or Th2 predominance of nephritogenic immune responses for the pattern and outcome of GN. Unlike other autoimmune conditions, GN results from a variety of different immune responses and has a range of histologic features and immune effectors in glomeruli. This review assesses the data available from studies of experimental and human GN that address the Th1 or Th2 predominance of nephritogenic immune responses and their relevance to the different histopathological patterns and outcomes of GN. In particular, the evidence that Th1-predominant nephritogenic immune responses are associated with severe proliferative and crescentic GN is presented.
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              A Th1 Response Is Essential for Induction of Crescentic Glomerulonephritis in Mice

              Crescentic glomerulonephritis can be induced in rodents by injection of heterologous antibodies against the glomerular basement membrane. There is evidence that glomerular inflammation in that model represents a delayed–type hypersensitivity response to the heterologous immunoglobulin, whereas the antibody response is not important. The aim of the present study was to test this hypothesis. Delayed–type hypersensitivity is mediated by T cells with the Th1 phenotype. We compared mice immunized with rabbit immunoglobulin G in complete Freund’s adjuvant or in incomplete Freund’s adjuvant, producing, respectively, Th1– or Th2–biased responses to the antigen. Intravenous injection of rabbit antimouse glomerular basement membrane serum provoked proteinuria, infiltration with T cells and macrophages, as well as profound histological damage in the group treated with complete Freund’s adjuvant. There was no evidence of glomerulonephritis in the group which received incomplete Freund’s adjuvant. Deposits of mouse IgG along the glomerular basement membrane were similar in both groups. Thus, a Th1 response appears to be essential for the induction of glomerulonephritis in this model.
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                Author and article information

                Journal
                NEF
                Nephron
                10.1159/issn.1660-8151
                Nephron
                S. Karger AG
                1660-8151
                2235-3186
                2001
                2001
                21 March 2001
                : 87
                : 4
                : 314-320
                Affiliations
                aFirst Department of Internal Medicine and Division of Blood Purification, School of Medicine, Kanazawa University, Kanazawa; bDepartment of Internal Medicine, Kanazawa National Hospital, Kanazawa; cKurobe Municipal Hospital, Kurobe; dDepartment of Molecular Preventive Medicine, School of Medicine, University of Tokyo, Japan
                Article
                45936 Nephron 2001;87:314–320
                10.1159/000045936
                11287774
                © 2001 S. Karger AG, Basel

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                Page count
                Figures: 3, Tables: 1, References: 26, Pages: 7
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/45936
                Categories
                Original Paper

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