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      CX3CL1/CX3CR1 Axis, as the Therapeutic Potential in Renal Diseases: Friend or Foe?

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          Abstract

          The fractalkine receptor chemokine (C-X3-C motif) receptor 1 (CX3CR1) and its highly se-lective ligand CX3CL1 mediate chemotaxis and adhesion of immune cells, which are involved in the pathogenesis and progression of numerous inflammatory disorders and malignancies. The CX3CL1/CX3CR1 axis has recently drawn attention as a potential therapeutic target because it is in-volved in the ontogeny, homeostatic migration, or colonization of renal phagocytes. We performed a Medline/PubMed search to detect recently published studies that explored the relationship between the CX3CL1/CX3CR1 axis and renal diseases and disorders, including diabetic nephropathy, renal allograft rejection, infectious renal diseases, IgA nephropathy, fibrotic kidney disease, lupus nephritis and glo-merulonephritis, acute kidney injury and renal carcinoma. Most studies demonstrated its role in promot-ing renal pathopoiesis; however, several recent studies showed that the CX3CL1/CX3CR1 axis could also reduce renal pathopoiesis. Thus, the CX3CL1/CX3CR1 axis is now considered to be a double-edged sword that could provide novel perspectives into the pathogenesis and treatment of renal diseases and disorders.

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          The natural history of chronic allograft nephropathy.

          Brian Nankivell, Richard J Borrows, Caroline L S Fung … (2003)
          With improved immunosuppression and early allograft survival, chronic allograft nephropathy has become the dominant cause of kidney-transplant failure. We evaluated the natural history of chronic allograft nephropathy in a prospective study of 120 recipients with type 1 diabetes, all but 1 of whom had received kidney-pancreas transplants. We obtained 961 kidney-transplant-biopsy specimens taken regularly from the time of transplantation to 10 years thereafter. Two distinctive phases of injury were evident as chronic allograft nephropathy evolved. An initial phase of early tubulointerstitial damage from ischemic injury (P<0.05), prior severe rejection (P<0.01), and subclinical rejection (P<0.01) predicted mild disease by one year, which was present in 94.2 percent of patients. Early subclinical rejection was common (affecting 45.7 percent of biopsy specimens at three months), and the risk was increased by the occurrence of a prior episode of severe rejection and reduced by tacrolimus and mycophenolate therapy (both P<0.05) and gradually abated after one year. Both subclinical rejection and chronic rejection were associated with increased tubulointerstitial damage (P<0.01). Beyond one year, a later phase of chronic allograft nephropathy was characterized by microvascular and glomerular injury. Chronic rejection (defined as persistent subclinical rejection for two years or longer) was uncommon (5.8 percent). Progressive high-grade arteriolar hyalinosis with luminal narrowing, increasing glomerulosclerosis, and additional tubulointerstitial damage was accompanied by the use of calcineurin inhibitors. Nephrotoxicity, implicated in late ongoing injury, was almost universal at 10 years, even in grafts with excellent early histologic findings. By 10 years, severe chronic allograft nephropathy was present in 58.4 percent of patients, with sclerosis in 37.3 percent of glomeruli. Tubulointerstitial and glomerular damage, once established, was irreversible, resulting in declining renal function and graft failure. Chronic allograft nephropathy represents cumulative and incremental damage to nephrons from time-dependent immunologic and nonimmunologic causes. Copyright 2003 Massachusetts Medical Society
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            TLRs and innate immunity.

            Bruce Beutler (2009)
            One of the most fundamental questions in immunology pertains to the recognition of non-self, which for the most part means microbes. How do we initially realize that we have been inoculated with microbes, and how is the immune response ignited? Genetic studies have made important inroads into this question during the past decade, and we now know that in mammals, a relatively small number of receptors operate to detect signature molecules that herald infection. One or more of these signature molecules are displayed by almost all microbes. These receptors and the signals they initiate have been studied in depth by random germline mutagenesis and positional cloning (forward genetics). Herein is a concise description of what has been learned about the Toll-like receptors, which play an essential part in the perception of microbes and shape the complex host responses that occur during infection.
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              Role of chemokines in tumor growth.

              Dayanidhi Raman, Paige Baugher, Yee Mon Thu … (2007)
              Chemokines play a paramount role in the tumor progression. Chronic inflammation promotes tumor formation. Both tumor cells and stromal cells elaborate chemokines and cytokines. These act either by autocrine or paracrine mechanisms to sustain tumor cell growth, induce angiogenesis and facilitate evasion of immune surveillance through immunoediting. The chemokine receptor CXCR2 and its ligands promote tumor angiogenesis and leukocyte infiltration into the tumor microenvironment. In harsh acidic and hypoxic microenvironmental conditions tumor cells up-regulate their expression of CXCR4, which equips them to migrate up a gradient of CXCL12 elaborated by carcinoma-associated fibroblasts (CAFs) to a normoxic microenvironment. The CXCL12-CXCR4 axis facilitates metastasis to distant organs and the CCL21-CCR7 chemokine ligand-receptor pair favors metastasis to lymph nodes. These two chemokine ligand-receptor systems are common key mediators of tumor cell metastasis for several malignancies and as such provide key targets for chemotherapy. In this paper, the role of specific chemokines/chemokine receptor interactions in tumor progression, growth and metastasis and the role of chemokine/chemokine receptor interactions in the stromal compartment as related to angiogenesis, metastasis, and immune response to the tumor are reviewed.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Curr Gene Ther
                Journal ID (iso-abbrev): Curr Gene Ther
                Journal ID (publisher-id): CGT
                Title: Current Gene Therapy
                Publisher: Bentham Science Publishers
                ISSN (Print): 1566-5232
                ISSN (Electronic): 1875-5631
                Publication date (Electronic): December 2017
                Publication date (Print): December 2017
                Volume: 17
                Issue: 6
                Pages: 442-452
                Affiliations
                [1]Transplantation Center of the 3rd Xiangya Hospital, Central South University , Changsha, , Hunan, 410013 , China
                Author notes
                [* ]Address correspondence to these authors at Transplantation Center, the 3 rd Xiangya Hospital, Central South University, 138 Tongzipo Rd, Changsha 410013, China; Tel: +86-731-88618320; E-mails: chke1972@ 123456163.com ; myz_china@ 123456aliyun.com
                Article
                Publisher ID: CGT-17-442
                DOI: 10.2174/1566523218666180214092536
                PMC ID: 5902862
                PubMed ID: 29446734
                SO-VID: 6892469f-b950-43da-9304-c6486d9572bb
                Copyright © © 2017 Bentham Science Publishers
                License:

                This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) ( https://creativecommons.org/licenses/by-nc/4.0/legalcode), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

                History
                Date received : 05 May 2017
                Date revision received : 06 October 2017
                Date accepted : 14 January 2018
                Categories
                Subject: Article

                ScienceOpen disciplines: Molecular medicine
                Keywords: fractalkine,cx3cl1,chemokine receptor,cx3cr1,renal disease,kidney transplantation
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: fractalkine, cx3cl1, chemokine receptor, cx3cr1, renal disease, kidney transplantation

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