Regulation and function of CX3CR1 and its ligand CX3CL1 in kidney disease
Attraction, retention, and differentiation of leukocytes to and within the kidney are governed by chemokines. The chemokine CX3CL1 (fractalkine) and its receptor CX3CR1 are exemplary in this regard as they are highly expressed and further upregulated in a range of kidney diseases. CX3CL1 is chiefly...
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| Veröffentlicht in: | Cell and tissue research 2021-08, Vol.385 (2), p.335-344 |
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| description | Attraction, retention, and differentiation of leukocytes to and within the kidney are governed by chemokines. The chemokine CX3CL1 (fractalkine) and its receptor CX3CR1 are exemplary in this regard as they are highly expressed and further upregulated in a range of kidney diseases. CX3CL1 is chiefly produced by renal endothelium and tubular epithelium, where it promotes leukocyte attraction. Recent data suggest that in addition to established soluble mediators, cellular interactions may enhance CX3CL1 expression. The receptor CX3CR1 is essential in myeloid phagocyte homing to the kidney at homeostasis, after acute cell depletion and in inflammation. CX3CR1 and its ligand are highly regulated in human kidney diseases such as IgA nephritis, systemic lupus erythematosus, and inflammatory conditions such as transplant rejection. A mechanistic role of CX3CR1 has been established in experimental models of nephrotoxic nephritis and renal candidiasis. It is debated in fibrosis. Recent publications demonstrate a role for CX3CR1
+
myeloid cells in radio-contrast-agent and sepsis-induced kidney damage. Systemically, circulating CX3CR1
+
monocytes reversibly increase in individuals with renal impairment and correlate with their cardiovascular risk. In this review, we discuss role and regulatory mechanisms of the CX3CL1-CX3CR1 axis in both localized and systemic effects of renal inflammation. |
| doi_str_mv | 10.1007/s00441-021-03473-0 |
| format | Article |
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+
myeloid cells in radio-contrast-agent and sepsis-induced kidney damage. Systemically, circulating CX3CR1
+
monocytes reversibly increase in individuals with renal impairment and correlate with their cardiovascular risk. In this review, we discuss role and regulatory mechanisms of the CX3CL1-CX3CR1 axis in both localized and systemic effects of renal inflammation.</description><identifier>ISSN: 0302-766X</identifier><identifier>EISSN: 1432-0878</identifier><identifier>DOI: 10.1007/s00441-021-03473-0</identifier><identifier>PMID: 34009468</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Animals ; Biomedical and Life Sciences ; Biomedicine ; Candidiasis ; Cardiovascular diseases ; Chemokine CX3CL1 - immunology ; Chemokines ; CX3C Chemokine Receptor 1 - immunology ; CX3CR1 protein ; Diabetic nephropathy ; Endothelium ; Epithelium ; Fibrosis ; Fractalkine ; Graft rejection ; Homeostasis ; Human Genetics ; Humans ; Immunoglobulin A ; Inflammation ; Kidney - pathology ; Kidney diseases ; Kidney Diseases - immunology ; Leukocytes ; Ligands ; Molecular Medicine ; Monocytes ; Myeloid cells ; Nephritis ; Proteomics ; Review ; Sepsis ; Systemic lupus erythematosus</subject><ispartof>Cell and tissue research, 2021-08, Vol.385 (2), p.335-344</ispartof><rights>The Author(s) 2021</rights><rights>2021. The Author(s).</rights><rights>COPYRIGHT 2021 Springer</rights><rights>The Author(s) 2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c572t-ffe0ebef6579dd08a6bbc769cf2ffced0633b624541636431d1cf37b49e6b5b53</citedby><cites>FETCH-LOGICAL-c572t-ffe0ebef6579dd08a6bbc769cf2ffced0633b624541636431d1cf37b49e6b5b53</cites><orcidid>0000-0002-3217-5433 ; 0000-0002-6620-2401</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00441-021-03473-0$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00441-021-03473-0$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34009468$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>von Vietinghoff, Sibylle</creatorcontrib><creatorcontrib>Kurts, Christian</creatorcontrib><title>Regulation and function of CX3CR1 and its ligand CX3CL1 in kidney disease</title><title>Cell and tissue research</title><addtitle>Cell Tissue Res</addtitle><addtitle>Cell Tissue Res</addtitle><description>Attraction, retention, and differentiation of leukocytes to and within the kidney are governed by chemokines. The chemokine CX3CL1 (fractalkine) and its receptor CX3CR1 are exemplary in this regard as they are highly expressed and further upregulated in a range of kidney diseases. CX3CL1 is chiefly produced by renal endothelium and tubular epithelium, where it promotes leukocyte attraction. Recent data suggest that in addition to established soluble mediators, cellular interactions may enhance CX3CL1 expression. The receptor CX3CR1 is essential in myeloid phagocyte homing to the kidney at homeostasis, after acute cell depletion and in inflammation. CX3CR1 and its ligand are highly regulated in human kidney diseases such as IgA nephritis, systemic lupus erythematosus, and inflammatory conditions such as transplant rejection. A mechanistic role of CX3CR1 has been established in experimental models of nephrotoxic nephritis and renal candidiasis. It is debated in fibrosis. Recent publications demonstrate a role for CX3CR1
+
myeloid cells in radio-contrast-agent and sepsis-induced kidney damage. Systemically, circulating CX3CR1
+
monocytes reversibly increase in individuals with renal impairment and correlate with their cardiovascular risk. In this review, we discuss role and regulatory mechanisms of the CX3CL1-CX3CR1 axis in both localized and systemic effects of renal inflammation.</description><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Candidiasis</subject><subject>Cardiovascular diseases</subject><subject>Chemokine CX3CL1 - immunology</subject><subject>Chemokines</subject><subject>CX3C Chemokine Receptor 1 - immunology</subject><subject>CX3CR1 protein</subject><subject>Diabetic nephropathy</subject><subject>Endothelium</subject><subject>Epithelium</subject><subject>Fibrosis</subject><subject>Fractalkine</subject><subject>Graft rejection</subject><subject>Homeostasis</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Immunoglobulin A</subject><subject>Inflammation</subject><subject>Kidney - pathology</subject><subject>Kidney diseases</subject><subject>Kidney Diseases - immunology</subject><subject>Leukocytes</subject><subject>Ligands</subject><subject>Molecular Medicine</subject><subject>Monocytes</subject><subject>Myeloid cells</subject><subject>Nephritis</subject><subject>Proteomics</subject><subject>Review</subject><subject>Sepsis</subject><subject>Systemic lupus erythematosus</subject><issn>0302-766X</issn><issn>1432-0878</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kV1rFDEUhoModrv6B7yQAcG7qScfk5ncCGXRWlgQikLvQiZzMps6m9TJTKH_3uxubbsgEvJ1znNecvIS8o7CGQWoPyUAIWgJLE8ual7CC7KggrMSmrp5SRbAgZW1lNcn5DSlGwAqpFSvyQkXAErIZkEur7CfBzP5GAoTusLNwe4v0RWra766ovuwn1Ix-H533EXXtPCh-OW7gPdF5xOahG_IK2eGhG8f9iX5-fXLj9W3cv394nJ1vi5tVbOpdA4BW3SyqlXXQWNk29paKuuYcxY7kJy3kolKUMml4LSj1vG6FQplW7UVX5LPB93bud1iZzFMoxn07ei3ZrzX0Xh9nAl-o_t4p5uK5b5lFvjwIDDG3zOmSd_EeQz5zZpVDWsUU0I9Ub0ZUPvgYhazW5-sPpe1qoAr2FFn_6Dy6HDrbQzofI4fFXx8VrBBM0ybFId59-fpGGQH0I4xpRHdY4cU9M5-fbBfZ_v13v68Lsn753_zWPLX7wzwA5ByKvQ4PvX-H9k_Lya36Q</recordid><startdate>20210801</startdate><enddate>20210801</enddate><creator>von Vietinghoff, Sibylle</creator><creator>Kurts, Christian</creator><general>Springer Berlin Heidelberg</general><general>Springer</general><general>Springer Nature B.V</general><scope>C6C</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7QR</scope><scope>7RV</scope><scope>7SS</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-3217-5433</orcidid><orcidid>https://orcid.org/0000-0002-6620-2401</orcidid></search><sort><creationdate>20210801</creationdate><title>Regulation and function of CX3CR1 and its ligand CX3CL1 in kidney disease</title><author>von Vietinghoff, Sibylle ; Kurts, Christian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c572t-ffe0ebef6579dd08a6bbc769cf2ffced0633b624541636431d1cf37b49e6b5b53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Candidiasis</topic><topic>Cardiovascular diseases</topic><topic>Chemokine CX3CL1 - immunology</topic><topic>Chemokines</topic><topic>CX3C Chemokine Receptor 1 - immunology</topic><topic>CX3CR1 protein</topic><topic>Diabetic nephropathy</topic><topic>Endothelium</topic><topic>Epithelium</topic><topic>Fibrosis</topic><topic>Fractalkine</topic><topic>Graft rejection</topic><topic>Homeostasis</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Immunoglobulin A</topic><topic>Inflammation</topic><topic>Kidney - pathology</topic><topic>Kidney diseases</topic><topic>Kidney Diseases - immunology</topic><topic>Leukocytes</topic><topic>Ligands</topic><topic>Molecular Medicine</topic><topic>Monocytes</topic><topic>Myeloid cells</topic><topic>Nephritis</topic><topic>Proteomics</topic><topic>Review</topic><topic>Sepsis</topic><topic>Systemic lupus erythematosus</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>von Vietinghoff, Sibylle</creatorcontrib><creatorcontrib>Kurts, Christian</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell and tissue research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>von Vietinghoff, Sibylle</au><au>Kurts, Christian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regulation and function of CX3CR1 and its ligand CX3CL1 in kidney disease</atitle><jtitle>Cell and tissue research</jtitle><stitle>Cell Tissue Res</stitle><addtitle>Cell Tissue Res</addtitle><date>2021-08-01</date><risdate>2021</risdate><volume>385</volume><issue>2</issue><spage>335</spage><epage>344</epage><pages>335-344</pages><issn>0302-766X</issn><eissn>1432-0878</eissn><abstract>Attraction, retention, and differentiation of leukocytes to and within the kidney are governed by chemokines. The chemokine CX3CL1 (fractalkine) and its receptor CX3CR1 are exemplary in this regard as they are highly expressed and further upregulated in a range of kidney diseases. CX3CL1 is chiefly produced by renal endothelium and tubular epithelium, where it promotes leukocyte attraction. Recent data suggest that in addition to established soluble mediators, cellular interactions may enhance CX3CL1 expression. The receptor CX3CR1 is essential in myeloid phagocyte homing to the kidney at homeostasis, after acute cell depletion and in inflammation. CX3CR1 and its ligand are highly regulated in human kidney diseases such as IgA nephritis, systemic lupus erythematosus, and inflammatory conditions such as transplant rejection. A mechanistic role of CX3CR1 has been established in experimental models of nephrotoxic nephritis and renal candidiasis. It is debated in fibrosis. Recent publications demonstrate a role for CX3CR1
+
myeloid cells in radio-contrast-agent and sepsis-induced kidney damage. Systemically, circulating CX3CR1
+
monocytes reversibly increase in individuals with renal impairment and correlate with their cardiovascular risk. In this review, we discuss role and regulatory mechanisms of the CX3CL1-CX3CR1 axis in both localized and systemic effects of renal inflammation.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>34009468</pmid><doi>10.1007/s00441-021-03473-0</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-3217-5433</orcidid><orcidid>https://orcid.org/0000-0002-6620-2401</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Cell and tissue research, 2021-08, Vol.385 (2), p.335-344 |
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| subjects | Animals Biomedical and Life Sciences Biomedicine Candidiasis Cardiovascular diseases Chemokine CX3CL1 - immunology Chemokines CX3C Chemokine Receptor 1 - immunology CX3CR1 protein Diabetic nephropathy Endothelium Epithelium Fibrosis Fractalkine Graft rejection Homeostasis Human Genetics Humans Immunoglobulin A Inflammation Kidney - pathology Kidney diseases Kidney Diseases - immunology Leukocytes Ligands Molecular Medicine Monocytes Myeloid cells Nephritis Proteomics Review Sepsis Systemic lupus erythematosus |
| title | Regulation and function of CX3CR1 and its ligand CX3CL1 in kidney disease |
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