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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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Autores principales: von Vietinghoff, Sibylle, Kurts, Christian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8523406/
https://www.ncbi.nlm.nih.gov/pubmed/34009468
http://dx.doi.org/10.1007/s00441-021-03473-0
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author von Vietinghoff, Sibylle
Kurts, Christian
author_facet von Vietinghoff, Sibylle
Kurts, Christian
author_sort von Vietinghoff, Sibylle
collection PubMed
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.
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spelling pubmed-85234062021-11-04 Regulation and function of CX3CR1 and its ligand CX3CL1 in kidney disease von Vietinghoff, Sibylle Kurts, Christian Cell Tissue Res Review 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. Springer Berlin Heidelberg 2021-05-19 2021 /pmc/articles/PMC8523406/ /pubmed/34009468 http://dx.doi.org/10.1007/s00441-021-03473-0 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Review
von Vietinghoff, Sibylle
Kurts, Christian
Regulation and function of CX3CR1 and its ligand CX3CL1 in kidney disease
title Regulation and function of CX3CR1 and its ligand CX3CL1 in kidney disease
title_full Regulation and function of CX3CR1 and its ligand CX3CL1 in kidney disease
title_fullStr Regulation and function of CX3CR1 and its ligand CX3CL1 in kidney disease
title_full_unstemmed Regulation and function of CX3CR1 and its ligand CX3CL1 in kidney disease
title_short Regulation and function of CX3CR1 and its ligand CX3CL1 in kidney disease
title_sort regulation and function of cx3cr1 and its ligand cx3cl1 in kidney disease
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8523406/
https://www.ncbi.nlm.nih.gov/pubmed/34009468
http://dx.doi.org/10.1007/s00441-021-03473-0
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