Mouse CD163 deficiency strongly enhances experimental collagen-induced arthritis

Pia Svendsen; Anders Etzerodt; Bent W. Deleuran; Søren K. Moestrup

doi:10.1038/s41598-020-69018-7

Mouse CD163 deficiency strongly enhances experimental collagen-induced arthritis

Pia Svendsen, Anders Etzerodt, Bent W. Deleuran, Søren K. Moestrup^*

^*Kontaktforfatter

Danish Institute for Advanced Study

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

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Abstrakt

The scavenger receptor CD163 is highly expressed in macrophages in sites of chronic inflammation where it has a not yet defined role. Here we have investigated development of collagen-induced arthritis (CIA) and collagen antibody-induced arthritis (CAIA) in CD163-deficient C57BL/6 mice. Compared to wild-type mice, the CIA in CD163-deficient mice had a several-fold higher arthritis score with early onset, prolonged disease and strongly enhanced progression. Further, the serum anti-collagen antibody isotypes as well as the cytokine profiles and T cell markers in the inflamed joints revealed that CD163-deficient mice after 52 days had a predominant Th2 response in opposition to a predominant Th1 response in CD163+/+ mice. Less difference in disease severity between the CD163+/+ and CD163−/− mice was seen in the CAIA model that to a large extent induces arthritis independently of T-cell response and endogenous Th1/Th2 balance. In conclusion, the present set of data points on a novel strong anti-inflammatory role of CD163.

Originalsprog	Engelsk
Artikelnummer	12447
Tidsskrift	Scientific Reports
Vol/bind	10
Udgave nummer	1
ISSN	2045-2322
DOI	https://doi.org/10.1038/s41598-020-69018-7
Status	Udgivet - 2020

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10.1038/s41598-020-69018-7Licens: CC BY

Open Access VersionForlagets udgivne version, 1,67 MBLicens: CC BY

Citationsformater

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title = "Mouse CD163 deficiency strongly enhances experimental collagen-induced arthritis",

abstract = "The scavenger receptor CD163 is highly expressed in macrophages in sites of chronic inflammation where it has a not yet defined role. Here we have investigated development of collagen-induced arthritis (CIA) and collagen antibody-induced arthritis (CAIA) in CD163-deficient C57BL/6 mice. Compared to wild-type mice, the CIA in CD163-deficient mice had a several-fold higher arthritis score with early onset, prolonged disease and strongly enhanced progression. Further, the serum anti-collagen antibody isotypes as well as the cytokine profiles and T cell markers in the inflamed joints revealed that CD163-deficient mice after 52 days had a predominant Th2 response in opposition to a predominant Th1 response in CD163+/+ mice. Less difference in disease severity between the CD163+/+ and CD163−/− mice was seen in the CAIA model that to a large extent induces arthritis independently of T-cell response and endogenous Th1/Th2 balance. In conclusion, the present set of data points on a novel strong anti-inflammatory role of CD163.",

author = "Pia Svendsen and Anders Etzerodt and Deleuran, {Bent W.} and Moestrup, {S{\o}ren K.}",

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AU - Svendsen, Pia

AU - Etzerodt, Anders

AU - Deleuran, Bent W.

AU - Moestrup, Søren K.

PY - 2020

Y1 - 2020

N2 - The scavenger receptor CD163 is highly expressed in macrophages in sites of chronic inflammation where it has a not yet defined role. Here we have investigated development of collagen-induced arthritis (CIA) and collagen antibody-induced arthritis (CAIA) in CD163-deficient C57BL/6 mice. Compared to wild-type mice, the CIA in CD163-deficient mice had a several-fold higher arthritis score with early onset, prolonged disease and strongly enhanced progression. Further, the serum anti-collagen antibody isotypes as well as the cytokine profiles and T cell markers in the inflamed joints revealed that CD163-deficient mice after 52 days had a predominant Th2 response in opposition to a predominant Th1 response in CD163+/+ mice. Less difference in disease severity between the CD163+/+ and CD163−/− mice was seen in the CAIA model that to a large extent induces arthritis independently of T-cell response and endogenous Th1/Th2 balance. In conclusion, the present set of data points on a novel strong anti-inflammatory role of CD163.

AB - The scavenger receptor CD163 is highly expressed in macrophages in sites of chronic inflammation where it has a not yet defined role. Here we have investigated development of collagen-induced arthritis (CIA) and collagen antibody-induced arthritis (CAIA) in CD163-deficient C57BL/6 mice. Compared to wild-type mice, the CIA in CD163-deficient mice had a several-fold higher arthritis score with early onset, prolonged disease and strongly enhanced progression. Further, the serum anti-collagen antibody isotypes as well as the cytokine profiles and T cell markers in the inflamed joints revealed that CD163-deficient mice after 52 days had a predominant Th2 response in opposition to a predominant Th1 response in CD163+/+ mice. Less difference in disease severity between the CD163+/+ and CD163−/− mice was seen in the CAIA model that to a large extent induces arthritis independently of T-cell response and endogenous Th1/Th2 balance. In conclusion, the present set of data points on a novel strong anti-inflammatory role of CD163.

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DO - 10.1038/s41598-020-69018-7

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Mouse CD163 deficiency strongly enhances experimental collagen-induced arthritis

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