Suppression of IL-23-mediated psoriasis-like inflammation by regulatory B cells

Abstract Psoriasis is an inflammatory cutaneous disease mediated by T-cell dependent immune responses; however, B cells are also considered to play an important role its development. Regulatory B cells (Bregs) regulate immune responses negatively through interleukin-10 (IL-10) production. This study...

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Autores principales: Kie Mizumaki, Motoki Horii, Miyu Kano, Akito Komuro, Takashi Matsushita
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Publicado: Nature Portfolio 2021
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Acceso en línea:https://doaj.org/article/2b95ef059a404b65b2c89cf4f0c0be14
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spelling oai:doaj.org-article:2b95ef059a404b65b2c89cf4f0c0be142021-12-02T15:23:39ZSuppression of IL-23-mediated psoriasis-like inflammation by regulatory B cells10.1038/s41598-021-81588-82045-2322https://doaj.org/article/2b95ef059a404b65b2c89cf4f0c0be142021-01-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-81588-8https://doaj.org/toc/2045-2322Abstract Psoriasis is an inflammatory cutaneous disease mediated by T-cell dependent immune responses; however, B cells are also considered to play an important role its development. Regulatory B cells (Bregs) regulate immune responses negatively through interleukin-10 (IL-10) production. This study aimed to investigate the role of Bregs in IL-23-mediated psoriasis-like inflammation in mice. Psoriasis-like inflammation was induced in B cell-specific phosphatase and tensin homolog (PTEN)-deficient mice, in which Bregs were significantly expanded, and in their controls, by intradermal injection of 20 μL phosphate-buffered saline (PBS) containing 0.5 μg rmIL-23 into one ear, every other day for 16 days. IL-23-mediated psoriasis-like inflammation was suppressed in B cell-specific PTEN-deficient mice along with decreased ear thickness and epidermal thickness on day 15. Moreover, adoptive transfer of B1 B cells suppressed IL-23-mediated psoriasis-like inflammation. rmIL-23-injected B cell-specific PTEN-deficient mice showed expanded regulatory T cells (Tregs) in the spleen and draining lymph nodes along with increased Bregs. Further, T helper (Th) 17 differentiation in the rmIL-23-injected ear was suppressed in B cell-specific PTEN-deficient mice. Overall, these results indicate that increased Bregs suppress IL-23-mediated psoriasis-like inflammation through Treg expansion and inhibition of Th17 differentiation. Thus, targeting Bregs may be a feasible treatment strategy for psoriasis.Kie MizumakiMotoki HoriiMiyu KanoAkito KomuroTakashi MatsushitaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-13 (2021)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Kie Mizumaki
Motoki Horii
Miyu Kano
Akito Komuro
Takashi Matsushita
Suppression of IL-23-mediated psoriasis-like inflammation by regulatory B cells
description Abstract Psoriasis is an inflammatory cutaneous disease mediated by T-cell dependent immune responses; however, B cells are also considered to play an important role its development. Regulatory B cells (Bregs) regulate immune responses negatively through interleukin-10 (IL-10) production. This study aimed to investigate the role of Bregs in IL-23-mediated psoriasis-like inflammation in mice. Psoriasis-like inflammation was induced in B cell-specific phosphatase and tensin homolog (PTEN)-deficient mice, in which Bregs were significantly expanded, and in their controls, by intradermal injection of 20 μL phosphate-buffered saline (PBS) containing 0.5 μg rmIL-23 into one ear, every other day for 16 days. IL-23-mediated psoriasis-like inflammation was suppressed in B cell-specific PTEN-deficient mice along with decreased ear thickness and epidermal thickness on day 15. Moreover, adoptive transfer of B1 B cells suppressed IL-23-mediated psoriasis-like inflammation. rmIL-23-injected B cell-specific PTEN-deficient mice showed expanded regulatory T cells (Tregs) in the spleen and draining lymph nodes along with increased Bregs. Further, T helper (Th) 17 differentiation in the rmIL-23-injected ear was suppressed in B cell-specific PTEN-deficient mice. Overall, these results indicate that increased Bregs suppress IL-23-mediated psoriasis-like inflammation through Treg expansion and inhibition of Th17 differentiation. Thus, targeting Bregs may be a feasible treatment strategy for psoriasis.
format article
author Kie Mizumaki
Motoki Horii
Miyu Kano
Akito Komuro
Takashi Matsushita
author_facet Kie Mizumaki
Motoki Horii
Miyu Kano
Akito Komuro
Takashi Matsushita
author_sort Kie Mizumaki
title Suppression of IL-23-mediated psoriasis-like inflammation by regulatory B cells
title_short Suppression of IL-23-mediated psoriasis-like inflammation by regulatory B cells
title_full Suppression of IL-23-mediated psoriasis-like inflammation by regulatory B cells
title_fullStr Suppression of IL-23-mediated psoriasis-like inflammation by regulatory B cells
title_full_unstemmed Suppression of IL-23-mediated psoriasis-like inflammation by regulatory B cells
title_sort suppression of il-23-mediated psoriasis-like inflammation by regulatory b cells
publisher Nature Portfolio
publishDate 2021
url https://doaj.org/article/2b95ef059a404b65b2c89cf4f0c0be14
work_keys_str_mv AT kiemizumaki suppressionofil23mediatedpsoriasislikeinflammationbyregulatorybcells
AT motokihorii suppressionofil23mediatedpsoriasislikeinflammationbyregulatorybcells
AT miyukano suppressionofil23mediatedpsoriasislikeinflammationbyregulatorybcells
AT akitokomuro suppressionofil23mediatedpsoriasislikeinflammationbyregulatorybcells
AT takashimatsushita suppressionofil23mediatedpsoriasislikeinflammationbyregulatorybcells
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