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Suppression of IL-23-mediated Psoriasis-like Inflammation by Regulatory B Cells

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Journal Sci Rep
Specialty Science
Date 2021 Jan 23
PMID 33483537
Citations 10
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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.

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References
1.
Mizoguchi A, Mizoguchi E, Takedatsu H, Blumberg R, Bhan A . Chronic intestinal inflammatory condition generates IL-10-producing regulatory B cell subset characterized by CD1d upregulation. Immunity. 2002; 16(2):219-30. DOI: 10.1016/s1074-7613(02)00274-1. View

2.
Lu J, Xu X, Li Y, Yu N, Ding Y, Shi Y . Local reinfusion of B10 cells is effective in the treatment of pustular psoriasis. Dermatol Ther. 2020; 33(4):e13645. DOI: 10.1111/dth.13645. View

3.
Mauri C . Regulation of immunity and autoimmunity by B cells. Curr Opin Immunol. 2010; 22(6):761-7. DOI: 10.1016/j.coi.2010.10.009. View

4.
Alrefai H, Muhammad K, Rudolf R, Pham D, Klein-Hessling S, Patra A . NFATc1 supports imiquimod-induced skin inflammation by suppressing IL-10 synthesis in B cells. Nat Commun. 2016; 7:11724. PMC: 4894959. DOI: 10.1038/ncomms11724. View

5.
Hayashi M, Yanaba K, Umezawa Y, Yoshihara Y, Kikuchi S, Ishiuji Y . IL-10-producing regulatory B cells are decreased in patients with psoriasis. J Dermatol Sci. 2015; 81(2):93-100. DOI: 10.1016/j.jdermsci.2015.11.003. View