Collagen epitope expression on B cells is sufficient to confer tolerance to collagen-induced arthritis

Andersson, S.; Eneljung, Tove; Tengvall, Sara; Jirholt, Pernilla; Stern, Anna; Henningsson, Louise; Liang, Bibo; Thorarinsdottir, Katrin; Kihlberg, Jan; Holmdahl, Rikard; Mårtensson, Inga‐Lill; Gustafsson, Kenth; Gjertsson, Inger

doi:10.1186/s13075-016-1037-7

Cited by 7 publications

(7 citation statements)

References 48 publications

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“…It has been known that B cells play the immunomodulatory role physiologically 34 35 . Recent studies suggest that B cell participated in the tumor-associated regulatory immune response 36 37 .…”

Section: Discussionmentioning

confidence: 99%

Characterization of c-Maf+Foxp3− Regulatory T Cells Induced by Repeated Stimulation of Antigen-Presenting B Cells

Chien

Chen

et al. 2017

Sci Rep

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The role of B cells in the development of CD4+ regulatory T cells has been emphasized recently. Our previous studies have demonstrated that the antigen-presenting splenic B cells converted naïve CD4+CD25− T cells into CD4+CD25+Foxp3− T cells without additional cytokines or chemicals with regulatory activity and that referred to as Treg-of-B cells. The present study further showed that Treg-of-B cells increased the IL-10-producing population, and the expression of c-Maf, inducible T-cell co-stimulator (ICOS) as well as cytotoxic T-lymphocyte-associated protein 4 (CTLA4) after repeated stimulation of B cells in a cell-cell contact-dependent manner. Long-term cultured Treg-of-B cells exerted IL-10 and CTLA4-mediated antigen-specific suppressive activity; moreover, the single antigen-specific Treg-of-B cells inhibited in a non-antigen-specific fashion. In conclusion, these results suggest that repeated stimulation of B cells induced IL-10-producing CD4+Foxp3− regulatory T cells in a contact-dependent manner and these Treg-of-B cells possess IL-10 and CTLA4-dependent suppressive function.

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Section: Discussionmentioning

confidence: 99%

Characterization of c-Maf+Foxp3− Regulatory T Cells Induced by Repeated Stimulation of Antigen-Presenting B Cells

Chien

Chen

et al. 2017

Sci Rep

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“…Genetically B-cell-deficient mice delayed recovery from experimental autoimmune encephalomyelitis and suggested B cells might contribute to immune modulation [ 46 ]. Collagen fragments expressed on B cell MHC class II sufficiently delayed the onset and decreased the severity of arthritis [ 47 ]. The role of B cells in oral tolerance has been investigated because B-cell-deficient mice exhibit a defective oral tolerogenic response characterized by lower levels of IL-10 and TGF-β in the spleen and gut-associated lymphoid tissues [ 48 ].…”

Section: Main Textmentioning

confidence: 99%

Regulatory T cells induced by B cells: a novel subpopulation of regulatory T cells

Chien

Chiang

2017

J Biomed Sci

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Regulatory T cells play a crucial role in the homeostasis of the immune response. In addition to CD4+Foxp3+ regulatory T cells, several subsets of Foxp3- regulatory T cells, such as T helper 3 (Th3) cells and type 1 regulatory T (Tr1) cells, have been described in mice and human. Accumulating evidence shows that naïve B cells contribute to tolerance and are able to promote regulatory T cell differentiation. Naïve B cells can convert CD4+CD25- T cells into CD25+Foxp3- regulatory T cells, named Treg-of-B cells by our group. Treg-of-B cells express LAG3, ICOS, GITR, OX40, PD1, and CTLA4 and secrete IL-10. Intriguingly, B-T cell-cell contact but not IL-10 is essential for Treg-of-B cells induction. Moreover, Treg-of-B cells possess both IL-10-dependent and IL-10-independent inhibitory functions. Treg-of-B cells exert suppressive activities in antigen-specific and non-antigen-specific manners in vitro and in vivo. Here, we review the phenotype and function of Foxp3+ regulatory T cells, Th3 cells, Tr1 cells, and Treg-of-B cells.

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“…B cells play a role in the induction of both immune tolerance and activation ( Andersson et al., 2016 ; Ashour and Niederkorn, 2006 ; Sun et al., 2008 ). A previous study has indicated that naive B cells induce regulatory T-cell production by forming a mature immunologic synapse at the contact zone ( Reichardt et al., 2007 ).…”

Section: Discussionmentioning

confidence: 99%

Regulatory T cells induced by B cells suppress NLRP3 inflammasome activation and alleviate monosodium urate-induced gouty inflammation

Huang

Chiang

2021

iScience

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Summary Regulatory T cells induced by B cells (Treg-of-B cells), a distinct Foxp3 - Treg cell subset, have established the roles in the suppression of inflammatory conditions, including asthma and intestinal inflammation. However, little is known about the regulatory effects of Treg-of-B cells on innate immunity. Herein, we examined whether Treg-of-B cells could regulate macrophage function and prevent NLRP3-associated diseases, particularly inflammatory gouty arthritis. Treg-of-B cells, but not thymus-derived Treg or effector T cells, inhibited inflammasome-mediated IL-1β secretion, caspase-1 activation, and NLRP3 production by LPS/ATP stimulation in a cell contact-dependent manner. In addition, Treg-of-B cells inhibited monosodium urate-induced NLRP3 inflammasome activation in vitro via NF-κB signaling. Treg-of-B cells ameliorated gouty inflammation in a mouse air pouch model by reducing neutrophil and leukocyte influx and cytokine and chemokine production. Our results demonstrated that Treg-of-B cells exerted regulatory effects on innate immunity by suppressing NLRP3 inflammasome activation and feasible for future therapeutic applications.

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Collagen epitope expression on B cells is sufficient to confer tolerance to collagen-induced arthritis

Cited by 7 publications

References 48 publications

Characterization of c-Maf+Foxp3− Regulatory T Cells Induced by Repeated Stimulation of Antigen-Presenting B Cells

Characterization of c-Maf+Foxp3− Regulatory T Cells Induced by Repeated Stimulation of Antigen-Presenting B Cells

Regulatory T cells induced by B cells: a novel subpopulation of regulatory T cells

Regulatory T cells induced by B cells suppress NLRP3 inflammasome activation and alleviate monosodium urate-induced gouty inflammation

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