Abstract
BackgroundFoxp3 is a key regulator of the development and function of regulatory T cells (Tregs), and its expression is thought to be T cell-restricted. We found that B cells in mice can express Foxp3 and B cells expressing Foxp3 may play a role in preventing the development of collagen-induced arthritis (CIA) in DBA/1J mice.MethodsFoxp3 expression was modulated in CD19+ B cells by transfection with shRNA or using an over-expression construct. In addition, Foxp3-transfected B cells were adoptively transferred to CIA mice. We found that LPS or anti-IgM stimulation induced Foxp3 expression in B cells. Foxp3-expressing B cells were found in the spleens of mice.ResultsOver-expression of Foxp3 conferred a contact-dependent suppressive ability on proliferation of responder T cells. Down-regulation of Foxp3 by shRNA caused a profound induction in proliferation of responder T cells. Adoptive transfer of Foxp3+CD19+ B cells attenuated the clinical symptoms of CIA significantly with concomitant suppression of IL-17 production and enhancement of Foxp3 expression in CD4+ T cells from splenocytes.ConclusionOur data indicate that Foxp3 expression is not restricted to T cells. The expression of Foxp3 in B cells is critical for the immunoregulation of T cells and limits autoimmunity in a mouse model.
Highlights
Foxp3 is a key regulator of the development and function of regulatory T cells (Tregs), and its expres‐ sion is thought to be T cell-restricted
We investigated the existence of Foxp3-expressing B cells, and their regulatory roles in mice arthritis model, by testing whether they could regulate the proliferation of effector T cells in vitro through a cell-to-cell contact-dependent mechanism
We found a therapeutic effect of Foxp3+ B cells in autoimmune arthritis by performing cell transfer studies in collagen-induced arthritis (CIA) mice, an animal model of Rheumatoid arthritis (RA)
Summary
Foxp is a key regulator of the development and function of regulatory T cells (Tregs), and its expres‐ sion is thought to be T cell-restricted. We found that B cells in mice can express Foxp and B cells expressing Foxp may play a role in preventing the development of collagen-induced arthritis (CIA) in DBA/1J mice. Foxp3-transfected B cells were adoptively transferred to CIA mice. Foxp3-expressing B cells were found in the spleens of mice. Several studies have shown that absence of B cells exacerbated pathologic inflammatory responses in autoimmune diseases [12, 14]. Experimental studies have demonstrated that the absence or loss of Bregs exacerbates symptoms in several experimental autoimmune disease model including collagen-induced arthritis (CIA) [15,16,17,18,19,20,21]. Bregs showed therapeutic properties in autoimmune arthritis mice models [18, 22]
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