Abstract
Galectin-1 (Gal-1) is required for the development of B cells in the bone marrow (BM), however very little is known about the contribution of Gal-1 to the development of B cell regulatory function. Here, we report an important role for Gal-1 in the induction of B cells regulatory function. Mice deficient of Gal-1 (Gal-1−/−) showed significant loss of Transitional-2 (T2) B cells, previously reported to include IL-10+ regulatory B cells. Gal-1−/− B cells stimulated in vitro via CD40 molecules have impaired IL-10 and Tim-1 expression, the latter reported to be required for IL-10 production in regulatory B cells, and increased TNF-α expression compared to wild type (WT) B cells. Unlike their WT counterparts, T2 and T1 Gal-1−/− B cells did not suppress TNF-α expression by CD4+ T cells activated in vitro with allogenic DCs (allo-DCs), nor were they suppressive in vivo, being unable to delay MHC-class I mismatched skin allograft rejection following adoptive transfer. Moreover, T cells stimulated with allo-DCs show an increase in their survival when co-cultured with Gal-1−/− T2 and MZ B cells compared to WT T2 and MZ B cells. Collectively, these data suggest that Gal-1 contributes to the induction of B cells regulatory function.
Highlights
B cells are generally thought to contribute to graft rejection through the production of alloantibody and due to their capacity to efficiently present alloantigens[1]
To understand whether Gal-1 plays a role in the regulatory function of B cells, IL-10 and T-cell immunoglobulin and mucin domain 1 (Tim-1) expression in B cells isolated from wild type (WT) (C57BL/6 (B6)) mice and Gal-1−/− mice housed under the aforementioned condition were analysed
It has been previously shown that CD40 stimulation is required for IL-10 production and Tim-1 expression by B cells[30,31,32], both molecules have been identified as markers for regulatory B cells[11,33]
Summary
B cells are generally thought to contribute to graft rejection through the production of alloantibody and due to their capacity to efficiently present alloantigens[1]. Adoptive transfer of T2 and T1 B cells, but not follicular (FO) B cells, from naïve mice housed in conventional animal facilities prolonged the skin allograft survival[10]. The transfer of T2 B cells from mice rendered tolerant to MHC-class I mismatched skin grafts by donor splenocyte transfusion and anti-CD40L treatment, but not naïve nor alloantigen experienced T2 B cells, can prolong skin graft survival and suppress T cell activation[17]. The role of Gal-1 in the control of the immune responses mediated by T cells is well characterized, less is known about its function in B cells. Gal-1−/− mice were used to investigate the contribution of Gal-1 in the generation and function of regulatory B cells
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
