Authors
Laurie Baert, Adrien Caffiers, Agnes Yang, Sae Rome Choi, Suman Bose, SangKon Oh
Published in
bioRxiv : the preprint server for biology. Oct 18, 2026. Epub Oct 18, 2026.
Abstract
B cells can control inflammation, but the factors governing B cell-mediated immune regulatory network remain unclear. We report that IL-2/CD40L enable class-switched memory (CSM) B cells to acquire an immunosuppressive phenotype characterized by the expression of surface TIGIT as well as multiple other inhibitory receptors (PD-1, LAG-3, GITR, CD39, and CTLA-4) and soluble molecules (IL-10, granzyme B, and IL-35). TIGIT + CSM B cells expressing functional CCR9 exhibit significant defects in total immunoglobulin secretion, while preserving IgA2 secretion. Furthermore, IL-2/CD40L-induced ex vivo -generated TIGIT + CSM B cells suppress human T cell-mediated inflammation in a xenogeneic mouse model of acute graft-versus-host disease, while promoting IL-10-producing regulatory T cell (Treg) response. These findings identify IL-2/CD40L as key drivers of a B cell-mediated immune regulatory network, especially by generating TIGIT + CSM B cells that can further promote Treg response. This study supports the development of TIGIT + B cell-based therapy models for inflammatory diseases.
IL-2/CD40L can generate and maintain immunosuppressive TIGIT + B cells in humans. TIGIT + B cells expressing CCR9 have defects in antibody secretion, but not IgA2. TIGIT + B cells suppress inflammation, while promoting Treg response in vivo . IL-2/CD40L can thus build a robust B cell-mediated immune regulatory network.
PMID:
42920441
Bibliographic data and abstract were imported from PubMed on 24 Oct 2026.
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