B cells in pancreatic cancer stroma

Figure 1 B-cell role in pancreatic cancer. B cells mature in plasma cells, which can produce immunoglobulin G, and are able to reprogram the M1 macrophage phenotype to M2 via Bruton’s tyrosine kinase activation. B regulatory cells are able to produce immune-suppressive cytokines, which inhibit the anti-tumour immune response, leading to tumour growth. Furthermore, in presence of hypoxia, stromal fibroblasts can secrete chemokine (C-X-C motif) ligand 13, which recruit B regulatory cells (CD1d^hiCD5⁺) and B1 B cells, resulting in faster tumour growth. Clusters of B cells, with follicular dendritic cells and T cells, are sites for T cell priming and B cell maturation and differentiation into antibody-producing cells, with anti-tumoral effect. TLS: Tertiary lymphoid structures; IL-35: Interleukin-35; CXCL-13: Chemokine (C-X-C motif) ligand 13.