Enteroantigen (eAg)‐binding B lymphocytes in the mouse – phenotype, distribution, function and eAg‐specific antibody secretion

Studies reporting beneficial effects of B lymphocytes in autoimmune diseases have been accumulating and a regulatory role for certain B cell subsets is hence getting more and more recognition. Recently, B cells were shown to exhibit a regulatory effect in a T cell transfer model of colitis. Here, B cells exposed to enteroantigen ( eA g) ex vivo abrogated the colitogenic effect if co‐transplanted with Treg‐depleted (CD4+CD25−) T cells into severe combined immune deficiency (SCID) mice. These data may imply a role for B cells that bind eAg (eAg+ B cells) in the immunopathology of colitis. Here, we report the detection of a subset of eAg+ B cells, including both B2 and B1 lineages, and show that these cells are present in all peripheral lymphoid organs of the mouse including the peritoneal cavity. eAg+ B cells are far more efficient as eAg‐presenting cells than unfractionated splenocytes or eAg− B cells in causing proliferation of eAg‐specific T cells. In comparison with eAg− B cells, eAg+ B cells secrete a significant amount of IL ‐10 in vitro , suggesting an anti‐inflammatory potential. Compared with wild‐type B cells, B cell receptor ( BCR ) transgenic, hen egg lysozyme‐specific B cells show inferior eAg binding and T cell stimulatory activity suggesting involvement of the BCR in eAg binding and processing. After activation of CD19 + B cells by eAg and hybridization with hypoxanthine‐aminopterin‐thymidine (HAT) sensitive ×63 lymphoma cells followed by cloning at limiting dilution conditions, around 10% of the hybridoma cells secrete eAg‐specific antibodies.