B-1 cell protective role in murine primary Mycobacterium bovis bacillus Calmette-Guerin infection.

B-1 cells were first described in the early 1980s and are distinct from conventional B lymphocytes in respect to phenotype, morphology, ontogeny, tissular distribution and function. Although many years have been past since their description, B-1 cells role within the immune system is still unclear. Years ago, our lab demonstrated that B-1 cells were able to differentiate into macrophage-like mononuclear phagocytes that could migrate to the acute inflammatory focus induced by a foreign body in vivo. We also showed that B-1 cells were pivotal for the formation of foreign-body giant cells. Studies using B-1-cell-defiecient mice (Xid mice), suggested B-1 cells have a participation in immune responses to infections. This led us to investigate whether B-1 cells would also have a participation in a model of infection-generated chronic inflammation. Using Xid mice and adoptive transfer of cultured B-1 cells, we investigated the influence of these cells on some of the immune events triggered by Mycobacterium bovis bacillus Calmette-Guerin (BCG) infection in mice. We found that B-1 cells are present in the BCG-induced pulmonary lesions and can migrate from peritoneal cavity to the infected lung, modulate the histological pattern of the inflammation, influence the influx of other cells to the infected lung and favor the resistance to the mycobacteria. Altogether, our results demonstrate that peritoneal B-1 cells play a key role in the inflammatory reaction to BCG, clarifying a new aspect of the biology of these versatile cells.