Enhanced resistance to Nocardia brasiliensis infection in mice depleted of antigen-specific B cells.

This study deals with the roles of T and B cells in Nocardia brasiliensis infection in mice. Nocardia injected into the animals' footpads caused inflammatory responses and mycetomas in situ, resulting in granulomatous lesions of subcutaneous tissues and eventual bone destruction. These clinical features resemble those of humans infected with Nocardia. The effect, if any, of antibody was studied by passively transferring anti-Nocardia serum into either immunologically normal or T-deficient infected mice. Such transfers had no protective function in either group. To the contrary, the antibody seemed to favor infection and worsen bone disease compared to that in mice not given antibody. Furthermore, passive transfer of the antibody along with injection of Nocardia coated with the antibody magnified the severity of subsequent symptoms. Although these experiments ruled out any role for antibody in protection from Nocardia, they did not directly prove T cell participation in such resistance. Therefore, the role of T cells during Nocardia infection was examined further by transferring spleen cells depleted of B lymphocytes bearing receptors for a Nocardia extract (NE). Lethally irradiated mice reconstituted with a population depleted of NE-specific B cells totally lacked the ability to form antibodies to NE; however, they mounted effective delayed-type hypersensitivity reactions and completely controlled their Nocardia infection, establishing the importance of cell-mediated immunity in halting this disease process.