Abstract
Protective immunity against infection with Mycobacterium tuberculosis is imparted by T cells rather than antibodies, but B cells can play a role as antigen-presenting cells and in granuloma formation. We re-evaluated the role of B cells in the course of tuberculous infection in μ-chain knock-out (Ig−) mice. Surprisingly, the organs of M. tuberculosis-infected Ig− mice were found to have three-to eight-fold elevated counts of viable bacilli compared with normal littermates at 3–6 weeks post-infection. Splenic interferon-gamma responses to whole antigen were unimpaired, whilst proliferation to certain mycobacterial peptides was found to be diminished. However, bacille Calmette–Guérin (BCG) vaccination significantly reduced the infection in Ig− mice. The mechanisms by which B cells can influence primary tuberculous infection need further study.
Keywords: tuberculosis, B cells, antibodies, mouse infection
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