Journal
JOURNAL OF IMMUNOLOGY
Volume 180, Issue 5, Pages 3329-3338Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.180.5.3329
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Funding
- NHLBI NIH HHS [R01 HL071241] Funding Source: Medline
- NIAID NIH HHS [P01 AI063537, T32 AI007506, R01 AI03377414, R01 AI50732, U54 AI05715805, P30 AI051519] Funding Source: Medline
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The critical role of cellular immunity during tuberculosis (TB) has been extensively studied, but the impact of Abs upon this infection remains poorly defined. Previously, we demonstrated that B cells are required for optimal protection in Mycobacterium tuberculosis-infected mice. Fc gamma R modulate immunity by engaging Igs produced by B cells. We report that C57BL/6 mice deficient in inhibitory Fc gamma RIIB (RIIB-/-) manifested enhanced mycobacterial containment and diminished immunopathology compared with wild-type controls. These findings corresponded with enhanced pulmonary Th1 responses, evidenced by increased IFN-gamma-producing CD4(+) T cells, and elevated expression of MHC class II and costimulatory molecules B7-1 and B7-2 in the lungs. Upon M. tuberculosis infection and immune complex engagement, RIIB-/- macrophages produced more of the p40 component of the Th1-promoting cytokine IL-12. These data strongly suggest that Fc gamma RIIB engagement can dampen the TB Th1 response by attenuating IL-12p40 production or activation of APCs. Conversely, C57BL/6 mice lacking the gamma-chain shared by activating Fc gamma R had enhanced susceptibility and exacerbated immunopathology upon M. tuberculosis challenge, associated with increased production of the immunosuppressive cytokine IL-10. Thus, engagement of distinct Fc gamma R can divergently affect cytokine production and susceptibility during M. tuberculosis infection.
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