| First Author | Maglione PJ | Year | 2008 |
| Journal | J Immunol | Volume | 180 |
| Issue | 5 | Pages | 3329-38 |
| PubMed ID | 18292558 | Mgi Jnum | J:131525 |
| Mgi Id | MGI:3773928 | Doi | 10.4049/jimmunol.180.5.3329 |
| Citation | Maglione PJ, et al. (2008) Fc{gamma} Receptors Regulate Immune Activation and Susceptibility during Mycobacterium tuberculosis Infection. J Immunol 180(5):3329-38 |
| abstractText | 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. FcgammaR modulate immunity by engaging Igs produced by B cells. We report that C57BL/6 mice deficient in inhibitory FcgammaRIIB (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 FcgammaRIIB 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 FcgammaR had enhanced susceptibility and exacerbated immunopathology upon M. tuberculosis challenge, associated with increased production of the immunosuppressive cytokine IL-10. Thus, engagement of distinct FcgammaR can divergently affect cytokine production and susceptibility during M. tuberculosis infection. |
