TLR2-dependent mast cell activation contributes to the control of Mycobacterium tuberculosis infection

Abstract Mast Cells (MCs) express toll-like receptor 2 (TLR2), a receptor known to be triggered by several major mycobacterial ligands and involved in resistance against Mycobacterium tuberculosis (MTB) infection. This study investigated whether adoptive transfer of TLR2 positive MCs (TLR2 +/+ ) corrects the increased susceptibility of TLR2 −/− mice to MTB infection. TLR2 −/− mice displayed increased mycobacterial burden, diminished myeloid cell recruitment and proinflammatory cytokine production accompanied by defective granuloma formation. The reconstitution of these mice with TLR2 +/+ MCs, but not TLR2 −/− , confers better control of the infection, promotes the normalization of myeloid cell recruitment associated with reestablishment of the granuloma formation. In addition, adoptive transfer of TLR2 +/+ MC to TLR2 −/− mice resulted in regulation of the pulmonary levels of IL-β, IL-6, TNF-α, enhanced Th1 response and activated CD8 + T cell homing to the lungs. Our results suggest that activation of MCs via TLR2 is required to compensate the defect in protective immunity and inability of TLR2 −/− mice to control MTB infection.