MyD88 signalling in myeloid cells is sufficient to prevent chronic mycobacterial infection

摘要: Tuberculosis is a chronic infectious disease caused by Mycobacterium tuberculosis that responsible for almost 1.5 million deaths per year. Sensing of mycobacteria the host's immune system relies on different families receptors present innate cells. Amongst them, several members TLR family are involved in activation cells mycobacteria, yet vivo contribution individual TLRs to protective response remains controversial. On contrary, MyD88, adaptor molecule most TLRs, plays non-redundant role protection against and mice with complete germline deletion MyD88 succumb very early infection. expressed both non-immune cells, but it not clear whether control requires ubiquitous or cell-type specific expression. Therefore, using novel conditional switch-on mouse models, we aimed investigate importance signalling DCs macrophages induction effector mechanisms mycobacterial We conclude reactivation CD11c- lysozyme M-expressing myeloid during bovis Bacille Calmette-Guerin infection sufficient restore systemic local inflammatory cytokine production pathogen burden.