Peter A. Sieling

TL;DR: It is shown that TLR2 activation leads to killing of intracellular Mycobacterium (M.) tuberculosis in both mouse and human macrophages, providing evidence that mammalian TLRs have retained not only the structural features of Drosophila Toll that allow them to respond to microbial ligands, but also the ability directly to activate antimicrobial effector pathways at the site of infection.

TL;DR: It is shown here that human CD1b presents the defined mycobacterial lipoglycan lipoarabinomannan (LAM) to alpha beta T cell receptor-bearing lymphocytes, which resulted in T cells activated by LAM producing interferon gamma and were cytolytic.

TL;DR: It is shown that human dermal microvessel endothelial cells (HMEC) and human umbilical vein endothelial Cells express predominantly TLR-4 but very weakTLR-2 and respond vigorously to LPS but not to Mycobacterium tuberculosis 19-kDa lipoprotein.

TL;DR: Data suggest that P. acnes triggers inflammatory cytokine responses in acne by activation of TLR2, which may provide a novel target for treatment of this common skin disease.

TL;DR: A new 'detour' pathway for presentation of antigens from a phagosome-contained pathogen shows the functional significance of infection-induced apoptosis in the activation of CD8 T cells specific for both protein and glycolipid antigENS in tuberculosis.