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The non-canonical inflammasome triggers host cell death and inflammation upon recognition of cytosolic LPS. A recent report in Cell now shows that Outer Membrane Vesicles (OMVs) of extracellular Gram-negative bacteria can deliver LPS into the host cell cytosol.
Changing exposure to intestinal helminths, or alterations in our intestinal microbiome, have been independently proposed to underlie the increasing incidence of chronic inflammatory diseases including allergy, autoimmunity and inflammatory bowel disease (IBD) observed in developed nations. A recent study in Science links these findings by showing that intestinal helminth infection can prevent the outgrowth of a common intestinal bacterium that causes IBD in genetically susceptible mice.
Asymmetric division in CD8 T cells produces two daughter cells expressing different levels of c-Myc with distinct metabolic profiles. Manipulating this asymmetric partitioning of c-Myc skews T cell responses and potentially allows the development of more effective vaccines and cancer immunotherapies.
The autophagy-related process LC3-Associated Phagocytosis, or LAP, is known to control the degradation of engulfed cells and microorganisms. Now Martinez et al. discover that LAP controls immune responses to dying cells and its inhibition leads to development of Systemic Lupus Erythematosus-like disease.
The tumor microenvironment is recognized as a critical regulator of cancer progression, and multiple roles are also emerging for the microenvironment in modulating response to therapeutic intervention. A recent study by Wang and colleagues identified IFN-γ as a central effector of CD8+ T cell-mediated regulation of glutathione and cysteine metabolism in fibroblasts, which consequently abrogates stromal-induced resistance through modulation of cisplatin intracellular content in ovarian cancer cells.
