Inflammasome-induced extracellular vesicles harbour distinct RNA signatures and alter bystander macrophage responses.

Infectious organisms and damage of cells can activate inflammasomes, which mediate tissue inflammation and adaptive immunity. These mechanisms evolved to curb the spread of microbes and to induce repair of the damaged tissue. Chronic activation of inflammasomes, however, contributes to non-resolving inflammatory responses that lead to immuno-pathologies.

IRGB10 Exposes Bacteria's Intimate Secrets.

When bacteria infect a cell, the bacterial membrane partially shields microbial structures from the immune system, preventing detection and clearance. In a recent issue of Cell, Man et al. (2016) show that the interferon-inducible protein IRGB10 liberates bacterial ligands for sensing by both the AIM2 and the non-canonical NLRP3 inflammasomes.

Efficient induction of antitumor immunity by synthetic toll-like receptor ligand-peptide conjugates.

Chemical conjugates comprising synthetic Toll-like receptor ligands (TLR-L) covalently bound to antigenic synthetic long peptides (SLP) are attractive vaccine modalities, which can induce robust CD8(+) T-cell immune responses. Previously, we have shown that the mechanism underlying the power of TLR-L SLP conjugates is improved delivery of the antigen together with a dendritic cell activation signal. In the present study, we have expanded the approach to tumor-specific CD4(+) as well as CD8(+) T-cell responses and in vivo studies in two nonrelated aggressive tumor models.