Issues

Naip knockout mice provide genetic evidence for the specificity of NAIP1, 2, and 5 in recognizing bacterial T3SS needle protein, rod protein, and flagellin, respectively. Naip1^−/−, Naip2^−/−, and Naip5^−/− mice underscore the physiological contribution of the NAIP proteins in innate defense against cytosolic bacteria.

Vance et al. provide genetic proof for the specificity and essentiality of NAIP proteins for inflammasome responses to specific bacterial ligands in vivo.

Wang et al. report that TREM2 protects mice from Alzheimer's disease by enabling resident microglia to insulate and alter Aβ plaque structure, thereby limiting neuritic damage.

Accumulation of β-amyloid peptide is a key step in Alzheimer’s disease pathogenesis. Yuede et al. propose a novel method to track β-amyloid levels in vivo.

Zook et al. use a novel mouse model to demonstrate a requirement for the transcription factor ETS1 in the development and function of group 2 innate lymphoid cells.

As an alternative to mitophagy, neutrophils spontaneously extrude mitochondrial (mt) DNA devoid of oxidized residues (Ox). Activated lupus neutrophils or healthy neutrophils treated with IFN/αRNP release ox-mtDNA bound to TFAM, which induces high levels of IFN-α in pDCs.

B cell–intrinsic IFN-γ receptor signaling through STAT1 is required for the generation of spontaneous germinal centers, which can lead to pathogenic autoantibody production.

Jackson et al. propose a role for B cell–intrinsic IFN-γ receptor signaling in spontaneous germinal center activation and autoantibody production.

Cambier et al. show that the tyrosine phosphatase SHP-1 and the inositol phosphatase SHIP-1 are required to maintain B cell anergy.

Ploegh et al. raised an alpaca single-domain antibody (VHH) against the inflammasome adaptor ASC. VHH_ASC blocks inflammasome activation in vitro and in living cells, and demonstrates a role of the ASC CARD domain in cross-linking ASC Pyrin domain filaments.

Rossjohn, Brooks, Vivian, and colleagues provide the most complete picture to date of the impact of KIR3DL1 polymorphism on HLA class I recognition, which can be used to both reevaluate previous work on the involvement of KIR3DL1 in disease as well as inform future disease association studies.

Russell et al. show that activation of Mycobacterium tuberculosis–infected macrophages in vitro and in vivo enhances drug tolerance and renders the bacilli more refractory to drug-dependent killing.

D’Amico et al. show that Dkk1 exerts immune-suppressive effects by directly targeting β-catenin in murine and human MDSCs and promoting their activation in cancer.

Genestier et al. shed light on the cellular origin of peripheral T cell lymphoma (PTCL), showing that in both mice and humans, unconventional CD1d-restricted T cells may give rise to PTCL.

Yang et al. identify a feedback loop between gankyrin, an oncoprotein overexpressed in human hepatocellular carcinoma (HCC), and Nrf2. The positive feedback modulates a series of antioxidant enzymes that lower intracellular reactive oxygen species to confer protection from mitochondrial damage and cell death.