E. Latz

Cytosolic sodium accumulation is a common danger signal triggering endocytic dysfunction and NLRP3 inflammasome activation

The paper shows that cytosolic sodium accumulation triggers NLRP3 inflammasome activation in response to various danger signals in human macrophages.

Butyrate and propionate are microbial danger signals that activate the NLRP3-inflammasome in human macrophages in the presence of TLR stimulation

The paper shows that butyrate and propionate activate the NLRP3 inflammasome in human macrophages when combined with TLR agonists, through HDAC inhibition and epigenetic changes.

NLRP3-induced systemic inflammation controls the development of JAK2V617F mutant myeloproliferative neoplasms

This study shows that NLRP3 inflammasome activation drives JAK2V617F mutant myeloproliferative neoplasms by promoting inflammation, platelet production, and fibrosis, and that its inhibition can reverse disease features.

Retention of ES cell-derived 129S genome drives NLRP1 hypersensitivity and transcriptional deregulation in Nlrp3-/- mice

The paper identifies retention of 129S genome in Nlrp3-/- mice causing NLRP1 hypersensitivity and transcriptional changes, and introduces a conditional Nlrp3 allele to resolve phenotypes.

Microbiome ssRNA as an environmental cue to activate TLR13-dependent tissue-protective programs in CD5Lhi hepatic macrophages

The paper shows that microbiome ssRNA activates TLR13 in hepatic macrophages to drive tissue-protective responses, leading to resistance against acute liver injury in Rnaset2-/- mice.

Epigenetic regulation of innate immune genes and enhanced interleukin-10 expression underlie chronic subclinical Plasmodium chabaudi infection

This study identifies epigenetic regulation of innate immune genes and increased IL-10 expression as mechanisms underlying chronic subclinical Plasmodium chabaudi infection in mice.

Aortic valve disease augments vesicular microRNA-145-5p to regulate the calcification of valvular interstitial cells via cellular crosstalk

This study identifies miR-145-5p as a key regulator of aortic valve calcification through EV-mediated crosstalk, showing it suppresses ZEB2 to enhance ALPL expression and promote calcification in valvular interstitial cells.

TLR7/8 stress response drives histiocytosis in SLC29A3 disorders

This study identifies TLR7/8 as drivers of histiocytosis in SLC29A3 disorders by responding to lysosomal nucleoside stress and enhancing monocyte proliferation and phagocyte maturation.

Suppression of systemic T cell immunity to viral infection during liver injury is prevented by inhibition of interferon and IL-10 signaling

The paper shows that liver injury suppresses systemic T cell immunity to viral infection, which can be reversed by inhibiting interferon and IL-10 signaling in preclinical models and human patients.

Nucleic acid receptor ligands improve vaccination efficacy against the filarial nematode Litomosoides sigmodontis

This study shows that adding nucleic acid receptor agonists to a vaccine against the filarial nematode Litomosoides sigmodontis improves immune response and reduces worm burden by 73%.

P38 kinases mediate NLRP1 inflammasome activation after ribotoxic stress response and virus infection

This study identifies p38 kinases as a central signaling hub for NLRP1 inflammasome activation in response to ribotoxic stress and virus infection.

Directionality of PYD filament growth determined by the transition of NLRP3 nucleation seeds to ASC elongation

The paper determines the directionality of PYD filament growth by showing ASC elongates exclusively on the B-end of NLRP3 filaments, enabling a transition from NLRP3 nucleation to ASC elongation.

Cryo-EM structure of the NLRP3 decamer bound to the cytokine release inhibitory drug CRID3

The paper determines the cryo-EM structure of NLRP3 bound to CRID3, revealing how the inhibitor stabilizes the protein and provides insights for drug development.

Clostridium difficile Toxin B activates the NLRP3 inflammasome in human macrophages, demonstrating a novel regulatory mechanism for the Pyrin inflammasome

The paper shows that C. difficile toxin B activates the NLRP3 inflammasome in human macrophages, not the Pyrin inflammasome, and that Pyrin activation can be restored with prolonged priming.

STAT3 Serine phosphorylation is required for TLR4 metabolic reprogramming and IL-1β expression

This study shows that STAT3 Ser727 phosphorylation is essential for TLR4-induced metabolic reprogramming and IL-1β production in inflammation.

AGC kinase members phosphorylate ubiquitin.

This study identifies AGC kinases as enzymes that phosphorylate ubiquitin, showing that kinase recruitment to ubiquitin, rather than peptide specificity alone, drives ubiquitin phosphorylation.

BTK operates a phospho-tyrosine switch to regulate NLRP3 inflammasome activity

The paper shows BTK modulates NLRP3 inflammasome activity through phosphorylation of tyrosine residues, affecting localization, oligomerization, and IL-1β release.

Sensing soluble uric acid by Naip1-Nlrp3 platform

The paper investigates how soluble uric acid is sensed by the Naip1-Nlrp3 inflammasome platform in murine macrophages and shows its role in IL-1β production and inflammation.

IRAK1-mediated coincidence detection of microbial signals licenses inflammasome activation

This study identifies IRAK1-mediated supramolecular organizing centers that coordinate multiple immune pathways to license inflammasome activation in response to microbial signals.

Platelets fuel the inflammasome activation of innate immune cells

This study shows platelets enhance inflammasome activation in immune cells, increasing IL-1β production, and identifies a platelet gene signature linked to autoinflammatory diseases.

Charcot-Leyden Crystals activate the NLRP3 inflammasome and cause IL-1β inflammation

This study shows that Charcot-Leyden crystals activate the NLRP3 inflammasome, leading to IL-1β release and inflammation in vitro and in vivo.