Neutrophil extracellular traps and extracellular histones potentiate Th17 inflammation and bone destruction in animal models of periodontitis. Findings in patients with periodontitis provide human relevance and support further exploration of NET-mediated pathology in human disease.

Steady-state and emergency myelopoiesis require different rates of mature cell production to maintain or restore homeostasis. This study demonstrates that mitochondrial pyruvate is specifically required for steady-state but not emergency myelopoiesis. Reciprocally, glutaminolysis specifically promotes emergency but not steady-state myelopoiesis.

Lockhart et al. demonstrate that exposure to food protein drives an antigen-specific CD4⁺ T cell response characterized at steady state by accumulation at the intestinal epithelium and tissue-specialized transcriptional imprinting. This process is disrupted upon either allergic sensitization or tolerance.

The role of B cells in T1D remains poorly understood. We identified an activated B cell subset that is enriched in insulin reactivity and increased in the blood and pLN of T1D donors. This subset has capacity to secrete antibodies and potential to serve as APCs to T cells.

Obesity is associated with enhanced breast cancer mortality, yet the mechanisms underlying this relationship remain poorly understood. McDowell et al. provide insight into the role of obesity on myeloid-driven cancer metastasis by identifying how monocyte development is skewed to promote prometastatic neutrophil effector functions.

A novel ILC2 subset was identified in the mouse intestine that constitutively expresses IL-4. Although the absence of the gut microbiota had marginal effects, feeding mice with a vitamin B1-deficient diet compromised the number of intestinal IL-4⁺ ILC2s.

E3 ubiquitin ligase ZNRF1 is activated by c-Src kinase following TLR3 activation and, in turn, promotes TLR3 ubiquitination and trafficking to lysosomes for degradation. This leads to properly regulated interferon production and alveolar barrier repair to prevent secondary bacterial superinfection.