ITLN1, whose expression is regulated by the unfolded protein response, coats a subset of microorganisms, including Akkermansia muciniphila, allows them to thin the inner mucus layer, and increases colitis severity. ITLN1 upregulation in UC may drive similar outcomes.

We report a new mechanism of immune evasion by SARS-CoV-2 based on direct disabling CTLs to form immune synapses through Spike protein binding to ACE2. This mechanism could contribute to the failure of the immune system to control SARS-CoV-2 infection.

The authors identify a tumor-suppressing angiocrine function of CCL2 which is inhibited by tumor-derived adrenomedullin acting via its receptor on endothelial cells. Disinhibition of endothelial CCL2 results in reduced tumor progression through inhibition of adrenomedullin formation by tumor cells.

Zhou et al. establish murine models of anti-CTLA-4–mediated intestinal irAEs. These reveal common immune signatures and the importance of fecal microbiome dysbiosis as irAE-driving mechanisms, which enable preclinical therapeutic interventions. Key immune features are validated in a cohort of melanoma patients with ICB-associated intestinal irAEs.

Using systemic EC–pericyte crosstalk analysis, this study identifies the NO–sGC as a key signaling that mediates EC–pericyte communication in the lung vasculature and demonstrates that pharmacological activation of the NO–sGC signaling promotes vascular integrity and mitigates inflammation-induced lung injury.

Integrins mediate the localization of innate-like B cells to the marginal zone of the spleen. By analyzing mice with β1-integrin deficiency in mature B cells, Andreani et al. show that β1-integrin is also required for normal differentiation and function of marginal zone B cells.

Loss of the dNTPase and DNA repair enzyme SAMHD1 is associated with cancer and causes systemic autoimmunity. We show transformation-promoting spontaneous DNA damage and MDA5-driven, but cGAS/STING-dependent, chronic type I interferon production in SAMHD1-deficient mice.