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A toxin produced by the bacterium Bordetella pertussis preferentially binds to non-activated integrin complement receptor 3 outside of its ligand-binding I-domain and efficiently blocks downstream signaling of the integrin through elevation of cytosolic cAMP.

Cross-species multiomics network modeling revealed tissue-specific regulatory genes, pathways, and networks shared between mouse and human or unique to each species for atherosclerosis and coronary artery disease.

The combination of molecular imaging, genetic and pharmacological approaches revealed that BCR signaling and PKCβ-dependent activation of focal adhesion kinase (FAK) is required for B cell mechanosensing.

In-depth proteomic analyses of intestinal tissue-resident intraepithelial T lymphocytes reveals how these cells are adapted to the intestinal environment through increased cholesterol and lipid metabolism, tailored metabolic profiles, receptors for interacting with epithelial cells, and tightly regulated signalling pathways.

Pre-existing enhancers interpret T cell signaling strength in an analogue manner to direct quantitative changes in gene expression within the context of an overall digital response.

A molecular interpretation is provided for why some inhibitory immunoreceptors prefer to recruit SHP1 but others prefer SHP2.

Gene editing to generate precisely matched primary human T cell populations demonstrates that the common autoimmune risk allele in the tyrosine phosphatase, PTPN22, promotes signaling in cells expressing a low-avidity, self-reactive TCR specific for a diabetes-associated self-antigen.

The adaptor protein Grb2 is able to enhance the activity of the cytoplasmic tyrosine kinase Btk through a novel mechanism, revealing a new role for Grb2 in B-cell signaling.

Compositional changes alter actin binding by phase separated T cell signaling clusters, enabling cluster movement by distinct actin networks.