A mouse model of atopic dermatitis provides mechanistic evidence for an association between allergic disease and skin cancer.

Studying the earliest events in B cell activation reveals that the B cell antigen receptor is opened and activated via the phosphorylation and binding by the spleen tyrosine kinase (Syk).

Sialoside-based pattern recognition by Siglecs directly regulates toll-like receptor signaling and a sialidase inhibitor protects against endotoxemia.

Peptide immunotherapy in mice depends upon sustained expression of co-inhibitory protein PD-1 in T cells.

T cell receptor signaling is regulated by newly polymerized F-actin foci at the immunological synapse.

Angiopoietin-like proteins signal through notch via receptor interaction and can regulate Notch cleavage/activation.

By contributing to the maintenance of ROS homeostasis, CD33-related Siglecs control oxidative damage and influence rate of aging and lifespan.

Atypical memory B cells (MBCs) appear to differentiate from classical MBCs during chronic exposure to the malaria parasite Plasmodium falciparum, and may interfere with the acquisition of immunity to the disease.

The B cell receptors of naïve B cells need higher levels of mechanical force to be fully activated than those of memory B cells.

Degradation of kinase LynA protects macrophages from activation unless cells sense a receptor-binding pathogen or inflammation