The receptor EBI2 is essential for correctly positioning CD4+ dendritic cells in the spleen so that they can present blood-borne antigens to T cells and thereby provoke an antibody response.

Goblet cells secrete mucins—which are key components of mucus—in a process that is regulated by calcium ions, which enter the goblet cells via a mechanism involving a channel protein called TRPM5.

Quantitative observations of single-molecule binding between antigen and T cell receptor (TCR) in living primary T cells reveals unbinding kinetics, stoichiometry and signaling molecule recruitment, providing insights into the mechanisms of antigen recognition by the immune system.

A single point mutation in a Ras activator leads to aberrant constitutive mTOR signaling in peripheral T cells that consequently accumulate as abnormal T helper cells and stimulate the production of autoantibodies by B cells.

Real time measurements of c-di-GMP in individual cells reveal an unexpected mechanism by which the chemotaxis machinery controls c-di-GMP heterogeneity, thereby regulating flagellar-based motility.

The T cell repertoire can display immunodominance to an epitope as a result of optimal positive selection in the thymus by one self-peptide/MHC ligand.

Experiment-driven quantitative model of IL-2 secretion demonstrates how T cells integrate their digital antigen responses into an analog-scaled output.

The p21-activated kinase 2 (Pak2) is an essential regulator that governs the actin cytoskeleton-dependent signaling to ensure normal thymocyte development, maturation and egress.

MHC class II-mediated self-antigen presentation by lymph node stromal cells controls regulatory T cell homeostasis, thus safeguarding immune tolerance.

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