Ninghai Wang

TL;DR: It is shown that a T-cell-specific, SLAM-associated protein (SAP), which contains an SH2 domain and a short tail, acts as an inhibitor by blocking recruitment of the SH2-domain-containing signal-transduction molecule SHP-2 to a docking site in the SLAM cytoplasmic region.

TL;DR: The topography of N KT cell ligand recognition determines the availability of a cosignaling pathway that is essential for NKT cell lineage development.

TL;DR: The aberrant immune responses in SAP-deficient mice show that SAP controls several distinct key T cell signal transduction pathways, which explains in part the complexity of the XLP phenotypes.

TL;DR: It appears therefore that the SAP/SH2D1A gene controls signaling via the SLAM family of surface receptors and thus may play a fundamental role in T cell and APC interactions during viral infections.

TL;DR: It is shown that T cell receptor–induced interleukin (IL)-4 secretion by SLAM−/− CD4+ cells is down-regulated, whereas interferon γ production by CD4+, and that the coreceptor SLAM plays a central role at the interface of acquired and innate immune responses.