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CD1d presents endogenous and exogenous lipid antigens to natural killer T cells. Wilson, Teyton and colleagues (p 810) and Jones, Cerundolo and colleagues (p 819) have solved the crystal structures of mouse and human CD1d, respectively, in complex with an agonist ligand. The image depicts a cross-sectional view of the structure and shows snug positioning of the α -galactosylceramide ligand in the grooves of CD1d. See also News and Views by Godfrey and Rossjohn (p 754). Artwork by Lewis Long (adapted from an image by Robert Esnouf).
The US has entered a new period of fiscal restraint. What does this mean for basic research? Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, discusses the way forward for research scientists in the US.
Cells of the innate and adaptive immune systems often require signals emanating from diverse cell surface receptors for full activation. For dendritic cells, synergistic stimulation by different pairs of Toll-like receptors provides the host with a mechanism to react rapidly and specifically to different pathogens.
Toll-like receptors are crucial in modulating immune responses. Glycogen synthase kinase 3 is involved in Toll-like receptor signaling and regulates the production of proinflammatory cytokines and septic shock.
Contrary to results of previous studies using high frequencies of T cell receptor–transgenic T cells, new data indicate that when naive precursor frequencies approach endogenous levels, CD8+ effector and central memory T cell lineage commitment is fixed.
Structural studies of CD1d presentation of α-galactosylceramide have shown that the lipid component fits snugly in the cleft, whereas the galactosyl head group protrudes upward, with key contact points between CD1d and the antigen conserved between mouse and human structures.
Stimulation of the vagus nerve via the α7 nicotinic acetylcholine receptor can dampen macrophage function. This anti-inflammatory pathway seems to signal through the Jak2-STAT3 pathway.