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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.
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.
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.
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.
After leaving lymphoid tissues, do T cells receive additional signals for survival and differentiation at effector sites? A unique cell population in the intestinal lamina propria may provide such a signal via the costimulatory molecule CD70.
Tumors that develop in immunocompetent hosts show reduced immunogenicity because of selective pressure to escape destruction by immune cells. Type I interferons are involved in shaping this evasive response but, unexpectedly, tumor cells are not the main targets of these interferons.
Notch is essential for T lineage cell differentiation. Three new papers look at when Notch signaling is required and how it affects different cell types.
The function of CD14 in LPS signaling has remained enigmatic. Examination of the responses of cells and mice with defective CD14 shows that this molecule seems to modulate specific LPS recognition by TLR4.
Some microbes can circumvent phagocytosis by interfering with membrane transport systems. Brucella do this by making cyclic glucan molecules that interfere with lipid raft–mediated vacuole maturation.
The MAP3K kinases are thought to mediate signaling 'downstream' of the Toll-like receptors. Analysis of the MAP3K ASK1 demonstrates additional complexity in Toll-like receptor signaling pathways involving reactive oxygen species.
Cross-priming of cytotoxic T cells requires the transfer of antigens to dendritic cells from other cells. Careful analysis indicates that the antigens are peptides in association with chaperone proteins.
Hypermutation of antibody-producing B cells occurs in germinal centers, but how autoimmunity from the generation of potentially self-reactive antibodies is avoided has remained puzzling. Characterization of a new mouse mutant, sanroque, indicates previously unknown tolerance mechanisms act at this stage.
HIV pathogenesis is thought of as a chronic infection involving slow degradation of immunity that ultimately leads to AIDS. This scenario, however, could reflect the decay of an immune system mortally wounded during acute HIV infection.
The function of prostaglandin E2 in allergy has long been ambiguous. Now a comprehensive assessment of prostaglandin E2 receptor–deficient mice demonstrates the main anti-inflammatory function of this prostaglandin in allergic lung disease.
A newly identified crystal structure for an autoimmune TCR bound to peptide-MHC shows a highly unusual docking mode. Is this an anomaly or a new twist on MHC restriction?
