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How do commensal gut bacteria coexist with the host without causing uncontrolled inflammation? The answer may lie in the induction of the association of PPAR-γ with NF-κB.
The immune system uses many sensors to detect and report microbial invaders. Most of these sensors are associated with immune cells, but the extracellular matrix also seems to be essential for this sentinel duty.
Murr1, a protein linked to copper homeostasis, is shown in a recent Nature paper to inhibit the degradation of IκBα. This unexpected action of Murr1, which blunts both basal and stimulus-coupled activation of the NF-κB transcription factor, is key in making resting CD4 T lymphocytes nonpermissive for HIV infection.
The Toll-like receptor (TLR) family targets pathogen-derived molecules in regions unlikely to change under selection pressures. For TLR5, which recognizes the protein flagellin, the function of the targeting motif is key.
Mast cells are not only important in IgE-associated disorders but also contribute to host defense against bacteria. One way they do this is by enhancing T cell recruitment and lymph node enlargement during bacterial infection.
TLR ligands mediate adjuvant effects. Unlike lipopolysaccharide, poly(I:C) is capable of using a TLR-Trif–independent pathway to induce costimulatory molecule upregulation on antigen-presenting cells.
Although natural killer T cells are activated during infection, it is not clear how this process occurs. Closer examination indicates that recognition of endogenous ligands and interleukin 12, rather than bacterial products, may drive the activation process.
The importance of cross-priming in vivo is controversial because its relative contribution in the presence of conventional priming is unclear. However, data from the examination of a conserved tyrosine residue in the cytoplasmic tail of MHC class I favor the cross-priming hypothesis.
Patients with type 2 Hermansky-Pudlak syndrome are immunodeficient. Mutations in AP-3 that prevent movement of lytic granules along microtubules in CD8+ T cells help explain these patients' susceptibility to infection.
Tim-3, a member of the T cell immunoglobulin mucin family, is expressed by TH1 cells. Analysis of Tim-3–Tim3 ligand signaling now shows this pathway is intimately involved in the counter-regulation of T helper type 1 immune responses.
The LFA-1 integrin is known to mediate adhesion between T cells and antigen-presenting cells. New evidence, however, is provided for its role in transmitting signals that promote T cell activation and differentiation.
Peptide chemokines were initially thought to govern effector T cell migration to inflamed tissues. Several studies now show that the leukotriene B4 is intimately involved in T cell homing.
Dendritic cells require a special 'license' to present exogenous antigens to CD8+ T cells. Such permission may be provided by type I interferons during viral infections.
Certain infectious diseases, autoimmune disorders and cancers are associated with T cell receptor ζ chain down-regulation. Interferon-γ production by T helper type 1 cells seems to be pivotal in this process.