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The transcription factor XBP1 is activated after endoplasmic reticulum stress. Glimcher and colleagues show that XBP1 can also be activated by TLR2 and TLR4 signaling pathways, in which it sustains proinflammatory cytokine production.
The AIM2 inflammasome induces maturation of the proinflammatory cytokines IL-1β and IL-18. Using AIM2-deficient mice, Fitzgerald and colleagues and Alnemri and colleagues show that the AIM2 inflammasome is essential for host defense against cytosolic bacteria and DNA viruses.
The AIM2 inflammasome induces maturation of the proinflammatory cytokines IL-1β and IL-18. Using AIM2-deficient mice, Fitzgerald and colleagues and Alnemri and colleagues show that the AIM2 inflammasome is essential for host defense against cytosolic bacteria and DNA viruses.
Vaccines elicit neutralizing antibodies to protect organisms against viral infection. Carroll and colleagues show that medullary lymph node dendritic cells capture influenza virus via SIGN-R1 and are necessary for humoral antiviral immunity.
How and where invariant natural killer T cells encounter glycolipids in vivo remains unclear. Batista and colleagues use multiphoton microscopy to show that CD169+ macrophages present lipid antigens to invariant natural killer T cells in lymph nodes.
Surveillance for blood-borne pathogens by immune cells occurs chiefly in the spleen and liver. Kubes and colleagues show that liver Kupffer cells directly sample the bloodstream and are the predominant antigen-presenting cell for invariant natural killer T cells
Leukocytes enter inflamed tissues by initiating selectin-dependent rolling on reactive endothelia. Mantovani and colleagues show that the long pentraxin PTX3 competes for P-selectin and acts to limit neutrophil extravasation.
The mechanism of T cell avidity maturation has remained elusive. Geisler and co-workers show that induction of the phospholipase PLC-γ1 via the alternative p38 pathway is required for avidity maturation in naive human T cells.
California has one of the most prestigious public university systems. However, budget woes and lack of clear strategic planning may undermine its continued success.
Members of the transient receptor potential vanilloid ion-channel family are expressed in a wide variety of cells and function as sensors of mechanical stress. The second such family member, TVRP2, is now also linked to phagocytosis in macrophages.
Transient formation of reactive oxygen species (ROS) accompanies B cell signaling and activation. Now the voltage-gated proton channel HVCN1 has been linked to ROS formation and B cell activation.
A new study demonstrates that commitment to the CD8 lineage in the thymus requires sequential T cell antigen receptor (TCR) and interleukin 7 (IL-7) signaling. The TCR signal first induces IL-7 responsiveness, then recognition of IL-7 induces the nuclear factor Runx3, which specifies the CD8 lineage.
Hematopoietic stem cell self-renewal is tightly regulated. Regulation of the stability of c-Myc protein contributes to this control of hematopoietic stem cell quiescence and repopulation.
The immunological mechanisms of diabetes onset in NOD mice are poorly characterized. Unanue and co-workers find that insulin peptide–reactive (but not insulin protein–reactive) type B T cells can cause diabetes.
Dendritic cells classically require cognate licensing by helper T cells to cross-prime cytotoxic T cells. Kurts and colleagues have found an alternative mechanism of cognate licensing mediated by natural killer T cells.
Quiescence must be actively maintained in cells of the immune response. Beutler and colleagues describe a new mutant mouse, elektra, with defective control of T cell and monocyte quiescence; this defect maps to Slfn2.
The importance of natural killer cell 'licensing' in vivo remains unclear. Lanier and co-workers now report that 'unlicensed' natural killer cells are more protective than 'licensed' cells during viral infection.