Volume 11 Issue 5, May 2010

A diverse group of immunologists gathered recently at Asilomar, California, to discuss advances in the theory and practice of their field. The pristine setting and informal atmosphere have always made this a unique and memorable conference.

Dendritic cells can internalize and degrade invading pathogens in phagosomes, yet some HIV-1 particles can evade this degradation process and productively infect dendritic cells. New data show that HIV-1 replication is triggered by signal-transduction events through Toll-like receptor 8 and DC-SIGN.

A critical aspect of innate immune function is the coordinated regulation of inflammatory gene expression. Now an unexpected discovery shows that certain signaling components of the unfolded protein response are required for optimal gene induction by Toll-like receptors.

Intracellular pathogens face a diverse array of innate immune receptors. New data show that a single receptor, AIM2, functions to detect bacterial or viral DNA in the cytosol, inducing a protective inflammasome response.

The 'choice' between the CD4⁺CD8⁻ and CD4⁻CD8⁺ T cell lineage involves genomic specification via a set of transcription factors. A new study shows that the zinc-finger protein MAZR is another member of this transcription factor network.

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.

The mechanism by which influenza virus activates the NLRP3 inflammasome is unknown. Iwasaki and colleagues show that the influenza virus M2 protein, a proton-selective ion channel, stimulates the NLRP3 inflammasome pathway.

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.

HIV-1 replication requires proviral production of full-length transcripts. Geijtenbeek and colleagues show that early Tat-independent HIV-1 replication coopts innate receptor signaling by DC-SIGN and TLR8 to promote RNA polymerase II elongation complexes at long terminal repeats.

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 double-positive thymocytes enter the invariant natural killer T cell lineage is still unclear. Alberola-Ila and co-workers show that c-Myb has a central role in this process.

MAZR is an important negative regulator of CD8 expression. Ellmeier and colleagues now demonstrate that MAZR directly regulates the transcription factor Th-POK locus and is therefore involved in CD4 and CD8 cell-fate 'decisions'.

Most antigenic peptides presented by MHC class I are produced by the proteasome. Van den Eynde and co-workers show that a MAGE-A3–derived peptide is produced directly by the cytosolic metallopeptidase IDE.