Volume 14 Issue 9, September 2013

A unique complex of the interferon receptor IFNAR1 and interferon-β (IFN-β) has been identified that signals independently of IFNAR2 and induces a distinct set of interferon-inducible genes and downstream IFN-β-specific functional responses.

Small phosphorylated prenyl metabolites are potent activators of γδ T cells in human peripheral blood, but the molecular mechanism underlying their antigenic potency has remained a mystery. New data identify BTN3A1 as a novel antigen-presentation molecule for both microbial and host-derived phosphorylated antigens.

In the absence of the SCARF1 scavenger system in mice, the load of 'dangerous' molecules can increase, inducing features of lupus in a sex-dependent process. These findings highlight the interplay of death and sex in the generation of autoimmunity.

CD11b⁺ dendritic cells (DCs) represent a subset of classical DCs that require signaling via the receptor Notch2 and lymphotoxin-β receptor and act as obligate source of interleukin 23 for protection against Citrobacter rodentium.

Sterols and oxysterol derivatives of cholesterol regulate diverse cellular processes. Nathanael Spann and Christopher Glass review the emerging data indicating that these endogenous compounds also serve key roles in almost all aspects of immunological function.

Type I interferons regulate immune responses by signaling via heterodimeric IFNAR1-IFNAR2 complexes. Hertzog and colleagues reveal a unique IFN-β–IFNAR1 signaling complex that is IFNAR2-independent and modulates expression of a distinct set of interferon-inducible genes.

V_γ9V_δ2-expressing cells are a prominent γδ T cell population, but little is known about how they recognize antigens. De Libero and colleagues identify CD277 as an actual antigen-presenting molecule that binds stimulatory phosphorylated antigens.

Failure to clear apoptotic cells can lead to autoinflammatory disease. Means and colleagues demonstrate that the receptor SCARF1 recognizes C1q-bound apoptotic cells, which leads to their clearance and prevents lupus-like symptoms.

The E3 ubiquitin ligases that modify the kinase RIP2 downstream of the receptor Nod2 remain unclear. Moynagh and colleagues show that Pellino3 ubiquitinates RIP2 for Nod2-induced activation of the transcription factor NF-κB.

IL-23 is needed to protect mucosal surfaces from bacterial pathogens. Murphy and colleagues identify a Notch-2-dependent CD11b⁺ dendritic cell population that produces IL-23 and is required for survival after infection with Citrobacter.

Inflammation induces changes in the extracellular matrix density and composition. Fowell and colleagues show that CD4⁺ effector T cells use integrin α_V for interstitial migration on fibronectin in inflamed tissues.

The signals controlling T_reg cell homeostasis and survival are still being determined. Liston and colleagues demonstrate that peripheral T_reg cells depend critically on IL-2 and the survival factor Mcl-1 but not on Bcl-2.

The adaptor Nck is known for linking TCR signaling to cytoskeleton regulation. Batista and colleagues show that in B cells, Nck recruits the adaptor BCAP to the BCR to activate the PI(3)K pathway.