Volume 9 Issue 10, October 2008

ThPOK is necessary for the differentiation of CD4⁺ helper T cells. Three new studies indicate that, unexpectedly, ThPOK is required only after initial specification to the CD4⁺ lineage.

The production of type I interferon—the first line of defense against virus infection and critical for innate immunity—in plasmacytoid dendritic cells relies on the mammalian target of rapamycin.

The mechanisms that lead to inflammation after necrotic cell death are poorly understood. New data show that the C-type lectin Mincle is involved in this process.

Mycobacterium tuberculosis grows in macrophages but escapes these cells by triggering their death. New findings delineate how this pathogen controls macrophage death to favor bacterial survival and avoid host immunity.

The transcription factor ThPOK is required for CD4⁺ T cell differentiation. Groups led by Taniuchi, Bosselut and Littman define distinct functions for ThPOK and other transcription factors in commitment versus specification of the CD4⁺ T cell lineage.

The transcription factor ThPOK is required for CD4⁺ T cell differentiation. Groups led by Taniuchi, Bosselut and Littman define distinct functions for ThPOK and other transcription factors in commitment versus specification of the CD4⁺ T cell lineage.

The transcription factor ThPOK is required for CD4⁺ T cell differentiation. Groups led by Taniuchi, Bosselut and Littman define distinct functions for ThPOK and other transcription factors in commitment versus specification of the CD4⁺ T cell lineage.

How T cell cytotoxic activity is induced remains incompletely defined. Yasutomo and colleagues now show that Notch2 signals, in direct cooperation with the transcription factor CREB1, promote granzyme B expression.

How calcium signaling affects dendritic cell (DC) maturation and/or migration is unclear. Launay and colleagues show that absence of the TRPM4 cation channel impairs DC migration but leaves DC maturation unaltered.

The mammalian target of rapamycin pathway regulates many essential cellular responses. Pulendran and colleagues show that this pathway is required for Toll-like receptor–mediated production of type I interferon by plasmacytoid dendritic cells.

Microbial sensors activate the Toll pathway in flies. Reichhart and colleagues identify the serine protease Grass, which acts in parallel with Persephone to cleave Toll-activating Spatzle in response to Gram-positive bacteria and fungi.

The molecular components of inflammasomes and what they sense are poorly defined. Vance and colleagues now show the carboxy-terminal 35 amino acids of flagellin activate the inflammasome in a Naip5-dependent way.

The C-type lectin family member Mincle is expressed mainly on macrophages. Saito and colleagues show that the nuclear protein SAP130, released by dead cells, is a ligand of Mincle that drives proinflammatory cytokine production by macrophages.

Virulent strains of Mycobacterium tuberculosis cause necrotic death of infected macrophages, which promotes bacterial dissemination. Remold and colleagues demonstrate that mycobacteria inhibit formation of the apoptotic envelope on macrophages, thus causing necrosis.