Reviews & Analysis

T cells are intrinsically more malleable than previously thought. Two studies now show that existing T helper type 2 cells can be converted into alternative CD4⁺ T helper cells that coexpress interleukins 9 and 10.

The protein kinase NIK is regulated by a complex of ubiquitin ligases that destroys it. When NIK-activating receptors are triggered, the ubiquitin ligase complex self-destructs.

The function of gene expression in the response of drosophila to viral infection is poorly understood. A report now demonstrates that the helicase Dicer-2 controls antiviral gene expression in addition to RNA interference–mediated gene silencing.

The molecular mechanisms by which the nervous system influences innate immunity to pathogens remain mysterious. Two new studies show that neuronal products modulate established innate immune signaling pathways operative in the Caenorhabditis elegans intestine.

Interferon-γ exerts many effects on the immune system. A new report shows that it induces both autophagy and Irgm1, a GTPase that protects activated CD4⁺ T cells from executing autophagy.

Major histocompatibility complex class II molecules present peptides to CD4⁺ T cells. New findings indicate that conventional and plasmacytoid dendritic cells handle these molecules differently after activation.

Cancer cells are more resistant to complement-mediated lysis and use this attribute to set up a locally immunosuppressive environment. However, new findings suggest that tumor-driven complement activation can also provide the tumor a growth advantage.

A flurry of studies has suggested the importance of the actin regulator coronin 1A in lymphocyte development. Now, mutants of this regulator are shown to cause immunodeficiency in both mice and humans.

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.

Definitive new data solidify and clarify the function of the adaptor TRADD in tumor necrosis factor receptor 1 signaling and show that in some situations, TRADD is also required for the transmission of Toll-like receptor signals.