Volume 9 Issue 12, December 2008

Although immunological research is of only recent origin in India, it is nevertheless rapidly becoming an area of choice for young researchers in this country.

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.

TGF-β promotes the differentiation of T_H-17 and regulatory T cells. Stockinger and colleagues show that TGF-β also directs differentiation of a unique interleukin 9–producing T cell subset.

Foxp3 is required for the generation and function of regulatory T cells. Kuchroo and colleagues find that interleukin 4 blocks the generation of these cells but promotes T helper cells that produce interleukins 9 and 10.

The E3 ubiquitin ligases Itch and Nedd4 target similar proteins in vitro. Oliver and colleagues find that unlike hyper-responsive Itch-mutant T cells, Nedd4-deficient T cells are hyporesponsive and contain excess Cbl-b.

Suppression of the kinase NIK prevents NF-κB signaling. The Cheng and Karin labs demonstrate that adaptor proteins TRAF2 and TRAF3 and ubiquitin ligases cIAP1 and cIAP2 regulate NIK degradation.

Suppression of the kinase NIK prevents NF-κB signaling. The Cheng and Karin labs demonstrate that adaptor proteins TRAF2 and TRAF3 and ubiquitin ligases cIAP1 and cIAP2 regulate NIK degradation.

Mature B cell survival requires signals from the BCR and from the BLyS receptor BR3. Michael Cancro and colleagues demonstrate crosstalk between these pathways, as BCR signals supply a substrate needed for BR3 signal transmission.

Foxo transcription factors are linked to complex regulatory circuits governed by the availability of phosphatidylinositol-3,4,5-trisphosphate. Rickert and colleagues show that Foxo1 has nonredundant functions at many stages of B cell development.

Classically activated macrophages are targets of intracellular bacteria such as Mycobacteria tuberculosis. Murray and colleagues find that such pathogens induce arginase 1 in these macrophages to block the production of antibacterial nitric oxide.

TLR9 binds unmethylated CpG DNA and sends signals from endolysosomes. Ploegh and colloeagues find that cleavage mediated by endolysosomal cathepsins is required for TLR9 activation.

In a variety of organisms, signals from the nervous system influence adaptive immunity. Tan and Kawli now show the importance of neuroendocrine inputs in the innate immunity of Caenorhabditis elegans to bacterial pathogens.

Dicer proteins direct RNA-interference activities. Imler and colleagues show that Dicer-2 induces Vago-dependent antiviral response in flies and that Dicer proteins are related to RIG-I viral sensors.