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The adaptor Fc receptor common γ-chain transduces signals for many immunoreceptors. Taki and colleagues find that this adaptor 'reroutes' interleukin 3 signals to induce interleukin 4 production and T helper 2 differentiation.
The costimulatory molecule ICOS is important for the development of both interleukin 17–producing and follicular T helper cells. Kuchroo and colleagues find that ICOS induces the transcription factor c-Maf, which regulates the population expansion of both helper cell types.
Lymphocytes exit lymph nodes and return to the bloodstream through the efferent lymphatics. Cyster and colleagues show that lymphocytes exit into cortical sinuses by a pathway dependent on sphingosine 1-phosphate receptor type 1.
Nonsignaling chemokine receptors are thought to function as chemokine 'decoys'. Rot and colleagues now show that the nonsignaling chemokine receptor DARC functions to unidirectionally transport inflammatory chemokines toward apical endothelial surfaces.
The functional importance of TCR-induced degradation of p105 NF-κB is unclear. Ley and colleagues now show it is required for regulatory and memory T cell differentiation and for mature T cell function.
ADAR1 is an adenosine deaminase that acts on double-stranded RNA. Orkin and colleagues show that ADAR1 protects hematopoietic stem cells from interferon-induced insult and is needed to maintain long-term hematopoiesis.
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.
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.
Chronic infection can lead to T cell exhaustion. Wherry and colleagues demonstrate that a hierarchy of inhibitory receptors coregulate CD8+ T cell exhaustion during chronic viral infection.
Mouse lymphoid tissue–inducer (LTi) cells require the transcription factor RORγt. Cupedo's group identifies RORγt+ human LTi cell equivalents as committed natural killer cell precursors, and teams led by Vivier and Diefenbach describe RORγt-expressing interleukin 22–producing natural killer cells in mouse gut.
A major challenge for vaccinologists is to understand vaccine immunogenicity. Pulendran and colleagues use systems biology to determine gene 'signatures' that predict CD8+ T cell and antibody responses to the yellow fever vaccine.
Mouse lymphoid tissue–inducer (LTi) cells require the transcription factor RORγt. Cupedo's group identifies RORγt+ human LTi cell equivalents as committed natural killer cell precursors, and teams led by Vivier and Diefenbach describe RORγt-expressing interleukin 22–producing natural killer cells in mouse gut.
Mouse lymphoid tissue–inducer (LTi) cells require the transcription factor RORγt. Cupedo's group identifies RORγt+ human LTi cell equivalents as committed natural killer cell precursors, and teams led by Vivier and Diefenbach describe RORγt-expressing interleukin 22–producing natural killer cells in mouse gut.
Interleukin 10 dampens inflammation and prevents excessive tissue damage during immune responses. Sotomayor and colleagues show that the histone deacetylase HDAC11 negatively regulates expression of the gene encoding interleukin 10 and immune tolerance.