Volume 10 Issue 1, January 2009

Anjana Rao recounts the contributions of two talented and productive postdoctoral fellows who purified and characterized the transcription factor NFAT.

On 24–27 September 2008, members of the scientific community gathered to discuss advances in innate immunity at the 'Toll meeting' in Cascais, Portugal. Before long, attendees noticed that 'Toll2008' might be a misnomer.

New findings show that a subpopulation of mucosal RORγt⁺ cells expresses natural killer cell receptors and produces interleukin 22. These innate immune cells may be pivotal in maintaining mucosal homeostasis.

Regulation of expression of the gene encoding interleukin 10 by the histone deacetylase HDAC11 emphasizes the ability of an antigen-presenting cell to induce immunity or tolerance in CD4⁺ T cells.

A systems biology approach provides correlates of successful vaccination, which allows a new method for measuring early vaccine efficiency and suggests hypotheses for the mechanisms that underlie immunogenicity.

ADAR1 catalyzes the deamination of adenosine to inosine in double-stranded RNA. This RNA-editing enzyme is now shown to be involved in hematopoiesis, where it acts to suppress interferon signaling and to block premature apoptosis.

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.

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.

Dendritic cells (DCs) can promote or inhibit T cell responses. Grogan and colleagues show that the T cell protein TIGIT, by engaging poliovirus receptor on DCs, promotes DC interleukin 10 production, which inhibits T cell activation.

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.

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.

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.

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.

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.

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.