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In response to activation, regulatory T cells undergo a differentiation program that enables them to produce interleukin 10 and access nonlymphoid tissues, as shown by Kallies and colleagues (p 304; see also News and Views by Ohkura and Sakaguchi, p 283). The original image is from the animation "Fighting Infection by Clonal Selection," created at the Walter and Eliza Hall Institute by Etsuko Uno and Drew Berry, and shows lymphocyte populations of distinct antigen specificities (various colors) in the lymph node. Artwork by Lewis Long.
Chronic inflammatory diseases represent a major challenge for both clinical research and patient care, and evidence indicates that these disorders develop as a result of complex gene-environment interactions. Better understanding of their cause-and-effect relationship is the basis for emerging proposals for therapy and prevention.
Analysis of the serine-threonine phosphoproteome leads to the intriguing find that phosphorylation of the histone deacetylase HDAC7 is key to cytotoxic T lymphocyte function.
The development and function of TCRαβ+CD8αα+ intraepithelial lymphocytes remain poorly understood. These cells are now shown to require transforming growth factor-β for development and proper expression of characteristic surface homodimers of CD8α.
Regulatory T cells adopt specialized differentiation programs controlled by transcription factors. The transcription factors Blimp-1 and IRF4 are now shown to be pivotal in the maturation of effector regulatory T cells.
Helminth parasites are adept at dampening immunity. New data showing that intracellular degradative pathways are manipulated have important implications for therapy.
The kinase mTOR has emerged as an important regulator of helper T cell differentiation. Powell and co-workers show that the mTOR complex mTORC1 selectively regulates TH1 and TH17 differentiation, whereas mTORC2 signaling is required for TH2 differentiation.
Regulatory T cells can adopt specialized differentiation programs in the periphery. Kallies and co-workers show that IRF4 and Blimp-1 control the acquisition of regulatory T cell effector functions, such as IL-10 production.
The molecular mechanisms that direct the development of intestinal intraepithelial lymphocytes (IELs) remain unclear. Chen and co-workers demonstrate a role for TGF-β in the development of TCRαβ+CD8αα+ IELs.
The transcription factor RORγt is expressed in many cell types. Eberl and colleagues show that intestinal homeostasis is regulated by an IL-25-dependent feedback pathway involving IL-22-expressing RORγt+ innate lymphoid cells.
CTLs can produce the regulatory cytokine IL-10 to prevent excess inflammation during clearance of viruses. Braciale and colleagues now unravel the molecular pathways involved in IL-10 expression by CTLs.
The NF-κB subunit RPS3 can contribute to the selection of nuclear targets by NF-κB. Lenardo and colleagues show that the kinase IκBβ phosphorylates RPS3 to promote its nuclear translocation, a process targeted by enteropathogenic Escherichia coli.
Parasites use multifarious means to manipulate and avoid sterilizing immunity. Melendez and colleagues show that a nematode product triggers macrophage autophagocytosis to degrade the adaptor MyD88 and suppress inflammatory responses.
TCR ligation triggers multiple signaling cascades. Cantrell and colleagues provide an unbiased phosphoproteomics analysis of CD8+ T cells showing that phosphorylation of the histone deacetylase HDAC7 is needed to maintain the identity of cytotoxic T lymphoctyes.