Tuesday, January 25, 2011

Hot off the presses! Feb 01 Nat Rev Immunol

The Feb 01 issue of the Nat Rev Immunol is now up on Pubget (About Nat Rev Immunol): if you're at a subscribing institution, just click the link in the latest link at the home page. (Note you'll only be able to get all the PDFs in the issue if your institution subscribes to Pubget.)

Latest Articles Include:

  • - Nat Rev Immunol 11(2):71 (2011)

  • - Nat Rev Immunol 11(2):72 (2011)

  • - Nat Rev Immunol 11(2):73 (2011)
  • Immunometabolism | Immunometabolism | PDF (126 KB)
    - Nat Rev Immunol 11(2):73 (2011)
    The inflammasome-mediated caspase-1 activation controls adipocyte differentiation and insulin sensitivity Stienstra, R.et al. Cell Metab. 12, 593–605 (2010)
  • Vaccines: Foes of fungi are just 17 | PDF (260 KB)
    - Nat Rev Immunol 11(2):74 (2011)
    The incidence of systemic fungal infections has increased throughout the world, and this has prompted much interest in developing effective vaccines against these pathogens. T helper 1 (TH1) cells are believed to be crucial for protection from pathogenic fungi, but the exact role of TH17 cells has remained unclear and both protective and pathological functions for these cells have been reported.
  • One Flu over? eschew the rest! | PDF (95 KB)
    - Nat Rev Immunol 11(2):74 (2011)
    Last year we had a vaccine surplus (Nature Rev. Immunol.
  • Macrophages: A transcription factor to call their own | PDF (222 KB)
    - Nat Rev Immunol 11(2):74 (2011)
    Not to be outdone by the ever-expanding list of T cell subsets and their defining transcription factors, macrophages are let in on the act by new research showing that interferon regulatory factor 5 (IRF5) is a subset-defining factor for M1 macrophages with both activating and repressive transcriptional functions.Monocyte-derived macrophages that are differentiated with granulocyte–macrophage colony stimulating factor (GM-CSF) adopt an M1 (classical) phenotype, which is associated with the production of pro-inflammatory cytokines such as interleukin-12 (IL-12).
  • Autoimmunity: Joint damage without antigen | PDF (139 KB)
    - Nat Rev Immunol 11(2):75 (2011)
    The development of various autoimmune diseases, including rheumatoid arthritis, is thought to be due to a breakdown in CD4+ T cell tolerance for a tissue-specific antigen. However, several lines of evidence have suggested that cognate antigen recognition by CD4+ T cells may not always be necessary.
  • Immune regulation: MicroRNAs keep microglia quiet | PDF (138 KB)
    - Nat Rev Immunol 11(2):76 (2011)
    MicroRNAs regulate gene expression in many biological processes, and now a new study shows that a brain-specific microRNA is a key regulator of microglial cell quiescence in the central nervous system (CNS), thereby helping to prevent CNS inflammation.Microglial cells are CNS-resident macrophages that, under normal conditions, have a resting phenotype that is characterized by low-level expression of CD45 and MHC class II molecules.

  • - Nat Rev Immunol 11(2):76 (2011)
  • Lymphocyte migration: Travel agents for two | PDF (167 KB)
    - Nat Rev Immunol 11(2):77 (2011)
    T helper 2 (TH2) cells are associated with protection from parasites but also drive immunopathological allergic responses. Dissecting the mechanisms that are involved in the migration of TH2 cells from lymph nodes to peripheral tissues has attracted much interest, as selectively inhibiting these pathways could be an effective new therapy for patients with allergies.
  • Haematopoiesis: Baby tolerance | PDF (183 KB)
    - Nat Rev Immunol 11(2):78 (2011)
    The human adaptive immune system starts to form at an early stage of fetal development (as early as gestation week 10), which contrasts with mice, in which the adaptive immune system only starts to develop around birth. Therefore, mechanisms must exist in humans to prevent a fetal immune response to maternal alloantigens.
  • Mucosal immunology | Dendritic cells | Tumour immunology | PDF (119 KB)
    - Nat Rev Immunol 11(2):78 (2011)
    Induction of colonic regulatory T cells by indigenous Clostridium species Atarashi, K.et al. Science23 Dec 2010 (doi: 10.1126/science.1198469)
  • Immunometabolism: an emerging frontier
    - Nat Rev Immunol 11(2):81 (2011)
    Immunometabolism is an emerging field of investigation at the interface between the historically distinct disciplines of immunology and metabolism. Accelerating interest in this area is being fuelled by the obesity epidemic and the relatively recent realization that obesity affects the immune system and promotes inflammation, and that obesity-induced inflammation potentially promotes a variety of chronic conditions and diseases. The multilevel interactions between the metabolic and immune systems suggest pathogenic mechanisms that may underlie many of the downstream complications of obesity and offer substantial therapeutic promise.
  • Adipokines in inflammation and metabolic disease
    - Nat Rev Immunol 11(2):85 (2011)
    The worldwide epidemic of obesity has brought considerable attention to research aimed at understanding the biology of adipocytes (fat cells) and the events occurring in adipose tissue (fat) and in the bodies of obese individuals. Accumulating evidence indicates that obesity causes chronic low-grade inflammation and that this contributes to systemic metabolic dysfunction that is associated with obesity-linked disorders. Adipose tissue functions as a key endocrine organ by releasing multiple bioactive substances, known as adipose-derived secreted factors or adipokines, that have pro-inflammatory or anti-inflammatory activities. Dysregulated production or secretion of these adipokines owing to adipose tissue dysfunction can contribute to the pathogenesis of obesity-linked complications. In this Review, we focus on the role of adipokines in inflammatory responses and discuss their potential as regulators of metabolic function.
  • Metabolism, migration and memory in cytotoxic T cells
    - Nat Rev Immunol 11(2):109 (2011)
    The transcriptional and metabolic programmes that control CD8+ T cells are regulated by a diverse network of serine/threonine kinases. The view has been that the kinases AKT and mammalian target of rapamycin (mTOR) control T cell metabolism. Here, we challenge this paradigm and discuss an alternative role for these kinases in CD8+ T cells, namely to control cell migration. Another emerging concept is that AMP-activated protein kinase (AMPK) family members control T cell metabolism and determine the effector versus memory fate of CD8+ T cells. We speculate that one link between metabolism and immunological memory is provided by kinases that originally evolved to control T cell metabolism and have subsequently acquired the ability to control the expression of key transcription factors that regulate CD8+ T cell effector function and migratory capacity.
  • Phenotypical and functional specialization of FOXP3+ regulatory T cells
    - Nat Rev Immunol 11(2):119 (2011)
    Forkhead box P3 (FOXP3)+ regulatory T (TReg) cells prevent autoimmune disease, maintain immune homeostasis and modulate immune responses during infection. To accomplish these tasks, TReg cell activity is precisely controlled, and this requires TReg cells to alter their migratory, functional and homeostatic properties in response to specific cues in the immune environment. We review progress in understanding the diversity of TReg cells, TReg cell function in different anatomical and inflammatory settings, and the influence of the immune environment on TReg cell activity. We also consider how these factors affect immune-mediated disease in the contexts of infection, autoimmunity, cancer and transplantation.
  • Presumed guilty: natural killer T cell defects and human disease
    - Nat Rev Immunol 11(2):131 (2011)
    Natural killer T (NKT) cells are important regulatory lymphocytes that have been shown in mouse studies, to have a crucial role in promoting immunity to tumours, bacteria and viruses, and in suppressing cell-mediated autoimmunity. Many clinical studies have indicated that NKT cell deficiencies and functional defects might also contribute to similar human diseases, although there is no real consensus about the nature of the NKT cell defects or whether NKT cells could be important for the diagnosis and/or treatment of these conditions. In this Review, we describe the approaches that have been used to analyse the NKT cell populations of various patient groups, suggest new strategies to determine how (or indeed, if) NKT cell defects contribute to human disease, and discuss the prospects for using NKT cells for therapeutic benefit.
  • Recognition of herpesviruses by the innate immune system
    - Nat Rev Immunol 11(2):143 (2011)
    Advances in innate immunity over the past decade have revealed distinct classes of pattern recognition receptors (PRRs) that detect pathogens at the cell surface and in intracellular compartments. This has shed light on how herpesviruses, which are large disease-causing DNA viruses that replicate in the nucleus, are initially recognized during cellular infection. Surprisingly, this involves multiple PRRs both on the cell surface and within endosomes and the cytosol. In this article we describe recent advances in our understanding of innate detection of herpesviruses, how this innate detection translates into anti-herpesvirus host defence, and how the viruses seek to evade this innate detection to establish persistent infections.

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