Thursday, August 25, 2011

Hot off the presses! Sep 01 Nat Rev Immunol

The Sep 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(9):567 (2011)
  • T cell responses: Anger management for TH17 cells
    - Nat Rev Immunol 11(9):568 (2011)
    A key feature of the intestinal immune system is its ability to promote tolerogenic responses to food antigens and commensal organisms. Now, Richard Flavell and colleagues have shown that the small intestine can also 'calm' pro-inflammatory T helper 17 (TH17) cells that are generated in extraintestinal sites.
  • Innate immunity: AT-rich DNA trapped in the cytoplasm
    - Nat Rev Immunol 11(9):569 (2011)
    Pathogen-derived DNA triggers the production of type I interferons (IFNs) and other pro-inflammatory cytokines. DNA sensors identified to date include Toll-like receptor 9 (TLR9) in endosomes, and DNA-dependent activator of IFN-regulatory factors (DAI; also known as ZBP1), RNA polymerase III, absent in melanoma 2 (AIM2) and IFNγ-inducible protein 16 (IFI16) in the cytoplasm.
  • Immunogenetics | Immunotherapy
    - Nat Rev Immunol 11(9):569 (2011)
    Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis The International Multiple Sclerosis Genetics Consortium & The Wellcome Trust Case Control Consortium 2. Nature 476, 214–219 (2011)
  • Innate immunity: MAVS build-ups for defence
    - Nat Rev Immunol 11(9):570 (2011)
    RIG-I-like receptors (RLRs) bind viral RNA and initiate the antiviral immune response through their interaction with mitochondrial antiviral signalling protein (MAVS; also known as CARDIF, VISA and IPS1). MAVS is localized on the mitochondrial membrane and activates kinases that are upstream of nuclear factor-κB and interferon-regulatory factor 3 (IRF3) by an unknown mechanism.
  • Immune regulation: Worming away from TB immunity
    - Nat Rev Immunol 11(9):570 (2011)
    The majority of helminth infections worldwide are concentrated in developing nations, where other diseases such as tuberculosis are endemic. It is known that a pre-existing helminth infection can impinge on immunity to Mycobacterium tuberculosis infection, but the underlying mechanism has yet to be described.
  • MHC molecules: Cod's wallop? It's first class!
    - Nat Rev Immunol 11(9):570 (2011)
    It is always fascinating to consider the distinct immune systems that have evolved in the natural world. A recent study in Nature has shown that, unlike other jawed vertebrates, the Atlantic cod does not encode MHC class II molecules.
  • Dendritic cells | HIV | Antibodies
    - Nat Rev Immunol 11(9):571 (2011)
    Flt3L controls the development of radiosensitive dendritic cells in the meninges and choroid plexus of the steady-state mouse brain Anandasabapathy, N.et al. J. Exp. Med. 208, 1695–1705 (2011)
  • T cells: mTOR lullabies for naive T cells
    - Nat Rev Immunol 11(9):572 (2011)
    Naive T cells are maintained in a quiescent state, which ensures their survival and preserves immune homeostasis. Writing in Nature Immunology, Yang et al.
  • Regulatory T cells: Pursuing a germinal centre career
    - Nat Rev Immunol 11(9):572 (2011)
    Antigen-primed B cells form germinal centres, where, helped by follicular helper T (TFH) cells, they develop into high-affinity plasma and memory B cells. This process is under stringent control to avoid uncontrolled B cell proliferation and production of autoantibodies.
  • Immune regulation: (micro)Control of IFNγ
    - Nat Rev Immunol 11(9):573 (2011)
    Although microRNAs are known to have roles in regulating immune responses, our understanding of the exact functions of individual microRNAs in the immune system is still in its infancy. Two papers, published in Immunity and Nature Immunology, now show that the microRNA miR-29 suppresses interferon-γ (IFNγ) production, although different mechanisms of action were reported.
  • Inflammation: A gutsy repair job
    - Nat Rev Immunol 11(9):574 (2011)
    Thymic stromal lymphopoietin (TSLP) has multiple effects on T cell responses, including promoting T helper 2 (TH2) cell responses and inducing regulatory T cells. It is produced by intestinal epithelial cells (IECs) in response to bacterial stimulation and has been suggested to have a role in regulating the colonic inflammation induced by dextran sulphate sodium (DSS-induced colitis); mice deficient for the TSLP receptor (Crlf2−/− mice) had increased production of TH1-type cytokines in the gut, and this increased the severity of DSS-induced colitis.
  • Flu 'super-antibody'
    - Nat Rev Immunol 11(9):574 (2011)
    A universal influenza vaccine has been something of a holy grail for vaccinologists, but the recent isolation of a neutralizing antibody that recognizes a conserved portion of the haemagglutinin glycoprotein of all 16 subtypes and neutralizes both group 1 and group 2 influenza A viruses (Science, 28 Jul 2011) has taken us a step closer to this possibility.
  • Human dendritic cell deficiency: the missing ID?
    - Nat Rev Immunol 11(9):575 (2011)
    Animal models and human in vitro systems indicate that dendritic cells (DCs) have a crucial role in priming naive T cells, but just how important are they in the intact human? Recent descriptions of human DC deficiency have begun to shed light on this question and to illuminate other puzzles of human DC biology, including their haematopoietic origin, developmental regulation and homeostatic equilibrium with other leukocytes. In this Review, we explore the recently described DC deficiency syndromes, discussing what these have taught us with regard to DC function in humans and the important issues that remain unsolved.
  • Modulation of the immune system by UV radiation: more than just the effects of vitamin D?
    - Nat Rev Immunol 11(9):584 (2011)
    Humans obtain most of their vitamin D through the exposure of skin to sunlight. The immunoregulatory properties of vitamin D have been demonstrated in studies showing that vitamin D deficiency is associated with poor immune function and increased disease susceptibility. The benefits of moderate ultraviolet (UV) radiation exposure and the positive latitude gradients observed for some immune-mediated diseases may therefore reflect the activities of UV-induced vitamin D. Alternatively, other mediators that are induced by UV radiation may be more important for UV-mediated immunomodulation. Here, we compare and contrast the effects of UV radiation and vitamin D on immune function in immunopathological diseases, such as psoriasis, multiple sclerosis and asthma, and during infection.
  • Homeostatic chemokine receptors and organ-specific metastasis
    - Nat Rev Immunol 11(9):597 (2011)
    It has been 10 years since the role of a chemokine receptor, CXCR4, in breast cancer metastasis was first documented. Since then, the field of chemokines and cancer has grown significantly, so it is timely to review the progress, analyse the studies to date and identify future challenges facing this field. Metastasis is the major factor that limits survival in most patients with cancer. Therefore, understanding the molecular mechanisms that control the metastatic behaviour of tumour cells is pivotal for treating cancer successfully. Substantial experimental and clinical evidence supports the conclusion that molecular mechanisms control organ-specific metastasis. One of the most important mechanisms operating in metastasis involves homeostatic chemokines and their receptors. Here, we review this field and propose a model of 'cellular highways' to explain the effects of homeostatic chemokines on cancer cells and how they influence metastasis.
  • The anti-inflammatory effects of exercise: mechanisms and implications for the prevention and treatment of disease
    - Nat Rev Immunol 11(9):607 (2011)
    Regular exercise reduces the risk of chronic metabolic and cardiorespiratory diseases, in part because exercise exerts anti-inflammatory effects. However, these effects are also likely to be responsible for the suppressed immunity that makes elite athletes more susceptible to infections. The anti-inflammatory effects of regular exercise may be mediated via both a reduction in visceral fat mass (with a subsequent decreased release of adipokines) and the induction of an anti-inflammatory environment with each bout of exercise. In this Review, we focus on the known mechanisms by which exercise — both acute and chronic — exerts its anti-inflammatory effects, and we discuss the implications of these effects for the prevention and treatment of disease.
  • Antiviral TRIMs: friend or foe in autoimmune and autoinflammatory disease?
    - Nat Rev Immunol 11(9):617 (2011)
    The concept that viral sensing systems, via their ability to drive pro-inflammatory cytokine and interferon production, contribute to the development of autoimmune and autoinflammatory disease is supported by a wide range of clinical and experimental observations. Recently, the tripartite motif-containing proteins (TRIMs) have emerged as having key roles in antiviral immunity — either as viral restriction factors or as regulators of pathways downstream of viral RNA and DNA sensors, and the inflammasome. Given their involvement in these pathways, we propose that TRIM proteins contribute to the development and pathology of autoimmune and autoinflammatory conditions, thus making them potential novel targets for therapeutic manipulation.
  • Reciprocal regulation of the neural and innate immune systems
    - Nat Rev Immunol 11(9):625 (2011)
    Innate immune responses are regulated by microorganisms and cell death, as well as by a third class of stress signal from the nervous and endocrine systems. The innate immune system also feeds back, through the production of cytokines, to regulate the function of the central nervous system (CNS), and this has effects on behaviour. These signals provide an extrinsic regulatory circuit that links physiological, social and environmental conditions, as perceived by the CNS, with transcriptional 'decision-making' in leukocytes. CNS-mediated regulation of innate immune responses optimizes total organism fitness and provides new opportunities for therapeutic control of chronic infectious, inflammatory and neuropsychiatric diseases.

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