Thursday, October 21, 2010

Hot off the presses! Oct 01 Nat Rev Immunol

The Oct 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 10(10):675 (2010)
  • Asthma and allergy: Complementing the IL-17 axis in asthma | PDF (202 KB)
    - Nat Rev Immunol 10(10):676 (2010)
    Although asthma is most commonly associated with an aberrant T helper 2 (TH2) cell response, severe disease is not associated with the exclusive production of TH2 cell-associated cytokines but is instead characterized by additional increased production of the pro-inflammatory cytokine interleukin-17A (IL-17A). However, studies of the role of IL-17A in mouse models of asthma have generated variable results and the exact role of this cytokine and the mechanisms that underlie its production remain poorly understood.
  • Infectious disease: The tuberculosis signature | PDF (208 KB)
    - Nat Rev Immunol 10(10):677 (2010)
    Anne O'Garra and colleagues, reporting in Nature, describe a gene expression signature that identifies individuals with active tuberculosis disease and may also indicate those individuals who are latently infected with Mycobacterium tuberculosis and go on to develop active disease. The tuberculosis signature was shown to be dominated by interferon (IFN)-induced genes.
  • T cells | T cell signalling | PDF (149 KB)
    - Nat Rev Immunol 10(10):677 (2010)
    The junctional adhesion molecule JAML is a costimulatory receptor for epithelial γδ T cell activation Witherden, D. A.et al. Science 329, 1205–1210 (2010)
  • Autoimmunity: Get me to the joint on time | PDF (200 KB)
    - Nat Rev Immunol 10(10):678 (2010)
    How leukocytes are recruited to joints to initiate and propagate autoantibody-induced arthritis is a complex and incompletely understood process. Previous studies have shown that the lipid chemoattractant leukotriene B4 (LTB4) and its receptor BLT1 are required for neutrophil recruitment in this disease.
  • Dendritic cells: An inner eye for HIV | PDF (270 KB)
    - Nat Rev Immunol 10(10):678 (2010)
    Dendritic cells (DCs) initiate protective immune responses following infection and 'see' dangerous microorganisms using receptors that recognize conserved microbial structures. However, DCs do not normally perceive HIV-1 as a danger but instead facilitate the infection of CD4+ T cells in a process that is known as trans-enhancement.
  • Catch of the day | PDF (125 KB)
    - Nat Rev Immunol 10(10):678 (2010)
    Fish oils have been hailed as a health 'wonder' food and have many reputed health benefits, including an ability to alleviate chronic inflammation. Now, scientists have identified a molecular pathway through which the omega-3 fatty acids, which are found in oily fish, exert anti-inflammatory effects (Cell, 3 Sep 2010).
  • Immune regulation: Innate T cells break the brakes | PDF (214 KB)
    - Nat Rev Immunol 10(10):679 (2010)
    Interleukin-23 (IL-23) has been associated with several autoimmune and chronic inflammatory conditions and many of the pathogenic effects of this cytokine have been attributed to its role in expanding T helper 17 (TH17) cell populations. A recent study in Immunity now describes another way in which this cytokine can promote inflammation, showing that IL-23-activated γδ T cells inhibit the functions of regulatory T (TReg) cells.
  • Tumour immunology: Tumour antigens cross the gap | PDF (151 KB)
    - Nat Rev Immunol 10(10):680 (2010)
    One of the obstacles in raising an effective immune response to tumours stems from the fact that dendritic cells (DCs) have distinct proteasomes from tumour cells and therefore process proteins into distinct peptide fragments for presentation to T cells. A new study by Rescigno and colleagues shows that bacteria induce the formation of gap junctions between tumour cells and DCs that allow the transfer of pre-processed tumour cell antigens to DCs for cross-presentation to CD8+ T cells.
  • Regulatory T cells: CD8+ TReg cells join the fold | PDF (635 KB)
    - Nat Rev Immunol 10(10):680 (2010)
    Most research to date on regulatory T (TReg) cells has focused on the CD4+FOXP3+ TReg cell population. Although a subset of CD8+ T cells has been shown to suppress CD4+ T cells, little is known about the exact function of CD8+ TReg cells.
  • Antigen presentation: Damage limitation: new role for immunoproteasomes | PDF (153 KB)
    - Nat Rev Immunol 10(10):681 (2010)
    New research published in Cell indicates that, in addition to promoting an adaptive immune response through increased antigen presentation, the main function of the immunoproteasome might be to protect cells from the damaging side effects of an innate inflammatory response.Cellular protein homeostasis is maintained in eukaryotic cells by the degradation of short-lived or defective proteins that are targeted to the 26S proteasome by polyubiquitylation.
  • Mucosal immunology: β-catenin calms the gut | PDF (186 KB)
    - Nat Rev Immunol 10(10):682 (2010)
    There are many gaps in our knowledge of how intestinal homeostasis and immune tolerance to the commensal microflora are maintained, but a study published in Science has provided another piece of the puzzle. Pulendran and colleagues show that β-catenin signalling promotes the induction of regulatory T (TReg) cells while suppressing T helper 1 (TH1) and TH17 cells in the gut by maintaining intestinal dendritic cells (DCs) in a tolerogenic state.
  • Allergy | T cell responses | PDF (153 KB)
    - Nat Rev Immunol 10(10):682 (2010)
    Basophils orchestrate chronic allergic dermatitis and protective immunity against helminths Ohnmacht, C.et al. Immunity1 Sep 2010 (doi:10.1016/j.immuni.2010.08.011)
  • Cellular sources and immune functions of interleukin-9
    - Nat Rev Immunol 10(10):683 (2010)
    Interleukin-9 (IL-9) has attracted renewed interest owing to the identification of its expression by multiple T helper (TH) cell subsets, including TH2 cells, TH9 cells, TH17 cells and regulatory T (TReg) cells. Here, we provide a broad overview of the conditions that are required for cells to produce IL-9 and describe the cellular targets and nature of the immune responses that are induced by IL-9.
  • Central roles of NLRs and inflammasomes in viral infection
    - Nat Rev Immunol 10(10):688 (2010)
    The immune response to viral infections is determined by a complex interplay between the pathogen and the host. Innate immune cells express a set of cytosolic sensors to detect viral infection. Recognition by these sensors induces the production of type I interferons and the assembly of inflammasome complexes that activate caspase-1, leading to production of interleukin-1β (IL-1β) and IL-18. Here, I discuss recent progress in our understanding of the central roles of NOD-like receptors (NLRs) and inflammasomes in the immune response during viral infections. This information will improve our understanding of host defence mechanisms against viruses and provide new avenues for interfering in the pathogenesis of infectious diseases.
  • Antiviral immune responses in the genital tract: clues for vaccines
    - Nat Rev Immunol 10(10):699 (2010)
    Mucosal surfaces are exploited as a portal of entry into hosts by a wide variety of microorganisms. Over the past decade, an advanced understanding of the immune system of the gastrointestinal and the respiratory mucosae has been gained. However, despite the fact that many viruses are transmitted sexually through the genital tract, the immune system of the male and female genital mucosae has received much less attention. Here, I describe and highlight differences in the innate and adaptive immune systems of the genital and intestinal mucosae, and discuss some of the challenges we face in the development of successful vaccines against sexually transmitted viral pathogens.
  • The impact of the extracellular matrix on inflammation
    - Nat Rev Immunol 10(10):712 (2010)
    The advent of in situ immunology and intravital analyses of leukocyte movement in tissues has drawn attention to the previously neglected extracellular matrix (ECM) and its role in modulating immune cell behaviour in inflamed tissues. The ECM exists in different biochemical and structural forms; both their individual components and three-dimensional ultrastructure impart specific signals to cells that modulate basic functions that are important for the early steps in inflammation, such as immune cell migration into inflamed tissues and immune cell differentiation. In chronically inflamed tissues, aberrant ECM expression and fragments of the ECM that are derived from tissue-remodelling processes can influence immune cell activation and survival, thereby actively contributing to immune responses at these sites.
  • Current perspectives of natural killer cell education by MHC class I molecules
    - Nat Rev Immunol 10(10):724 (2010)
    From the early days of natural killer (NK) cell research, it was clear that MHC genes controlled the specificity of mouse NK cell-dependent responses, such as the ability to reject transplanted allogeneic bone marrow and to kill tumour cells. Although several mechanisms that are involved in this 'education' process have been clarified, most of the mechanisms have still to be identified. Here, we review the current understanding of the processes that are involved in NK cell education, including how the host MHC class I molecules regulate responsiveness and receptor repertoire formation in NK cells and the signalling pathways that are involved.
  • The immune system and the gut microbiota: friends or foes?
    - Nat Rev Immunol 10(10):735 (2010)
    The mammalian intestine is home to a complex community of trillions of bacteria that are engaged in a dynamic interaction with the host immune system. Determining the principles that govern host–microbiota relationships is the focus of intense research. Here, we describe how the intestinal microbiota is able to influence the balance between pro-inflammatory and regulatory responses and shape the host's immune system. We suggest that improving our understanding of the intestinal microbiota has therapeutic implications, not only for intestinal immunopathologies but also for systemic immune diseases.

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