Friday, February 25, 2011

Hot off the presses! Mar 01 Nat Rev Immunol

The Mar 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(3):155 (2011)
  • Mucosal immunology: Acid attack | PDF (119 KB)
    - Nat Rev Immunol 11(3):156 (2011)
    Immune responses in the intestine must be tightly controlled to prevent harmful attacks against commensal organisms, food proteins and self antigens. Previous studies have shown that dendritic cells (DCs) contribute to immune homeostasis in the intestine by constitutively generating high levels of retinoic acid, which, together with transforming growth factor-β (TGFβ), promotes the development of regulatory T (TReg) cells.
  • Tumour immunology: Early exposure is inflammatory | PDF (154 KB)
    - Nat Rev Immunol 11(3):157 (2011)
    Sunburn during childhood has been associated with an increased risk of melanoma development, and in a recent Nature paper, M. Raza Zaidi, Glenn Merlino and colleagues have shown that changes in the immune response in the skin of young mice after exposure to ultraviolet B (UVB) light could help to promote melanoma development and progression.
  • Regulatory T cells | T cells | Innate immunity | PDF (121 KB)
    - Nat Rev Immunol 11(3):157 (2011)
    Killer cell Ig-like receptor (KIR) 3DL1 down-regulation enhances inhibition of type 1 diabetes by autoantigen-specific regulatory T cells Qin, H.et al. Proc. Natl Acad. Sci. USA 108, 2016–2021 (2011)
  • Macrophages: Iron macrophages | PDF (132 KB)
    - Nat Rev Immunol 11(3):158 (2011)
    Macrophages contribute to wound healing through the processes of inflammation, matrix deposition and tissue remodelling. However, local accumulation of activated macrophages and macrophage-derived pro-inflammatory factors can also lead to chronic inflammation, which impairs tissue repair.
  • Immune responses: IL-7 goes antiviral | PDF (152 KB)
    - Nat Rev Immunol 11(3):158 (2011)
    It is well appreciated that interleukin-7 (IL-7) has essential roles in lymphocyte development and homeostasis. A new study in Cell shows that IL-7 also has potent pro-immune functions during viral infection.
  • Keeping HIV out | PDF (94 KB)
    - Nat Rev Immunol 11(3):158 (2011)
    HIV infection paralyses the host's immune system, resulting in a fatal susceptibility to infections. According to a recent study, it is not only HIV-positive individuals who are unprotected against infections.
  • Evolution | B cells | Regulatory T cells | PDF (116 KB)
    - Nat Rev Immunol 11(3):159 (2011)
    A thymus candidate in lampreys Bajoghli, B.et al. Nature 470, 90–94 (2011) The adaptive immune system of lampreys consists of lymphocyte-like cells that express somatically diversified antigen receptors, termed variable lymphocyte receptors (VLRs).
  • T cells: Plastic TH17 cells | PDF (154 KB)
    - Nat Rev Immunol 11(3):160 (2011)
    Interleukin-17 (IL-17)-producing T helper cells (TH17 cells) are a unique subset of effector CD4+ T cells. However, TH17 cells that are generated in vitro have remarkable plasticity and can produce the TH1 cell-associated cytokine interferon-γ (IFNγ) and/or may lose the ability to produce IL-17.
  • B cells: Short- and long-term memory | PDF (241 KB)
    - Nat Rev Immunol 11(3):160 (2011)
    In a recent study in Science, Marc Jenkins and colleagues identify two populations of memory B cells that differ in terms of frequency, lifespan and activation potential.In a classical primary immune response, naive IgM+ B cells specific for the target antigen enter a germinal centre, where they undergo affinity maturation and immunoglobulin class switching.
  • Vaccines: Early and late protection from TB | PDF (196 KB)
    - Nat Rev Immunol 11(3):161 (2011)
    The one approved vaccine against tuberculosis (known as the Mycobacterium bovis bacillus Calmette–Guérin (BCG) vaccine) and those currently in clinical trials are designed to protect against initial infection, as they incorporate Mycobacterium tuberculosis antigens that are expressed early in the disease process. However, they do not prevent the establishment of latent persistent infection or the reactivation of clinical disease — a major need both for infected patients and for reducing further transmission.
  • Inflammation: ROSy outlook for TRAPS patients | PDF (195 KB)
    - Nat Rev Immunol 11(3):162 (2011)
    A paper published in the Journal of Experimental Medicine has furthered our growing understanding of the role of mitochondria, and the reactive oxygen species (ROS) that they produce, in inflammation. This study shows that mitochondrial ROS enhance pro-inflammatory cytokine production through the regulation of the mitogen-activated protein kinase (MAPK) pathway.
  • Inflammation: An innate signal for CNS disease | PDF (190 KB)
    - Nat Rev Immunol 11(3):162 (2011)
    Multiple sclerosis and the animal model experimental autoimmune encephalomyelitis (EAE) are thought to develop in genetically predisposed individuals after an environmental trigger activates myelin-specific T cells in the central nervous system (CNS). A recent study published in Immunity suggests that peptidoglycan (PGN), a component of bacterial cell walls, activates antigen-presenting cells (APCs) in the CNS to provide this trigger.
  • MicroRNAs: the fine-tuners of Toll-like receptor signalling
    - Nat Rev Immunol 11(3):163 (2011)
    Toll-like receptor (TLR) signalling must be tightly regulated to avoid excessive inflammation and to allow for tissue repair and the return to homeostasis after infection and tissue injury. MicroRNAs (miRNAs) have emerged as important controllers of TLR signalling. Several miRNAs are induced by TLR activation in innate immune cells and these and other miRNAs target the 3′ untranslated regions of mRNAs encoding components of the TLR signalling system. miRNAs are also proving to be an important link between the innate and adaptive immune systems, and their dysregulation might have a role in the pathogenesis of inflammatory diseases.
  • DCs and NK cells: critical effectors in the immune response to HIV-1
    - Nat Rev Immunol 11(3):176 (2011)
    Dendritic cells (DCs) and natural killer (NK) cells have central roles in antiviral immunity by shaping the quality of the adaptive immune response to viruses and by mediating direct antiviral activity. HIV-1 infection is characterized by a severe dysregulation of the antiviral immune response that starts during early infection. This Review describes recent insights into how HIV-1 infection affects DC and NK cell function, and the roles of these innate immune cells in HIV-1 pathogenesis. The importance of understanding DC and NK cell crosstalk during HIV infection for the development of effective antiviral strategies is also discussed.
  • Microbial manipulation of receptor crosstalk in innate immunity
    - Nat Rev Immunol 11(3):187 (2011)
    In the arms race of host–microbe co-evolution, successful microbial pathogens have evolved ingenious ways to evade host immune responses. In this Review, we focus on 'crosstalk manipulation' — the microbial strategies that instigate, subvert or disrupt the molecular signalling crosstalk between receptors of the innate immune system. This proactive interference undermines host defences and contributes to microbial adaptive fitness and persistent infections. Understanding how pathogens exploit host receptor crosstalk mechanisms and infiltrate the host signalling network is essential for developing interventions to redirect the host response and achieve protective immunity.
  • Immune cell regulation by autocrine purinergic signalling
    - Nat Rev Immunol 11(3):201 (2011)
    Stimulation of almost all mammalian cell types leads to the release of cellular ATP and autocrine feedback through a diverse array of purinergic receptors. Depending on the types of purinergic receptors that are involved, autocrine signalling can promote or inhibit cell activation and fine-tune functional responses. Recent work has shown that autocrine signalling is an important checkpoint in immune cell activation and allows immune cells to adjust their functional responses based on the extracellular cues provided by their environment. This Review focuses on the roles of autocrine purinergic signalling in the regulation of both innate and adaptive immune responses and discusses the potential of targeting purinergic receptors for treating immune-mediated disease.
  • Emerging inflammasome effector mechanisms
    - Nat Rev Immunol 11(3):213 (2011)
    Caspase 1 activation by inflammasome complexes in response to pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) induces the maturation and secretion of the pro-inflammatory cytokines interleukin-1β (IL-1β) and IL-18. Recent reports have begun to identify additional inflammasome effector mechanisms that proceed independently of IL-1β and IL-18. These include the induction of pyroptotic cell death, the restriction of bacterial replication, the activation of lipid metabolic pathways for cell repair and the secretion of DAMPs and leaderless cytokines. These non-canonical functions of caspase 1 illustrate the diverse mechanisms by which inflammasomes might contribute to innate immunity, repair responses and host defence.
  • Tissue-based class control: the other side of tolerance
    - Nat Rev Immunol 11(3):221 (2011)
    In this Essay, we offer a new perspective on how immune responses are regulated. We do not cover how they are turned on and off, but focus instead on the second major aspect of an immune response: the control of effector class. Although it is generally thought that the class of an immune response is tailored to fit the invading pathogen, we suggest here that it is primarily tailored to fit the tissue in which the response occurs. To this end, we cover such topics as the nature of T helper (TH) cell subsets (current and yet to be discovered), the nature of privileged sites, the difference between oral tolerance and oral vaccination, why the route of immunization matters, whether the TH1-type response is really the immune system's primary defense, and whether there might be a different role for some regulatory T cells.

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