Wednesday, June 24, 2009

Hot off the presses! Jul 01 Nat Rev Immunol

The Jul 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:

  • From the editors
    - Nat Rev Immunol 9(7):457 (2009)
  • T cell memory: Keeping energy levels up
    - Nat Rev Immunol 9(7):458 (2009)
  • HIV: Selective pressure
    - Nat Rev Immunol 9(7):459 (2009)
  • In brief: Autoimmunity, NKT cells, T cell responses
    - Nat Rev Immunol 9(7):459 (2009)
  • T cell memory: Live long with WNT
    - Nat Rev Immunol 9(7):460 (2009)
  • Immunization in the spotlight
    - Nat Rev Immunol 9(7):460 (2009)
  • T cell differentiation: Inhibiting TH17 cells
    - Nat Rev Immunol 9(7):460 (2009)
  • In brief: Inflammation, Antigen presentation
    - Nat Rev Immunol 9(7):461 (2009)
  • Antigen presentation: Basophils do it too
    - Nat Rev Immunol 9(7):462 (2009)
  • T cell responses: A new starting point
    - Nat Rev Immunol 9(7):462 (2009)
  • Antiviral immunity: TRIMming the response
    - Nat Rev Immunol 9(7):463 (2009)
  • Evolution: A common solution to an age-old problem
    - Nat Rev Immunol 9(7):464 (2009)
  • Signalling through C-type lectin receptors: shaping immune responses
    - Nat Rev Immunol 9(7):465-479 (2009)
    C-type lectin receptors (CLRs) expressed by dendritic cells are crucial for tailoring immune responses to pathogens. Following pathogen binding, CLRs trigger distinct signalling pathways that induce the expression of specific cytokines which determine T cell polarization fates. Some CLRs can induce signalling pathways that directly activate nuclear factor-B, whereas other CLRs affect signalling by Toll-like receptors. Dissecting these signalling pathways and their effects on host immune cells is essential to understand the molecular mechanisms involved in the induction of adaptive immune responses. In this Review we describe the role of CLR signalling in regulating adaptive immunity and immunopathogenesis and discuss how this knowledge can be harnessed for the development of innovative vaccination approaches.
  • New insights into the regulation of T cells by c family cytokines
    - Nat Rev Immunol 9(7):480-490 (2009)
    Common cytokine receptor -chain (c) family cytokines have crucial roles in the development, proliferation, survival and differentiation of multiple cell lineages of both the innate and adaptive immune systems. In this Review, we focus on our current understanding of the distinct and overlapping effects of interleukin-2 (IL-2), IL-7, IL-9, IL-15 and IL-21, as well as the IL-7-related cytokine thymic stromal lymphopoietin (TSLP), on the survival and proliferation of conventional T cells, T cells and regulatory T cells. This knowledge potentially allows for the therapeutic manipulation of immune responses for the treatment of cancer, autoimmunity, allergic diseases and immunodeficiency, as well as for vaccine development.
  • Cracking the BAFF code
    - Nat Rev Immunol 9(7):491-502 (2009)
    The tumour necrosis factor (TNF) family members B cell activating factor (BAFF) and APRIL (a proliferation-inducing ligand) are crucial survival factors for peripheral B cells. An excess of BAFF leads to the development of autoimmune disorders in animal models, and high levels of BAFF have been detected in the serum of patients with various autoimmune conditions. In this Review, we consider the possibility that in mice autoimmunity induced by BAFF is linked to T cell-independent B cell activation rather than to a severe breakdown of B cell tolerance. We also outline the mechanisms of BAFF signalling, the impact of ligand oligomerization on receptor activation and the progress of BAFF-depleting agents in the clinical setting.
  • MHC class I antigen presentation: learning from viral evasion strategies
    - Nat Rev Immunol 9(7):503-513 (2009)
    The cell surface display of peptides by MHC class I molecules to lymphocytes provides the host with an important surveillance mechanism to protect against invading pathogens. However, in turn, viruses have evolved elegant strategies to inhibit various stages of the MHC class I antigen presentation pathway and prevent the display of viral peptides. This Review highlights how the elucidation of mechanisms of viral immune evasion is important for advancing our understanding of virus–host interactions and can further our knowledge of the MHC class I presentation pathway as well as other cellular pathways.
  • CD95, BIM and T cell homeostasis
    - Nat Rev Immunol 9(7):514-519 (2009)
    The relative importance of the intrinsic and extrinsic apoptotic pathways in the control of haematopoietic cell homeostasis has been a matter of debate for many years. Cell death is omnipresent in this cellular compartment and ensures the removal of cells that are not properly equipped to assume their function as well as those that have assumed function but are no longer required. In this Review we focus on the roles of CD95 (also known as FAS) and BCL-2-interacting mediator of cell death (BIM), two major regulators of apoptosis in T cell homeostasis, with a particular emphasis on their cooperation in the shutdown of T cell responses.
  • Towards the identification of biomarkers of transplantation tolerance
    - Nat Rev Immunol 9(7):521-526 (2009)
    Although transplantation has been a standard medical practice for decades, the marked morbidity from the use of immunosuppressive drugs and poor long-term graft survival remain important limitations in the field. Achieving tolerance to transplanted organs should solve both problems, but has been an elusive goal. Recent advances in the human immunological toolbox have rekindled interest in studying the small number of transplant recipients who become tolerant to their grafts over time. The development of biomarkers of transplantation tolerance holds promise to improve the care of organ allograft recipients, to provide surrogate end points of tolerance induction strategies and to advance our understanding of the human immune response to both self and foreign antigens.

No comments: