Latest Articles Include:
- From the editors
- Nat Rev Immunol 9(10):669 (2009)
- T cells: Innate source of IL-17
- Nat Rev Immunol 9(10):671 (2009)
- Innate immunity: A protective fungal spore coat
- Nat Rev Immunol 9(10):672 (2009)
- Tumour immunology: Neutrophil plasticity
- Nat Rev Immunol 9(10):672 (2009)
- Common ills linked to memory loss
- Nat Rev Immunol 9(10):672 (2009)
- In brief: Inflammation, Natural killer cells, Immune regulation
- Nat Rev Immunol 9(10):673 (2009)
- Regulatory T cells: Eos: the sound of silence
- Nat Rev Immunol 9(10):674 (2009)
- Natural killer cells: Peace not war
- Nat Rev Immunol 9(10):674 (2009)
- Innate immunity: Help from 'friendly' bacteria
- Nat Rev Immunol 9(10):675 (2009)
- Dendritic cells: One SIGN, different paths
- Nat Rev Immunol 9(10):676 (2009)
- One jab protects from swine flu
- Nat Rev Immunol 9(10):676 (2009)
- Immune responses: Seeing is believing
- Nat Rev Immunol 9(10):677 (2009)
- Tolerance: SIRT1 keeps escapees quiet
- Nat Rev Immunol 9(10):677 (2009)
- Skin immune sentinels in health and disease
- Nat Rev Immunol 9(10):679-691 (2009)
Human skin and its immune cells provide essential protection of the human body from injury and infection. Recent studies reinforce the importance of keratinocytes as sensors of danger through alert systems such as the inflammasome. In addition, newly identified CD103+ dendritic cells are strategically positioned for cross-presentation of skin-tropic pathogens and accumulating data highlight a key role of tissue-resident rather than circulating T cells in skin homeostasis and pathology. This Review focuses on recent progress in dissecting the functional role of skin immune cells in skin disease. - Transcriptional control of the inflammatory response
- Nat Rev Immunol 9(10):692-703 (2009)
Inflammation is a multicomponent response to tissue stress, injury and infection, and a crucial point of its control is at the level of gene transcription. The inducible inflammatory gene expression programme — such as that triggered by Toll-like receptor signalling in macrophages — is comprised of several coordinately regulated sets of genes that encode key functional programmes; these are controlled by three classes of transcription factors, as well as various transcriptional co-regulators and chromatin modifications. Here, we discuss the mechanisms of and the emerging principles in the transcriptional regulation of inflammatory responses in diverse physiological settings. - Engineering lymphocyte subsets: tools, trials and tribulations
- Nat Rev Immunol 9(10):704-716 (2009)
Cell-based therapies with various lymphocyte subsets hold promise for the treatment of several diseases, including cancer and disease resulting from inflammation and infection. The ability to genetically engineer lymphocyte subsets has the potential to improve the natural immune response and correct impaired immunity. In this Review we focus on the lymphocyte subsets that have been modified genetically or by other means for therapeutic benefit, on the technologies used to engineer lymphocytes and on the latest progress and hurdles in translating these technologies to the clinic. - Monkeying around with HIV vaccines: using rhesus macaques to define 'gatekeepers' for clinical trials
- Nat Rev Immunol 9(10):717-728 (2009)
Rhesus macaques are an important animal model for the study of human disease and the development of vaccines against HIV and AIDS. HIV vaccines have been benchmarked in rhesus macaque preclinical challenge studies using chimeric viruses made up of parts of HIV and simian immunodeficency viruses. However, the lack of efficacy in a recent clinical trial calls for a re-evaluation of the scientific assumptions regarding the predictive value of using data generated from rhesus macaques as a 'gatekeeper' for the advancement of candidate vaccines into the clinic. In this context, there is significant consensus among HIV vaccinologists that next-generation HIV vaccines must generate 'better' immunity in rhesus macaques than clinically unsuccessful vaccines generated using validated assays. Defining better immunity is the core challenge of HIV vaccine development in this system and is the focus of this Review. - Complement regulators and inhibitory proteins
- Nat Rev Immunol 9(10):729-740 (2009)
The complement system is important for cellular integrity and tissue homeostasis. Complement activation mediates the removal of microorganisms and the clearance of modified self cells, such as apoptotic cells. Complement regulators control the spontaneously activated complement cascade and any disturbances in this delicate balance can result in damage to tissues and in autoimmune disease. Therefore, insights into the mechanisms of complement regulation are crucial for understanding disease pathology and for enabling the development of diagnostic tools and therapies for complement-associated diseases. - Learning immunology from the yellow fever vaccine: innate immunity to systems vaccinology
- Nat Rev Immunol 9(10):741-747 (2009)
Despite their great success, we understand little about how effective vaccines stimulate protective immune responses. Two recent developments promise to yield such understanding: the appreciation of the crucial role of the innate immune system in sensing microorganisms and tuning immune responses, and advances in systems biology. Here I review how these developments are yielding insights into the mechanism of action of the yellow fever vaccine, one of the most successful vaccines ever developed, and the broader implications for vaccinology. - Corrigendum: Structure and signalling in the IL-17 receptor family
- Nat Rev Immunol 9(10):747 (2009)
; published online 3 July 2009; corrected after print 7 August 2009 In the version of this article initially published, reference 22 was incorrectly stated to be the first report to directly compare Il17a-/- and Il17f-/- mice and to show that these cytokines have markedly different functions in vivo. In fact, this was first reported by reference 19: Yang, X. O. et al. Regulation of inflammatory responses by IL-17F. J. Exp. Med.205, 1063–1075 (2008)
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