Regulation Of The Innate And Adaptive Immune Response Against Pathogens And Their Products View Homepage


Ontology type: schema:MonetaryGrant     


Grant Info

YEARS

2001-2015

FUNDING AMOUNT

14320245 GBP

ABSTRACT

White blood cells or leucocytes originating in the bone marrow when functionally mature are found in blood and lymphoid tissue and respond to infectious organisms by producing various effector molecules important for the eradication of the pathogen. Amongst these cells, dendritic cells are key initiators of such immune responses and play a key role in activating leucocytes, known as CD4+ T helper cells and CD8+ T killer cells, which produce substances key to protect the host from pathogens such as viruses, bacteria and parasites. In addition, the CD4+ T helper cells produce patterns of molecules called cytokines which play an important role in regulating other white blood cells involved in eradication of infectious organisms, but these need to be regulated so as to inflict minimum damage to the host. This is important since these cytokines can also activate cells which give rise to pathology, such as autoimmunity or allergy. Our research involves the study at a molecular level of how dendritic cells and T helper cells can be activated to elicit the right kind of immune response, and how this immune response is regulated in infection (e.g. tuberculosis and influenza) to eradicate infectious organisms with minimum damage to the individual. Technical Summary The type of immune response and effector cytokines elicited to pathogens can determine the outcome of infection. A major lab research focus is the regulation and function of cytokines in immune responses, defining molecular mechanisms of induction of the immunosuppressive cytokine IL-10 versus that of proinflammatory cytokines in immune cells. Although a major function of IL-10 is to regulate inflammation and damage to the host, a penalty is that IL-10 can also contribute to chronic infection. Recently my lab research has been expanded to study of the immune response in tuberculosis (TB), still a major global cause of morbidity and mortality. We have shown that IL-10 can contribute to chronic infection with Mycobacterium tuberculosis (MTb) by diminishing protective T helper (Th)1 responses and the production of IFN-? in the lung. The immune response to MTb is complex and incompletely characterized, hindering development of new diagnostics, treatments and vaccines. Although T cells and the cytokines TNF, IFN-?? and IL-12, are important for immune control of MTb infection, there is an incomplete understanding of the host factors determining protection or pathogenesis in TB. Using an unbiased whole genome array analysis of the transcriptome in blood of TB patients, we have identified potential factors leading to TB pathogenesis. Modular, pathway and gene analyses revealed a striking interferon (IFN)-inducible neutrophil-driven signature of active TB correlating with extent of radiographic disease, which was represented by Type I IFN as well as IFN-?? -inducible genes. This forms the basis of a patent, and the work is now accepted for publication in the journal Nature. We are now in an excellent position to apply the knowledge obtained from our study of human TB to further develop mouse models of TB and define mechanisms and potential determinants of pathogenesis. We will build on our past results to investigate further the molecular mechanisms for induction of IL-10 production and function. IL-10 is produced by multiple cells of the innate and adaptive immune response and thus is not controlled by a strict trajectory of cellular differentiation and is under the control of both cell intrinsic and extrinsic positive and negative regulatory loops in macrophages. Such control mechanisms, although likely, have not as yet been shown in other immune cells. Thus we will continue to characterize mechanisms of induction and regulation of IL-10 in macrophages, dendritic cells and T cells to uncover common and/or distinct mechanisms for its production. We will use basic molecular tools to delineate mechanisms of IL-10 expression both in vitro and in vivo and also extend this to in vivo models of infection with intracellular pathogens, with emphasis on TB. Leading on from our findings in human TB, we will dissect further potential factors in TB pathogenesis, using improved mouse models of TB. We will also use our findings to improve and define transcriptional biomarkers to enhance TB diagnosis and distinguish it from other lung diseases, and define prognostic markers predictive of outcome of latent TB to help develop targeted therapies needed to reduce the burden of TB globally. Technologies used include cell culture, flow cytometry immunoassay, in vivo whole animal immune responses, biochemical and molecular analysis of intracellular signalling pathways and gene regulation (protein and DNA-based technology), microarray technology of host mRNA. More... »

URL

http://gtr.rcuk.ac.uk/project/B7E1854F-85CA-4A03-BC95-AACF025F2D33

Related SciGraph Publications

  • 2018-05. c-Maf controls immune responses by regulating disease-specific gene networks and repressing IL-2 in CD4+ T cells in NATURE IMMUNOLOGY
  • 2017-12. Signatures of malaria-associated pathology revealed by high-resolution whole-blood transcriptomics in a rodent model of malaria in SCIENTIFIC REPORTS
  • 2016-10. Characterization of progressive HIV-associated tuberculosis using 2-deoxy-2-[18F]fluoro-D-glucose positron emission and computed tomography in NATURE MEDICINE
  • 2015-12. HIV–tuberculosis-associated immune reconstitution inflammatory syndrome is characterized by Toll-like receptor and inflammasome signalling in NATURE COMMUNICATIONS
  • 2015-02. Type I interferons in infectious disease in NATURE REVIEWS IMMUNOLOGY
  • 2014. The Regulation of IL-10 Expression in INTERLEUKIN-10 IN HEALTH AND DISEASE
  • 2014. Interleukin-10: Cytokines in Anti-inflammation and Tolerance in CYTOKINE FRONTIERS
  • 2013-02. Brigitte Askonas (1923–2013) in NATURE
  • 2012-10. From IL-2 to IL-37: the expanding spectrum of anti-inflammatory cytokines in NATURE IMMUNOLOGY
  • 2011-10. Highlights of 10 years of immunology in Nature Reviews Immunology in NATURE REVIEWS IMMUNOLOGY
  • 2011-05. The role of IL-10 in immune regulation during M. tuberculosis infection in MUCOSAL IMMUNOLOGY
  • 2011-04. Quantitative events determine the differentiation and function of helper T cells in NATURE IMMUNOLOGY
  • 2010-08. An interferon-inducible neutrophil-driven blood transcriptional signature in human tuberculosis in NATURE
  • 2010-03. The regulation of IL-10 production by immune cells in NATURE REVIEWS IMMUNOLOGY
  • 2009-09. From IL-10 to IL-12: how pathogens and their products stimulate APCs to induce TH1 development in NATURE IMMUNOLOGY
  • 2008-06. Differentiation of human TH-17 cells does require TGF-β! in NATURE IMMUNOLOGY
  • 2007-09. Regula'ten' the gut in NATURE IMMUNOLOGY
  • 2007-06. TH1 cells control themselves by producing interleukin-10 in NATURE REVIEWS IMMUNOLOGY
  • 2006-06. ABIN-2 is required for optimal activation of Erk MAP kinase in innate immune responses in NATURE IMMUNOLOGY
  • 2005-04. Potential role of interleukin-10-secreting regulatory T cells in allergy and asthma in NATURE REVIEWS IMMUNOLOGY
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