Publications
187 results found
Anderson K, Shylakhter I, Tabrizi S, et al., 2012, Genome-wide scans provide evidence for positive selection of genes implicated in Lassa fever, Vol: 367 (1590)
Novembre J, Han E, 2012, Human population structure and the adaptive response to pathogen-induced selection pressure, Philosophical Transactions of the Royal Society of London: Biological Sciences, Vol: 367 (1590)
Williams-Blangero S, Criscione C, Vandeberg J, et al., 2012, Host genetics and population structure effects on parasitic disease, Philosophical Transactions of the Royal Society of London: Biological Sciences, Vol: 367 (1590)
Jobling M, 2012, The impact of recent events on human genetic diversity, Philosophical Transactions of the Royal Society of London: Biological Sciences, Vol: 367 (1590)
Jablonski N, Chaplin G, 2012, Human skin pigmentation, migration and disease susceptibility, Philosophical Transactions of the Royal Society of London: Biological Sciences, Vol: 367 (1590)
Oppenheimer S, 2012, Out-of-Africa, the peopling of continents and islands: tracing uniparental gene trees across the map, Philosophical Transactions of the Royal Society of London: Biological Sciences, Vol: 367 (1590)
Altmann DM, Balloux F, Boyton RJ, 2012, Diverse approaches to analysing the history of human and pathogen evolution: how to tell the story of the past 70 000 years Introduction, PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES, Vol: 367, Pages: 765-769, ISSN: 0962-8436
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- Citations: 4
Durrenberger PF, Ettorre A, Kamel F, et al., 2012, Innate Immunity in multiple sclerosis white matter lesions: expression of natural cytotoxicity triggering receptor 1 (NCR1), Journal of Neuroinflammation, Vol: 9, ISSN: 1742-2094
Boyton RJ, Altmann DM, 2012, Immune regulation in idiopathic bronchiectasis, ADVANCES AGAINST ASPERGILLOSIS I, Vol: 1272, Pages: 68-72, ISSN: 0077-8923
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- Citations: 5
Kamel F, Ettorre A, Durrenberger PF, et al., 2011, Altered invariant natural killer T cells in multiple sclerosis, Annual Congress of the British-Society-for-Immunology, Publisher: WILEY-BLACKWELL, Pages: 41-41, ISSN: 0019-2805
Ettorre A, Kamel FO, Durrenberger PF, et al., 2011, KIR expression as a biomarker of multiple sclerosis disease type, Annual Congress of the British-Society-for-Immunology, Publisher: WILEY-BLACKWELL, Pages: 172-172, ISSN: 0019-2805
Kamel F, Ettorre A, Durrenberger P, et al., 2011, Altered invariant natural killer T cells in Multiple Sclerosis., Immunology, Annual Congress of the British-Society-for-Immunology, Liverpool, ENGLAND, Publisher: Wiley-Blackwell
Bilton, 2011, Bronchiectasis, Bronchiectasis, Editors: Floto, Haworth, Publisher: EuropeanRespiratorySociety, ISBN: 9781849840125
This book provides a definitive guide to the management of patients with bronchiectasis.
Boyton R, Sander C, 2010, Respiratory Infections in HIV positive patients, Respiratory Infections, Editors: Sethi, Informa Healthcare USA Inc. 52 Vanderbilt Ave New York, NY 10017, Publisher: Informa Healthcare USA, Inc, Pages: 186-220
Reynolds C, Barkans J, Clark P, et al., 2009, Natural killer T cells in bronchial biopsies from human allergen challenge model of allergic asthma., J Allergy Clin Immunol, Vol: 124, Pages: 860-862
Campbell JD, Buckland KF, McMillan SJ, et al., 2009, Peptide immunotherapy in allergic asthma generates IL-10-dependent immunological tolerance associated with linked epitope suppression, JOURNAL OF EXPERIMENTAL MEDICINE, Vol: 206, Pages: 1535-1547, ISSN: 0022-1007
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- Citations: 168
Boyton RJ, 2009, Regulation of immunity in bronchiectasis, MEDICAL MYCOLOGY, Vol: 47, Pages: S175-S182, ISSN: 1369-3786
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- Citations: 15
Ingram RJ, Isaacs JD, Kaur G, et al., 2009, A role of cellular prion protein in programming T-cell cytokine responses in disease., FASEB J, Vol: 23, Pages: 1672-1684
The cellular prion protein (PrP(C)) is widely expressed in neural and non-neural tissues, but its function is unknown. Elucidation of the part played by PrP(C) in adaptive immunity has been a particular conundrum: increased expression of cell surface PrP(C) has been documented during T-cell activation, yet the functional significance of this activation remains unclear, with conflicting data on the effects of Prnp gene knockout on various parameters of T-cell immunity. We show here that Prnp mRNA is highly inducible within 8-24 h of T-cell activation, with surface protein levels rising from 24 h. When measured in parallel with CD69 and CD25, PrP(C) is a late activation antigen. Consistent with its up-regulation being a late activation event, PrP deletion did not alter T-cell-antigen presenting cell conjugate formation. Most important, activated PrP(0/0) T cells demonstrated much reduced induction of several T helper (Th) 1, Th2, and Th17 cytokines, whereas others, such as TNF-alpha and IL-9, were unaffected. These changes were investigated in the context of an autoimmune model and a bacterial challenge model. In experimental autoimmune encephalomyelitis, PrP-knockout mice showed enhanced disease in the face of reduced IL-17 responses. In a streptococcal sepsis model, this constrained cytokine program was associated with poorer local control of infection, although with reduced bacteremia. The findings indicate that PrP(C) is a potentially important molecule influencing T-cell activation and effector function.
Boyton RJ, Smith J, Jones M, et al., 2008, Human leucocyte antigen class II association in idiopathic bronchiectasis, a disease of chronic lung infection, implicates a role for adaptive immunity, CLINICAL AND EXPERIMENTAL IMMUNOLOGY, Vol: 152, Pages: 95-101, ISSN: 0009-9104
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- Citations: 26
Boyton R, 2008, The role of natural killer T cells in lung inflammation, Journal of Pathology, Vol: 214, Pages: 276-282
PMID: 18161753 [PubMed - indexed for MEDLINE] Invariant NK T cells (iNKT) bridge the innate and adaptive immune response, being characterized by the ability to use invariant T cell receptors to recognize glycolipid antigens presented by CD1d, leading to an explosive cytokine effector response. As such it has been proposed that iNKT cells perform important roles as both effector and regulatory cells in a wide range of disease settings. These roles have been characterized in experiments depending on the use of iNKT-null mice, due to lack of either CD1d expression or Jalpha18 and the use of CD1d tetramers loaded with the model glycolipid antigen, alpha-galactosylceramide (alphaGalCer). Several studies have examined lung disease, infectious and allergic, in humans and mice. While the lung itself does not carry an exceptionally large population of iNKT cells (compared with, say, the liver), it does appear to be a site at which these cells can exert a profound effect. Several models of bacterial, fungal and viral murine lung infection have been investigated that have sometimes produced conflicting results. Abrogation of iNKT cell function in knockouts is often associated with disease exacerbation, indicating a regulatory role in lung infection. Studies in murine asthma models and in patients have similarly probed the role of iNKT cells in these settings. While there are again somewhat contradictory findings, evidence suggests a likely role for iNKT cells in mediating airway hyper-responsiveness (AHR), but probably not in Th2 polarization or lung eosinophilia. In marginally different models, administration of alphaGalCer has either ameliorated or exacerbated AHR. Different studies of BAL from human asthma patients show variously that there is either a very enlarged population of iNKT cells in the asthmatic lung, or that there is no significant difference from controls. Taken together, there are some observations that argue compellingly for an important role of iNKT cell
Boyton RJ, Altmann DM, 2007, Natural killer cells, killer immunoglobulin-like receptors and human leucocyte antigen class I in disease, CLINICAL AND EXPERIMENTAL IMMUNOLOGY, Vol: 149, Pages: 1-8, ISSN: 0009-9104
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- Citations: 137
Reynolds C, Ozerovitch L, Wilson R, et al., 2007, Toll-like receptors 2 and 4 and innate immunity in neutrophilic asthma and idiopathic bronchiectasis, THORAX, Vol: 62, Pages: 279-279, ISSN: 0040-6376
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- Citations: 7
Boyton RJ, Altmann DM, Wright A, et al., 2007, Pulmonary infection with <i>Cryptococcus neoformans</i> in the face of underlying sarcoidosis, RESPIRATION, Vol: 74, Pages: 462-466, ISSN: 0025-7931
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- Citations: 8
Boyton RJ, Reynolds C, Wahid FN, et al., 2006, IFNγ and CXCR-1 gene polymorphisms in idiopathic bronchiectasis, TISSUE ANTIGENS, Vol: 68, Pages: 325-330, ISSN: 0001-2815
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- Citations: 17
Griesenbach U, Boyton RJ, Somerton L, et al., 2006, Effect of tolerance induction to immunodominant T-cell epitopes of Sendai virus on gene expression following repeat administration to lung, GENE THERAPY, Vol: 13, Pages: 449-456, ISSN: 0969-7128
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- Citations: 16
Boyton RJ, Smith J, Ward R, et al., 2006, HLA-C and killer cell immunoglobulin-like receptor genes in idiopathic bronchiectasis, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 173, Pages: 327-333, ISSN: 1073-449X
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- Citations: 56
Boyton RJ, Smith J, Ward J, et al., 2006, HLA-C and killer cell immunoglobulin-like receptor genes in idiopathic bronchiectasis, American Journal of Respiratory Critical Care Medicine, Vol: 173, Pages: 327-333
Wilson R, Boyton R, 2006, Bronchiectasis, Encyclopedia of Respiratory Medicine, Four-Volume Set, Pages: 259-268, ISBN: 9780123708793
Bronchiectasis is abnormal chronic dilatation of one or more bronchi due to loss of structural elements in the bronchial wall. There are a number of known causes and several associated conditions, but the underlying cause is not known in many cases. The prevalence is unknown, but thin-section computed tomography has increased its recognition. Symptoms are of chronic productive cough, breathlessness, recurrent exacerbations usually provoked by infection, and tiredness. There may be crackles over affected areas but not in all cases, and there may be wheezes due to airflow obstruction that is largely irreversible. Subsegmental airways are permanently dilated, tortuous, and contain excess secretions. Characteristically, the elastin layer of the wall is deficient, and muscle and cartilage show signs of destruction. Increased mucus production and impaired clearance predispose to bacterial infection, which stimulates chronic inflammation in which lymphocytes predominate within the wall and neutrophils in the lumen. The inflammation causes more damage, which in turn further impairs the lung defenses, leading to more infection and a vicious cycle of events. Treatment involves daily physiotherapy to drain affected areas and appropriate antibiotics to treat infection and thus reduce inflammation.
Boyton R, Wilson R, Altmann DM, 2006, DEFENSE SYSTEMS, Encyclopedia of Respiratory Medicine: Volume 1-4, ISBN: 9780123708793
The lung is the anatomical site not only for gaseous exchange, but also for high-turnover sampling of pathogens and other antigenic and allergenic material. It constitutes a vast mucosal surface area, constantly exposed to inhaled substances that, allowed free ingress, would cause substantial damage or death. Any defense mechanism must accommodate the fact that the respiratory tract is made up of delicate tissues required for gas exchange. The lung, therefore, requires a multilayered system of protection that allows a fast, efficient, and effective response able to deal with infectious pathogens and other foreign particles without damaging the lung itself in the process. This encompasses physical barriers, innate immune mechanisms, and the cellular and antibody adaptive immune response. The price of excessive or inappropriate inflammatory responses can be high and may lead to lung damage. The first line of defense against entry to the lung is from physical barriers such as mucus and cilia, followed by the innate immune response that includes a battery of mediators such as lactoferrin, lysozyme, collectins, and defensins. Release of these molecules leads directly to lysis of pathogens, or destruction through opsonization or the recruitment of inflammatory cells. Rapid activation of the innate immune response also comes through the triggering of Toll-like receptors (TLRs) and the chemotactic recruitment and activation of neutrophils. Natural killer (NK) cells provide a fast and effective immune surveillance response against infectious pathogens. Type I interferons exert a direct antiviral effect. The adaptive immune response contributes by making neutralizing antibodies and T lymphocytes orchestrate antigen-specific immune responses through their ability to differentiate self from nonself and provide memory. T lymphocyte populations of different cytokine phenotypes - so-called T-helper-1 (Th1) and T-helper-2 (Th2) - dramatically alter the balance between pathogen clea
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