Imperial College London

ProfessorRosemaryBoyton

Faculty of MedicineDepartment of Infectious Disease

Professor of Immunology and Respiratory Medicine
 
 
 
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Contact

 

r.boyton

 
 
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Location

 

8N22Commonwealth BuildingHammersmith Campus

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Summary

 

Publications

Publication Type
Year
to

106 results found

Boyton RJ, 2009, Regulation of immunity in bronchiectasis, MEDICAL MYCOLOGY, Vol: 47, Pages: S175-S182, ISSN: 1369-3786

Journal article

Ingram RJ, Isaacs JD, Kaur G, Lowther DE, Reynolds CJ, Boyton RJ, Collinge J, Jackson GS, Altmann DMet 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.

Journal article

Boyton RJ, Smith J, Jones M, Reynolds C, Ozerovitch L, Chaudhry A, Wilson R, Rose M, Altmann DMet 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

Journal article

Boyton RJ, 2008, Bronchiectasis, Medicine, Vol: 36, Pages: 315-320

Journal article

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

Journal article

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

Journal article

Reynolds C, Ozerovitch L, Wilson R, Altmann D, Boyton Ret 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

Journal article

Boyton RJ, Altmann DM, Wright A, Kon OMet al., 2007, Pulmonary infection with Cryptococcus neoformans in the face of underlying sarcoidosis, RESPIRATION, Vol: 74, Pages: 462-466, ISSN: 0025-7931

Journal article

Boyton RJ, Reynolds C, Wahid FN, Jones MG, Ozerovitch L, Ahmad T, Chaudhry A, Jewell DP, Kon OM, Smith J, Rose M, Newman-Taylor AJ, Cole P, Wilson R, Altmann DMet al., 2006, IFN gamma and CXCR-1 gene polymorphisms in idiopathic bronchiectasis, TISSUE ANTIGENS, Vol: 68, Pages: 325-330, ISSN: 0001-2815

Journal article

Griesenbach U, Boyton RJ, Somerton L, Garcia SE, Ferrari S, Owaki T, Ya-Fen Z, Geddes DM, Hasegawa M, Altmann DM, Alton EWFWet 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

Journal article

Boyton RJ, Smith J, Ward R, Jones M, Ozerovitch L, Wilson R, Rose M, Trowsdale J, Altmann DMet 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

Journal article

Boyton RJ, Smith J, Ward J, Jones M, Ozerovitch L, Wilson R, Rose M, Trowsdale Jet 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

Journal article

Boyton R, Altmann DM, 2006, Pneumonia: Fungal (Including Pathogens), Encyclopedia of Respiratory Medicine, Four-Volume Set, Pages: 431-440, ISBN: 9780123708793

© 2006 Elsevier Ltd. All rights reserved. Fungal infection generally originates from an exogenous, environmental source acquired by inhalation, ingestion, or trauma. Fungi are rarely associated with significant disease in the normal host, although many more cause serious disease in the immunocompromised host. Opportunistic fungal infections have become increasingly common, especially in AIDS patients, and constitute a major cause of morbidity and mortality in this group. Pathogenicity depends on the interplay between components of the host immune system and specific features of the fungal strain. Considerable efforts are underway to conduct genetic characterization of fungal virulence and host susceptibility factors in disease. Genome projects have been undertaken for a number of the key fungal pathogens. Here we consider the etiology, pathology, clinical features, management, and molecular mycology of Blastomycosis, Coccidioidomycocis, Histoplasmosis, Paracoccidioidomycosis, Aspergillosis, Candidosis, Cryptococcosis, and Mucormycosis.

Book chapter

Boyton R, Wilson R, Altmann DM, 2006, Defense Systems, Encyclopedia of Respiratory Medicine, Four-Volume Set, Pages: 1-7, ISBN: 9780123708793

© 2006 Elsevier Ltd All rights reserved. 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) - dramat

Book chapter

Altmann DM, 2006, Models of Sarcoidosis. Autoimmune Diseases, Drug Discovery Today: Disease Models, Vol: 3, Pages: 21-25

Journal article

Boyton R, 2006, Pneumonia: Fungal, Encyclopedia of Respiratory Medicine, Editors: Laurent, Shapiro, Oxford, UK, Publisher: Elsevier Limited

Book chapter

Boyton R, 2006, Notch, Encyclopedia of Respiratory Medicine, Editors: Laurent, Shapiro, Oxford, UK, Publisher: Elsevier Limited

Book chapter

Wilson R, Boyton R, 2006, Bronchiectasis, Encyclopedia of Respiratory Medicine, Editors: Laurent, Shapiro, Oxford, UK, Publisher: Elsevier Limited

Book chapter

Boyton R, 2006, Lung Defence, Encyclopedia of Respiratory Medicine, Editors: Laurent, Shapiro, Oxford, UK, Publisher: Elsevier Limited

Book chapter

Boyton RJ, Davies S, Fantino C, Reynolds C, Portugal K, Dewchand H, Altmann DMet al., 2005, Stat4-null non-obese diabetic mice: protection from diabetes and experimental allergic encephalomyelitis, but with concomitant epitope spread, INTERNATIONAL IMMUNOLOGY, Vol: 17, Pages: 1157-1165, ISSN: 0953-8178

Journal article

Boyton RJ, 2005, Infectious lung complications in patients with HIV/AIDS, CURRENT OPINION IN PULMONARY MEDICINE, Vol: 11, Pages: 203-207, ISSN: 1070-5287

Journal article

Ellmerich S, Mycko M, Takacs K, Waldner H, Wahid FN, Boyton RJ, King RHM, Smith PA, Amor S, Herlihy AH, Hewitt RE, Jutton M, Price DA, Hafler DA, Kuchroo VK, Altmann DMet al., 2005, High incidence of spontaneous disease in an HLA-DR15 and TCR transgenic multiple sclerosis model, JOURNAL OF IMMUNOLOGY, Vol: 174, Pages: 1938-1946, ISSN: 0022-1767

Journal article

Altmann D, Boyton R, 2005, Models of multiple sclerosis. Autoimmune diseases., Drug Discovery Today: Disease Models, Vol: 11, Pages: 405-410

Journal article

Ellmerich S, Takacs K, Mycko M, Waldner H, Wahid F, Boyton RJ, Smith PA, Amor S, Baker D, Hafler DA, Kuchroo VK, Altmann DMet al., 2004, Disease-related epitope spread in a humanized T cell receptor transgenic model of multiple sclerosis, EUROPEAN JOURNAL OF IMMUNOLOGY, Vol: 34, Pages: 1839-1848, ISSN: 0014-2980

Journal article

Griesenbach U, Boyton R, Somerton L, Garcia SE, Ferrari S, Owaki T, Tsugumine S, Geddes DM, Hasegawa M, Altmann D, Alton EWFWet al., 2004, Tolerisation of mice to allow repeated administration of recombinant Sendai virus vector to the airways, 7th Annual Meeting of the American-Society-of-Gene-Therapy, Publisher: ACADEMIC PRESS INC ELSEVIER SCIENCE, Pages: S274-S275, ISSN: 1525-0016

Conference paper

Boyton RJ, Altmann DM, 2004, Asthma: new developments in cytokine regulation, CLINICAL AND EXPERIMENTAL IMMUNOLOGY, Vol: 136, Pages: 13-14, ISSN: 0009-9104

Journal article

Boyton RJ, Mitchell DM, Kon OM, 2004, Pneumocystis pneumonia in humans is caused by P jiroveci not P carinii - Reply, THORAX, Vol: 59, Pages: 83-84, ISSN: 0040-6376

Journal article

Altmann DM, Boyton RJ, 2004, Models of multiple sclerosis, Drug Discovery Today: Disease Models, Vol: 1, Pages: 405-410, ISSN: 1740-6757

Multiple sclerosis, the most common disease of central nervous system demyelination, is widely believed to result from autoimmune attack of myelin by T lymphocytes. Several approaches are widely used to model the disease. In vitro studies address specific steps in disease such as mechanisms of T-cell activation by myelin epitopes, migration across the blood-brain barrier and demyelination. In vivo models encompass approaches based on experimental allergic encephalomyelitis, as well as transgenic and mutant strains. Using these models, many therapeutic strategies have been proposed. © 2004 Elsevier Ltd. All rights reserved.

Journal article

Miller R, 2004, Pneumocystis pneumonia in humans is caused by P jiroveci not P carinii, THORAX, Vol: 59, Pages: 83-83, ISSN: 0040-6376

Journal article

Boyton RJ, Mitchell D, Kon OM, 2004, HIV associated pneumonia in intensive care, Respiratory Management in Critical Care, Editors: Griffiths, Evans, London, UK, Publisher: BMJ Publishing Group, Pages: 120-124

Book chapter

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