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A. B. Kay

Bio: A. B. Kay is an academic researcher from Imperial College London. The author has contributed to research in topics: Eosinophil & Immunoglobulin E. The author has an hindex of 35, co-authored 73 publications receiving 6566 citations. Previous affiliations of A. B. Kay include National Institutes of Health & University of Edinburgh.


Papers
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Journal ArticleDOI
TL;DR: The treatment of allergic rhinitis (and other allergic diseases) consists of allergen avoidance (whenever possible and practical), anti-allergic medication, and immunotherapy for specific allergens as mentioned in this paper.
Abstract: Allergic Diseases and Their Treatment Allergic Rhinitis Allergic rhinitis is characterized by episodes of sneezing, itching, rhinorrhea, and nasal obstruction. Perennial allergic rhinitis should be distinguished from nonallergic, noninfectious forms of rhinitis, such as idiopathic (“vasomotor”) rhinitis, nonallergic rhinitis with eosinophilia syndrome, hormonal rhinitis, drug-induced rhinitis, and food-induced rhinitis. The treatment of allergic rhinitis (and other allergic diseases) consists of allergen avoidance (whenever possible and practical), antiallergic medication, and immunotherapy for specific allergens, which is also called hyposensitization or desensitization. Currently, the drugs usually used to treat allergic rhinitis are antihistamines and anticholinergic agents (for the relief of symptoms) and . . .

1,280 citations

Journal Article
TL;DR: It is suggested that multiple C-C chemokines, acting at least in part via CCR3, contribute to bronchial eosinophilia in both atopic and nonatopic asthma.
Abstract: Atopic (AA) and nonatopic (NAA) asthma are characterized by chronic inflammation and local tissue eosinophilia. Many C-C chemokines are potent eosinophil chemoattractants and act predominantly via the CCR3. We examined the expression of eotaxin, eotaxin-2, RANTES, monocyte chemoattractant protein-3 (MCP-3), MCP-4, and CCR3 in the bronchial mucosa from atopic (AA) and nonatopic (intrinsic; NAA) asthmatics and compared our findings with atopic (AC) and nonatopic nonasthmatic controls (NC). Cryostat sections were processed for immunohistochemistry (IHC), in situ hybridization (ISH), and double IHC/ISH. Compared with AC and NC, the numbers of EG2+ cells and the cells expressing mRNA for eotaxin, eotaxin-2, RANTES, MCP-3, MCP-4, and CCR3 were significantly increased in AA and NAA (p < 0.01). Nonsignificant differences in these variants were observed between AA and NAA and between AC and NC. Significant correlations between the cells expressing eotaxin or CCR3 and EG2+ eosinophils in the bronchial tissue were also observed for both AA (p < 0.01) and NAA (p = 0.01). Moreover, in the total asthmatic group (AA + NAA) there was a significant inverse correlation between the expression of eotaxin and that of the histamine PC20 (p < 0.05). Sequential IHC/ISH showed that cytokeratin+ epithelial cells, CD31+ endothelial cells, and CD68+ macrophages were the major sources of eotaxin, eotaxin-2, RANTES, MCP-3, and MCP-4. There was no significantly different distribution of cells expressing mRNA for these chemokines between atopic and nonatopic asthma. These findings suggest that multiple C-C chemokines, acting at least in part via CCR3, contribute to bronchial eosinophilia in both atopic and nonatopic asthma.

429 citations

Journal ArticleDOI
TL;DR: Several, short, overlapping Fel d 1 T-cell peptides have potential in treatment of cat allergy and patients on peptides had initial late asthmatic reactions, but could be desensitised to the higher dose of peptide.

361 citations

Journal ArticleDOI
TL;DR: Cell-mediated immunity may be causally related to the pathogenesis of acute severe asthma, although these values remained raised above control values for the observation period.

356 citations


Cited by
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31 Oct 1996-Nature
TL;DR: The existence of subsets of CD4+ helper T lymphocytes that differ in their cytokine secretion patterns and effector functions provides a framework for understanding the heterogeneity of normal and pathological immune responses.
Abstract: The existence of subsets of CD4+ helper T lymphocytes that differ in their cytokine secretion patterns and effector functions provides a framework for understanding the heterogeneity of normal and pathological immune responses. Defining the cellular and molecular mechanisms of helper-T-cell differentiation should lead to rational strategies for manipulating immune responses for prophylaxis and therapy.

4,578 citations

Journal ArticleDOI
Jean Bousquet, N. Khaltaev, Alvaro A. Cruz1, Judah A. Denburg2, W. J. Fokkens3, Alkis Togias4, T. Zuberbier5, Carlos E. Baena-Cagnani6, Giorgio Walter Canonica7, C. van Weel8, Ioana Agache9, Nadia Aït-Khaled, Claus Bachert10, Michael S. Blaiss11, Sergio Bonini12, L.-P. Boulet13, Philippe-Jean Bousquet, Paulo Augusto Moreira Camargos14, K-H. Carlsen15, Y. Z. Chen, Adnan Custovic16, Ronald Dahl17, Pascal Demoly, H. Douagui, Stephen R. Durham18, R. Gerth van Wijk19, O. Kalayci19, Michael A. Kaliner20, You Young Kim21, Marek L. Kowalski, Piotr Kuna22, L. T. T. Le23, Catherine Lemière24, Jing Li25, Richard F. Lockey26, S. Mavale-Manuel26, Eli O. Meltzer27, Y. Mohammad28, J Mullol, Robert M. Naclerio29, Robyn E O'Hehir30, K. Ohta31, S. Ouedraogo31, S. Palkonen, Nikolaos G. Papadopoulos32, Gianni Passalacqua7, Ruby Pawankar33, Todor A. Popov34, Klaus F. Rabe35, J Rosado-Pinto36, G. K. Scadding37, F. E. R. Simons38, Elina Toskala39, E. Valovirta40, P. Van Cauwenberge10, De Yun Wang41, Magnus Wickman42, Barbara P. Yawn43, Arzu Yorgancioglu44, Osman M. Yusuf, H. J. Zar45, Isabella Annesi-Maesano46, E.D. Bateman45, A. Ben Kheder47, Daniel A. Boakye48, J. Bouchard, Peter Burney18, William W. Busse49, Moira Chan-Yeung50, Niels H. Chavannes35, A.G. Chuchalin, William K. Dolen51, R. Emuzyte52, Lawrence Grouse53, Marc Humbert, C. M. Jackson54, Sebastian L. Johnston18, Paul K. Keith2, James P. Kemp27, J. M. Klossek55, Désirée Larenas-Linnemann55, Brian J. Lipworth54, Jean-Luc Malo24, Gailen D. Marshall56, Charles K. Naspitz57, K. Nekam, Bodo Niggemann58, Ewa Nizankowska-Mogilnicka59, Yoshitaka Okamoto60, M. P. Orru61, Paul Potter45, David Price62, Stuart W. Stoloff63, Olivier Vandenplas, Giovanni Viegi, Dennis M. Williams64 
Federal University of Bahia1, McMaster University2, University of Amsterdam3, National Institutes of Health4, Charité5, Catholic University of Cordoba6, University of Genoa7, Radboud University Nijmegen8, Transilvania University of Brașov9, Ghent University10, University of Tennessee Health Science Center11, University of Naples Federico II12, Laval University13, Universidade Federal de Minas Gerais14, University of Oslo15, University of Manchester16, Aarhus University17, Imperial College London18, Erasmus University Rotterdam19, George Washington University20, Seoul National University21, Medical University of Łódź22, Hai phong University Of Medicine and Pharmacy23, Université de Montréal24, Guangzhou Medical University25, University of South Florida26, University of California, San Diego27, University of California28, University of Chicago29, Monash University30, Teikyo University31, National and Kapodistrian University of Athens32, Nippon Medical School33, Sofia Medical University34, Leiden University35, Leiden University Medical Center36, University College London37, University of Manitoba38, University of Helsinki39, Finnish Institute of Occupational Health40, National University of Singapore41, Karolinska Institutet42, University of Minnesota43, Celal Bayar University44, University of Cape Town45, Pierre-and-Marie-Curie University46, Tunis University47, University of Ghana48, University of Wisconsin-Madison49, University of British Columbia50, Georgia Regents University51, Vilnius University52, University of Washington53, University of Dundee54, University of Poitiers55, University of Mississippi56, Federal University of São Paulo57, German Red Cross58, Jagiellonian University Medical College59, Chiba University60, American Pharmacists Association61, University of Aberdeen62, University of Nevada, Reno63, University of North Carolina at Chapel Hill64
01 Apr 2008-Allergy
TL;DR: The ARIA guidelines for the management of allergic rhinitis and asthma are similar in both the 1999 ARIA workshop report and the 2008 Update as discussed by the authors, but the GRADE approach is not yet available.
Abstract: Allergic rhinitis is a symptomatic disorder of the nose induced after allergen exposure by an IgE-mediated inflammation of the membranes lining the nose. It is a global health problem that causes major illness and disability worldwide. Over 600 million patients from all countries, all ethnic groups and of all ages suffer from allergic rhinitis. It affects social life, sleep, school and work and its economic impact is substantial. Risk factors for allergic rhinitis are well identified. Indoor and outdoor allergens as well as occupational agents cause rhinitis and other allergic diseases. The role of indoor and outdoor pollution is probably very important, but has yet to be fully understood both for the occurrence of the disease and its manifestations. In 1999, during the Allergic Rhinitis and its Impact on Asthma (ARIA) WHO workshop, the expert panel proposed a new classification for allergic rhinitis which was subdivided into 'intermittent' or 'persistent' disease. This classification is now validated. The diagnosis of allergic rhinitis is often quite easy, but in some cases it may cause problems and many patients are still under-diagnosed, often because they do not perceive the symptoms of rhinitis as a disease impairing their social life, school and work. The management of allergic rhinitis is well established and the ARIA expert panel based its recommendations on evidence using an extensive review of the literature available up to December 1999. The statements of evidence for the development of these guidelines followed WHO rules and were based on those of Shekelle et al. A large number of papers have been published since 2000 and are extensively reviewed in the 2008 Update using the same evidence-based system. Recommendations for the management of allergic rhinitis are similar in both the ARIA workshop report and the 2008 Update. In the future, the GRADE approach will be used, but is not yet available. Another important aspect of the ARIA guidelines was to consider co-morbidities. Both allergic rhinitis and asthma are systemic inflammatory conditions and often co-exist in the same patients. In the 2008 Update, these links have been confirmed. The ARIA document is not intended to be a standard-of-care document for individual countries. It is provided as a basis for physicians, health care professionals and organizations involved in the treatment of allergic rhinitis and asthma in various countries to facilitate the development of relevant local standard-of-care documents for patients.

3,769 citations

Journal ArticleDOI
TL;DR: This systematic review and meta-analyses confirmed the findings of a previous study published in “Rhinitis and Asthma: Causes and Prevention, 2nd Ed.” (2015) as well as new findings of “Mechanisms of Respiratory Disease and Allergology,” which confirmed the role of EMTs in the development of these diseases.
Abstract: Authors Jan L. Brozek, MD, PhD – Department of Clinical Epidemiology & Biostatistics and Medicine, McMaster University, Hamilton, Canada Jean Bousquet, MD, PhD – Service des Maladies Respiratoires, Hopital Arnaud de Villeneuve, Montpellier, France, INSERM, CESP U1018, Respiratory and Environmental Epidemiology Team, France, and WHO Collaborating Center for Rhinitis and Asthma Carlos E. Baena-Cagnani, MD – Faculty of Medicine, Catholic University of Cordoba, Cordoba, Argentina Sergio Bonini, MD – Institute of Neurobiology and Molecular Medicine – CNR, Rome, Italy and Department of Medicine, Second University of Naples, Naples, Italy G. Walter Canonica, MD – Allergy & Respiratory Diseases, DIMI, Department of Internal Medicine, University of Genoa, Genoa, Italy Thomas B. Casale, MD – Division of Allergy and Immunology, Department of Medicine, Creighton University, Omaha, Nebraska, USA Roy Gerth van Wijk, MD, PhD – Section of Allergology, Department of Internal Medicine, Erasmus Medical Centre, Rotterdam, the Netherlands Ken Ohta, MD, PhD – Division of Respiratory Medicine and Allergology, Department of Medicine, Teikyo University School of Medicine, Tokyo, Japan Torsten Zuberbier, MD – Department of Dermatology and Allergy, Charite Universitatsmedizin Berlin, Berlin, Germany Holger J. Schunemann, MD, PhD, MSc – Department of Clinical Epidemiology & Biostatistics and Medicine, McMaster University, Hamilton, Canada

3,368 citations

Journal ArticleDOI
TL;DR: Atopic asthma is associated with activation in the bronchi of the interleukin-3, 4, and 5 and GM-CSF gene cluster, a pattern compatible with predominant activation of the TH2-like T-cell population.
Abstract: Background. In atopic asthma, activated T helper lymphocytes are present in bronchial-biopsy specimens and bronchoalveolar-lavage (BAL) fluid, and their production of cytokines may be important in the pathogenesis of this disorder. Different patterns of cytokine release are characteristic of certain subgroups of T helper cells, termed TH1 and TH2, the former mediating delayed-type hypersensitivity and the latter mediating IgE synthesis and eosinophilia. The pattern of cytokine production in atopic asthma is unknown. Methods. We assessed cells obtained by BAL in subjects with mild atopic asthma and in normal control subjects for the expression of messenger RNA (mRNA) for interleukin-2, 3, 4, and 5, granulocytemacrophage colony-stimulating factor (GM-CSF), and interferon gamma by in situ hybridization with 32P-labeled complementary RNA. Localization of mRNA to BAL T cells was assessed by simultaneous in situ hybridization and immunofluorescence and by in situ hybridization after immunomagnetic enrichment or...

2,898 citations