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A. B. Kay

Researcher at National Institutes of Health

Publications -  25
Citations -  8013

A. B. Kay is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Eosinophil & Allergy. The author has an hindex of 23, co-authored 25 publications receiving 7957 citations. Previous affiliations of A. B. Kay include Imperial College London.

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Journal ArticleDOI

Predominant TH2-like bronchoalveolar T-lymphocyte population in atopic asthma

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.
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Eosinophils and mast cells in bronchoalveolar lavage in subjects with mild asthma. Relationship to bronchial hyperreactivity.

TL;DR: This study supports the hypothesis that bronchial hyperresponsiveness is secondary to epithelial cell damage mediated through eosinophil-derived granule products.
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Identification of activated T lymphocytes and eosinophils in bronchial biopsies in stable atopic asthma.

TL;DR: Examination of mucosal biopsies obtained from both central and subsegmental bronchi showed that the highest number of CD45-, DC3-, DC4-, and CD8-positive cells were found in the group with asthma, and there was a significant increase in the number of interleukin-2 receptor (CD25)-positive cells.
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Eosinophils, T-lymphocytes, mast cells, neutrophils, and macrophages in bronchial biopsy specimens from atopic subjects with asthma: comparison with biopsy specimens from atopic subjects without asthma and normal control subjects and relationship to bronchial hyperresponsiveness.

TL;DR: The results support the hypothesis that activated (CD25) T-lymphocytes release products which regulate recruitment of EOSs into the airway wall, and suggest that asthma is not associated with hyperplasia of either mucosal-type or connective tissue-type mast cell.
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Activation of CD4+ T cells, increased TH2-type cytokine mRNA expression, and eosinophil recruitment in bronchoalveolar lavage after allergen inhalation challenge in patients with atopic asthma

TL;DR: Cytokines produced by activated TH2-type CD4+ T cells in the airway may contribute to late asthmatic responses by mechanisms that include eosinophil accumulation.