TY - JOUR
T1 - Role of human basophils and mast cells in the pathogenesis of allergic diseases
AU - Schleimer, R. P.
AU - Fox, C. C.
AU - Naclerio, R. M.
AU - Plaut, M.
AU - Creticos, P. S.
AU - Togias, A. G.
AU - Warner, J. A.
AU - Kagey-Sobotka, A.
AU - Lichtenstein, L. M.
N1 - Funding Information:
From Johns Hopkins University School of Medicine, Division of Climcal Immunology at The Good Samaritan Hospital, Balti-more. Md. Publication #606 of the O’Neill Laboratories at The Good Sa-maritan Hospital, Baltimore, Mtl. Supported by National Institutes of Health grants Al 07290. AI 08270 (L. M. L.), and AI 20136 (R. P. S.). Reprint requests: L. M. Lichtenstein, M.D., Johns Hopkins Uni-versity School of Medicine at The Good Samaritan Hospital. 5601 I,och Raven Blvd., Baltimore, MD 21239.
PY - 1985/8
Y1 - 1985/8
N2 - The role of human basophils and mast cells in the pathogenesis of allergic diseases has been analyzed. Purified human basophils and mast cells release several known mediators of allergic reactions, including histamine, sulfidopeptide leukotrienes, kinin-forming enzymes, and, in the case of the mast cell, PGD2. These same mediators are released in vivo after experimental challenge in the upper airways with either allergen or cold, dry air, a stimulus used to simulate exercise-induced bronchospasm. The appearance of mast cell mediators in vivo after such challenges further implicates mast cells in the pathogenesis of allergic diseases of the airways that occur as a result of exposure to allergen or physical stimuli. During the LPR after experimental challenge of the upper airways, the pattern of mediators released (i.e., histamine, leukotrienes, and others, but no PGD2) suggests that basophils may contribute to the LPR. Antiallergic drugs that prevent mediator release in vitro, such as antihistamines, also prevent the appearance of mediators in vivo, strengthening both the validity of the in vitro test as a model of the disease and the hypothesis that mediator release is an essential element of the disease process. A model discussing the pathogenetic mechanism is presented.
AB - The role of human basophils and mast cells in the pathogenesis of allergic diseases has been analyzed. Purified human basophils and mast cells release several known mediators of allergic reactions, including histamine, sulfidopeptide leukotrienes, kinin-forming enzymes, and, in the case of the mast cell, PGD2. These same mediators are released in vivo after experimental challenge in the upper airways with either allergen or cold, dry air, a stimulus used to simulate exercise-induced bronchospasm. The appearance of mast cell mediators in vivo after such challenges further implicates mast cells in the pathogenesis of allergic diseases of the airways that occur as a result of exposure to allergen or physical stimuli. During the LPR after experimental challenge of the upper airways, the pattern of mediators released (i.e., histamine, leukotrienes, and others, but no PGD2) suggests that basophils may contribute to the LPR. Antiallergic drugs that prevent mediator release in vitro, such as antihistamines, also prevent the appearance of mediators in vivo, strengthening both the validity of the in vitro test as a model of the disease and the hypothesis that mediator release is an essential element of the disease process. A model discussing the pathogenetic mechanism is presented.
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U2 - 10.1016/0091-6749(85)90656-6
DO - 10.1016/0091-6749(85)90656-6
M3 - Article
C2 - 2410478
AN - SCOPUS:0022388825
SN - 0091-6749
VL - 76
SP - 369
EP - 374
JO - The Journal of allergy and clinical immunology
JF - The Journal of allergy and clinical immunology
IS - 2 PART 2
ER -