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The Journal of Immunology, 1968, 101: 989-1003.
Copyright © 1968 by The American Association of Immunologists, Inc.

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Immunoglobulin Production in Bronchial Mucosa and Bronchial Lymph Nodes, Particularly in Cystic Fibrosis of the Pancreas

Francisco J. Martinez-Tello1, Dietmar G. Braun2 and William A. Blanc3

From the Department of Pathology (Division of Developmental Pathology), College of Physicians and Surgeons, Columbia University, and Babies Hospital, Columbia-Presbyterian Medical Center, New York, New York, (F.J.M-T, W.A.B.) and the Rockefeller University, New York, (D.G.B.)

Abstract

The three main serum immunoglobulins were demonstrated immunohistologically in plasmacytes of the human bronchial mucosa. The majority of the Ig-producing cells produce IgA and only a minority of cells produce IgM. There was no immunoglobulin production in three newborn infants and one agammaglobulinemic child.

The number of plasma cells containing immunoglobulins increases significantly in the bronchial mucosa in chronic bronchopulmonary disease. Those containing IgA are the most abundant followed by those containing IgG. Cells containing IgM are not increased in number.

Parallel immunohistochemical studies of bronchial lymph nodes have shown an increased number of Ig-containing cells in chronic inflammation. In contrast to bronchial mucosa, IgG-containing cells are by far the most abundant.

Immunodiffusion studies suggested the presence of 11 S IgA in bronchial washings. Using immunofluorescent staining the "secretory piece" was found in the bronchial epithelium and bronchial glands as well as in bronchial secretions. The secretory piece was demonstrated immuno-histologically in the bronchial epithelium, glands and secretions of newborn infants and of an agammaglobulinemic patient.

In the particular case of CFP, immunologic and immunohistochemical studies suggest that there is no defect of the production and secretion of IgA in the bronchial mucosa. On the contrary, there is high IgA production. The role of IgA in the local defense mechanism in chronic bronchopulmonary processes is discussed.

Footnotes

1 Basic Research Fellow of the National Cystic Fibrosis Research Foundation.

2 United States Public Health Service International Post-Doctoral Research Fellow.

3 Career Scientist of the Health Research Council of the City of New York under Contract I-300.




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