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Localization of 11 S External Secretory IgA by Immunofluorescence in Tissues Lining the Oral and Respiratory Passages in Man^1,2,

From the Departments of Medicine and Microbiology, Columbia University College of Physicians and Surgeons, New York, New York and the Department of Microbiology, Baylor University College of Medicine, Houston, Texas

Abstract

The tissue localization of cells containing 11 S external secretory IgA was investigated using rhodamine- or fluorescein-labeled antisera specific either for the heavy polypeptide chain of 7 S serum IgA (anti-IgA) or for the characteristic extra-antigenic determinants of 11 S secretory IgA (anti-Piece). Both anti-Piece and anti-IgA caused fluorescence of: 1) cells at the periphery of lymphoid follicles and lining the crypts of the pharyngeal and palatine tonsils, and 2) scattered interstitial and serous acinar cells of the compound alveolar glands in the nasal submucosa and in the submaxillary and parotid salivary glands. Anti-IgA alone stained occasional cells in the lymphoid follicles of spleen and of lymph nodes taken from the lung, submandibular tissue and periaortic chain. Anti-Piece stained none of the latter tissues, and neither anti-Piece nor anti-IgA caused fluorescence of liver, pancreas or pulmonary alveolar cells.

When anti-IgA and anti-Piece, one labeled with fluorescein and the other with rhodamine, were applied to the same tissue sections, cells stained by anti-Piece were also stained by anti-IgA. Occasional cells in all tissues stained with anti-IgA alone when both conjugates were applied to the sections. These findings suggest that the complete 11 S external secretory IgA is formed in many cells lining the oral and respiratory passages. It is not necessary to postulate selective transport of 7 S serum IgA either from the interstitial fluid surrounding nasal and salivary glands or from the plasma to account for the high concentrations of 11 S IgA in external excretions.

Footnotes

This investigation was conducted under the sponsorship of the Commission on Influenza, Armed Forces Epidemiological Board, and was supported by the United States Army Medical Research and Development Command, Department of the Army, under research contract No. DA-49-007-MD-885. Support was also received from Research Grant AI-06814 of the National Institute of Allergy and Infectious Diseases, National Institutes of Health, United States Public Health Service.

² An abstract of this work appeared in Clin. Res., 15: 298, 1967.

³ Send reprint requests to: Roger D. Rossen, Department of Microbiology, Baylor University College of Medicine, Houston, Texas 77025

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