Immune systems of human nasopharyngeal and palatine tonsils: histomorphometry of lymphoid components and quantification of immunoglobulin-producing cells in health and disease.

Abstract

The relative contributions of the various lymphoid tissue compartments (follicle centre, mantle zone, extrafollicular area, and reticular epithelium) of clinically normal nasopharyngeal (adenoid) and palatine tonsils of young children (mean age 5, range 2–10 years) were found to be almost identical in the two organs. In adenoid hypertrophy and recurrent palatine tonsillitis a significant relative reduction of the contributions of follicle centres and mantle zones occurred along with an increase of the extrafollicular compartment. The tonsillar Ig-producing cell systems in health and disease were studied by paired immunohistochemical staining. Only occasional IgE-producing cells were seen in normal as well as in diseased specimens. A general predominance of IgG cells followed by the IgA, IgM and IgD classes was demonstrated in both organs. In the palatine tonsils the percentage class ratios (64·4:29·6:4·3:1·7) were virtually unaltered in disease. Conversely, the class ratios were changed from 54·2:35·2:7·4:3·3 in healthy adenoids to 70·3:23·3:4·7:1·7 in hypertrophy. Intensified B-cell stimulation associated with disease was indicated as the follicle centres tended to show an increased density of Ig-producing cells—at least in the palatine tonsils—and, moreover, showed a significant shift to IgG expression. Taking the histomorphometric data into account, a decreased number of extrafollicular Ig-producing cells per tissue unit was indicated in recurrent tonsillitis. This change was most likely secondary to the disease. Conversely, the hypertrophic adenoids showed significantly increased B-cell activity in the extrafollicular compartment—a raised number of IgG-producing cells being especially marked. A difference between the two organs in the response pattern of the Ig-producing cells, especially in the reticular epithelium, might be influenced by a contribution of the secretory immune system to the surface protection of the adenoids.