A rare case of adenoid cystic carcinoma of the external auditory canal with magnetic resonance imaging appearances is reported. Both T1 weighted and T2 weighted MR images showed the tumour as a hypointense mass, although there was marked contrast enhancement. Microscopic examination of the resected tumour showed a preponderance of solid tumour cell nests. According to previous reports, these pathological and radiological findings indicate a poor prognosis.

We investigated influences of adhesion factors on the migration of antigen-specific IgA-forming cells (ASAFCs) to the middle ear mucosa by means of an in vitro lymphocyte binding assay. Peyer's patch (PP) lymphocytes from guinea pigs with mucosal immunization, which are rich in ASAFCs, more frequently bound with the inflamed middle ear mucosa than those of PP and spleen cells from animals with systemic immunization, in which antigen-specific IgG-forming cells (ASGFCs) were induced (p > .001). The bindings were not affected by antigenic and nonantigenic stimuli to the middle ear mucosa for producing otitis media. On human middle ear mucosa from 10 patients with acute mastoiditis and chronic otitis media, endothelial cells of newly grown vessels were stained strongly with intercellular adhesion molecule (ICAM)-1, and weakly with vascular cell adhesion molecule (VCAM)-1, platelet endothelial cell adhesion molecule (PECAM), and endothelial leukocyte adhesion molecule (ELAM)-1. Many lymphocytes bound mainly to these endothelial cells, and a few cells were observed bound to the basal portion of epithelial cells. The binding of lymphocytes was significantly, but not completely, inhibited by anti-ICAM-1 antibody (p < .001). These findings suggest that PP lymphocytes with activated mucosal immunity more frequently migrate to the inflamed middle ear mucosa, and that those migrations, after extravasation, may be regulated by the interaction between various binding factors and their receptors on lymphocytes, which is different from that of adhesion molecules and their ligands in the extravasation.

We investigated the migration of antigen-specific IgA-forming cells to the middle ear mucosa. Antigen-specific lymphocytes of IgA and IgG classes were induced in guinea pigs according to an immunization strategy previously described. From those animals, chromium 51-labeled lymphocytes of Peyer's patches and spleen were transferred to radiated chimera recipients. The radioactivity levels of the middle ears with antigenic and nonantigenic stimuli were significantly higher than those of the control ears (p < .05). Those levels of radioactivity were influenced neither by origins and subsets of transferred cells nor by antigenic stimuli to the mucosa (p > .05). Many labeled cells were observed in the middle ear effusion, while few were found in the inflamed mucosa. These findings suggest that in the early stage of inflammation, lymphocytes, including antigen-specific T and B cells, may be recruited from the blood circulation to the inflamed middle ear mucosa by nonspecific inflammatory processes that may mask antigen-specific factors in lymphocyte migration.

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