The clinicopathologic features of 118 granular cell tumors (GCT) encountered at two affiliated hospitals were reviewed. A total of 110 patients were affected over this 32-year period of study (71 men, 39 women), and in 5% GCT were multiple. Patients ranged in age from 16 to 58 years (average 32 years) and were symptomatic for an average duration of 11 months prior to diagnosis. There was a greater than expected frequency of GCT among black patients (29%). Although tongue was the single most common anatomic site involved, relatively more GCT (44%) occurred in skin or subcutaneous tissue. Less common locations were breast parenchyma (10 cases), rectal mucosa and anus (6), vulva (4), esophagus and larynx (2 cases each). The correct preoperative diagnosis of this protean tumor was made in only three patients. GCT were surgically treated with the average diameter of resected tumor being 1.2 cm (range 0.2--3.5 cm). Pseudoepitheliomatous hyperplasia was noted in 11 tumors and in one vulvar GCT there was overlying in situ squamous cell carcinoma. Tumors were incompletely excised in 24 of 56 patients having adequate followup; only five of these 24 patients experienced a local recurrence of tumor. Malignant behavior was not observed. Results of histochemical and ultrastructural study are briefly discussed. The precise histogenesis of GCT is uncertain but Schwann cell origin is favored in most cases.

The binding of a T cell to an APC results in T cell actin cytoskeletal rearrangement leading to the formation of an immunological synapse. The APC cytoskeleton has been thought to play a passive role in this process. In this study, we demonstrate that dendritic cells (DC), unlike other APC, actively polarize their actin cytoskeleton during interaction with T cells. DC cytoskeletal rearrangement was critical for both the clustering and the activation of resting T cells. This study provides compelling evidence that the APC cytoskeleton plays an active role in the immunological synapse and may explain the unique ability of DC to activate resting T cells.

Langerhans cells and mast cells are both resident in large numbers in the skin and act as sentinel cells in host defense. The ability of mast cells to induce Langerhans cell migration from the skin to the draining lymph node in vivo was examined. Genetically mast cell-deficient (W/Wv) mice and control mice were sensitized with IgE Ab in the ear pinna. Seven to 14 days later, mice were challenged with Ag i.v. After a further 18–24 h, epidermal sheets and draining auricular lymph nodes were examined using Langerin/CD207 immunostaining. In mast cell-containing mice, a significant decrease in the number of Langerhans cells was observed at epidermal sites of mast cell activation. A significant increase in total cellularity and accumulation of Langerin-positive dendritic cells was observed in the auricular lymph nodes, draining the sites of IgE-mediated mast cell activation. These changes were not observed in W/Wv mice, but were restored by local mast cell reconstitution. Treatment of mast cell-containing mice with the H2 receptor antagonist cimetidine significantly inhibited the observed IgE/Ag-induced changes in Langerhans cell location. In contrast, Langerhans cell migration in response to LPS challenge was not mast cell dependent. These data directly demonstrate the ability of mast cells to induce dendritic cell migration to lymph nodes following IgE-mediated activation in vivo by a histamine-dependent mechanism.

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