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American Journal of Pathology, Vol 140, 847-857, Copyright © 1992 by American Society for Investigative Pathology

REGULAR ARTICLES

Mast-cell phenotype in indolent forms of mastocytosis. Ultrastructural features, fluorescence detection of avidin binding, and immunofluorescent determination of chymase, tryptase, and carboxypeptidase

N Weidner, RF Horan and KF Austen
Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts.

The factor(s) that causes excessive mast cell (MC) proliferation in indolent forms of mastocytosis is not known, nor is it known whether that proliferation is a regulated clonal expansion or merely a non- neoplastic hyperplasia. Human MCs display phenotypes that depend on the microenvironment. Thus, if the phenotype of MCs in mastocytosis lesions is determined to be abnormal for that tissue site (and therefore the MCs are refractory to microenvironmental signals) then a clonal process would be suggested. The authors determined the phenotypes of MCs from the lesional skin of 17 patients with indolent mastocytosis and the bone marrows of 9 patients. They compared them with the phenotypes of MCs from the lesional skin of 8 patients with various dermatitides, the skin of 2 patients with idiopathic anaphylaxis, and the breast skin of 15 control patients. MCs from all the skin specimens showed the characteristic skin MC phenotype, with predominantly scroll-poor granules by ultrastructure and containing tryptase and chymase by immunofluorescence detection (the MCTC immunophenotype). The skin MCs of each patient bound avidin and contained carboxypeptidase by immunofluorescence detection. MCs from the bone marrow of patients with indolent mastocytosis, the source of progenitors, also showed the scroll-poor and MCTC phenotypes. These findings do not support an unregulated clonal expansion in indolent forms of mastocytosis. They are consistent with a non-neoplastic hyperplasia or possibly a clonal process in which MCs remain responsive to microenvironmental regulation.


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Copyright © 1992 by the American Society for Investigative Pathology.