Abstract
In 1968, Macaulay coined the term lymphomatoid papulosis to describe the paradox of a clinically benign, self-healing skin eruption resembling pityriasis lichenoides acuta, in which the histology was unexpectedly that of a malignant lymphoma. 1 Willemze et al 2 subsequently classified lymphomatoid papulosis into two principal histologic types: type A, in which large atypical cells with characteristics of Reed-Sternberg (RS) cells are prominent; and type B, in which atypical cerebriform mononuclear cells similar to mycosis fungoides cells predominate. The presence of both histologic types in different but concurrent lesions and the finding of transitional forms in some biopsy specimens suggested that the two types were somehow related. Further clarification of the histogenesis of lymphomatoid papulosis, the relationship between the principal histologic types, and the nature of the atypical cells awaited the development of new monoclonal antibodies for their investigation. In this issue of theARCHIVES, Tokura
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