Abstract
Vassallo et al. (June 29 issue)1 depict a central role for the alveolar macrophage in the pathogenesis of pulmonary Langerhans'-cell histiocytosis. We made several observations in a series of five patients with biopsy-proved, CD1a+ pulmonary Langerhans'-cell histiocytosis at our institution. The patients were all young adults (age range, 22 to 31 years) who had smoked cigarettes. On histologic analyses, there were CD68+ histiocytes, including macrophages with “smoker's granules,” admixed with Langerhans' cells; angiotensin-converting–enzyme (ACE) antigen was expressed on non–Langerhans'-cell histiocytes within the lesion and surrounding alveoli. Histiocytes from a lesion of Langerhans'-cell histiocytosis were positive for the latency-associated peptide of transforming growth factor β1; and there were foci of myofibroblasts positive for α-smooth-muscle actin ( Figure 1 ).

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