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American Journal of Pathology, Vol 131, 191-198, Copyright © 1988 by American Society for Investigative Pathology
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M Chilosi, F Menestrina, P Capelli, L Montagna, M Lestani, G Pizzolo, A Cipriani, C Agostini, L Trentin and R Zambello
Istituto di Anatomia Patologica, University of Verona, Italy.
Proliferating cells have been immunophenotypically characterized in lymph node and bronchoalveolar lavage (BAL) samples obtained from patients with active and inactive sarcoidosis with the cell-cycle- related antigen Ki67. Ki67 monoclonal antibody was used by combined immunohistochemical methods together with antibodies recognizing macrophage- and T-cell-subset-related antigens using avidin-biotin peroxidase (ABC) and alkaline phosphatase-anti-alkaline phosphatase (APAAP) systems. Many proliferating Ki67+ cells were found in affected mediastinal lymph nodes. These cells were mainly located around granulomas and exhibited phenotypical markers of helper/inducer T cells (CD3+, CD4+). Ki67+ macrophages could not be detected in the same lesions with this technique. A different picture was found in BAL preparations where proportions of both T lymphocytes and macrophages were Ki67+. The presence of replicating lymphocytes could be correlated to disease activity, whereas the proportions of Ki67+ macrophages did not show significant differences between active and inactive disease. Interleukin-1 (IL-1) expression was investigated in the same samples with a specific antiserum. Epithelioid macrophages in granulomas and BAL macrophages in all cases exhibited cytoplasmic staining revealing an activated status. Interestingly, giant cells in granulomas were mainly devoid of IL-1 immunoreactivity. These studies support the concept that activated cells at different sites of ongoing inflammation play a central role in the mechanisms accounting for granuloma formation.
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