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(Chest. 1993;103:139S-143S.)
© 1993 American College of Chest Physicians

Cellular Immunity in Sarcoidosis and Hypersensitivity Pneumonitis

Recent Advances

Gianpietro Semenzato M.D., F.C.C.P.1; Renato Zambello M.D.1; Livio Trentin M.D.1; and Carlo Agostini M.D.1

1 The Padua University School of Medicine, Department of Clinical Medicine, First Medical Clinic and Clinical Immunology Branch, Padova, Italy.

We have concentrated on three immunologic phenomena which contribute to the T cell alveolitis in the respiratory tract of patients with sarcoidosis and HP Evidence has been presented that two mechanisms account for the increased number of pulmonary T cells in both diseases, ie, a cellular redistribution from the peripheral blood to the lung and an in situ proliferation. Furthermore, we demonstrated that, although the lung [unknown]/dgr pool may occasionally increase in patients with active sarcoidosis and HP, the majority of T cells isolated from the BAL of these patients express the agr/β TCR-related determinant WT31. Finally, the evaluation of the molecular organization of TCR on BAL lymphocytes has shown that antigens involved in sarcoid and HP immunoinflammatory processes favor the local cell proliferation of a limited number of clones. It would thus be logical to expect that a deletion of such restricted T cell subsets would have a beneficial impact on these diseases. Further molecular studies are needed to define the possibility that a TCR-focused attack might down-modulate the activity of a definite TCR-type positive T cell subset in the lung.







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Copyright © 1993 by the American College of Chest Physicians.