Identical expression of ELAM‐1, VCAM‐1, and ICAM‐1 in sarcoidosis and usual interstitial pneumonitis

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Abstract
Extravasation of leucocytes in tissues is mediated by leucocyte—endothelial cell interactions in which adhesion molecules play an important role. Until now, two pathways have been unravelled, i.e., the LFA‐1/ICAM‐1 and the VLA‐4/VCAM‐1 pathways. ELAM‐1 has been shown to be involved in granulocyte accumulation and recently also in lymphocyte migration. The role of HECA‐452 is under investigation. In this study we have investigated the expression of the above‐mentioned adhesion molecules in lung tissue of patients with pulmonary sarcoidosis and usual interstitial pneumonitis (UIP), and in mediastinal lymph nodes of patients with sarcoidosis. ICAM‐1 (CD54) was broadly distributed on the endothelium of all the vessels found in sarcoidosis and UIP. VCAM‐1 was present on the endothelium of the venules, capillaries, and arterioles in both sarcoidosis and UIP. ELAM‐1 reacted with endothelial cells lining venules and capillaries in chronic progressive sarcoidosis and in the active phase of UIP but not in the stationary phases of both diseases. HECA‐452 activity could be detected only on high endothelial venules within sarcoid lymph nodes. In lung tissues, macrophages bearing the ICAM‐1 antigen were present in sarcoid tissue but not in the interstitium and alveolar space of UIP. LFA‐1 (CD11a/CD18) and VLA‐4 (CD49d/CD29) were present on all leucocytes found but seemed to be more highly expressed on lymphocytes in sarcoidosis. These findings suggest that the LFA‐1/ICAM‐1 and VLA‐4/VCAM‐1 pathways are involved in leucocyte migration in both types of lung disease, while in the active phases of sarcoidosis and UIP, ELAM‐1 is also involved.