A COMPARISON OF THE ANTIGEN-PRESENTING CAPABILITIES OF CLASS-II MHC-EXPRESSING HUMAN LUNG EPITHELIAL AND ENDOTHELIAL-CELLS

Human lung alveolar epithelial cells constitutively express class II m ajor histocompatibility complex (MHC). Human lung microvascular endoth elial and small airway epithelial cells can be induced to express clas s II MHC by stimulation with the pro-inflammatory cytokine interferon- gamma. The levels of class II MHC on lung epithelial and endothelial c ells were comparable to those seen on an Epstein-Barr virus (EBV)-tran sformed B-cell line. However, the costimulatory molecules B7-1 and B7- 2 were not expressed. The ability of the class II MHC expressing human lung parenchymal cells to present alloantigen to CD4(+) T lymphocytes was investigated. Freshly isolated human alveolar epithelial cells (t ype II pneumocytes) and monolayers of interferon-gamma-stimulated smal l airway epithelial and lung microvascular endothelial cells were co-c ultured with allogeneic CD4(+) T lymphocytes and proliferation determi ned by [H-3]thymidine incorporation. A clear difference was observed b etween effects of the epithelial and endothelial cells on CD4(+) T-lym phocyte activation. Alveolar and small airway epithelial cells failed to stimulate the proliferation of allogeneic CD4(+) T lymphocytes wher eas lung microvascular endothelial cells did stimulate proliferation. This difference could not be explained by the levels of class II MHC o r the lack of B7-1 and B7-2 solely. Microvascular endothelial cells, a nd not alveolar or small airway epithelial cells, possess B7-independe nt costimulatory pathways.