CONSTITUTIVE EXPRESSION OF MHC AND ADHESION MOLECULES BY ALVEOLAR EPITHELIAL-CELLS (TYPE-II PNEUMOCYTES) ISOLATED FROM HUMAN LUNG AND COMPARISON WITH IMMUNOCYTOCHEMICAL FINDINGS

Highly purified populations of alveolar epithelial cells (type II pneu mocytes) were isolated from human lung specimens. These cells were cha racterised histochemically, by demonstrating the presence of intracell ular alkaline phosphatase, and morphologically, by electron microscopi c demonstration of lamellar bodies and microvilli. Expression of the e pithelial glycoprotein KEA-125, of MHC class I and class II (HLA-DR, - DP and -DQ) antigens and of the intercellular adhesion molecules ICAM- 1, VCAM-1, LFA-3 and B7 was quantified by flow cytometry. Comparison w as made between the expression of these molecules by isolated type II cells and by alveolar epithelium in normal human lung tissue after imm unocytochemical staining of frozen sections of donor lung. Isolated ty pe II pneumocytes expressed HEA-125 and class I MHC molecules and the class II MHC molecules HLA-DR and -DP; HLA-DQ was not detected. The in tercellular adhesion molecule ICAM-1 was expressed constitutively at l ow levels but there was minimal expression of VCAM-1, LFA-3 and B7. It was not possible to differentiate type II cells from the predominant type I pneumocytes on frozen sections. Alveolar epithelium expressed H EA-125, class I MHC antigens, the class II molecules HLA-DR, and -DP a nd the intercellular adhesion molecule LFA-3. Expression of the adhesi on molecules ICAM-1, VCAM-1 and B7 was variable. As with the isolates, HLA-DQ was not observed on alveolar epithelium. In conclusion, a repr oducible method for the isolation of pure populations of human type II pneumocytes has been developed. These cells were not damaged by the i solation procedure. It is not known whether alveolar epithelium can pr esent antigens to T lymphocytes. However, the expression of potentiall y immunogenic class II MHC antigens and of intercellular adhesion mole cules may facilitate pulmonary inflammation.