ADHESION MOLECULES (E-SELECTIN AND ICAM-1) IN PULMONARY ALLOGRAFT-REJECTION

Vascular endothelial cells act as antigen-presenting cells in the lung allograft and stimulate alloreactive host lymphocytes. Activated lymp hocytes and cytokines can induce expression of leukocyte-endothelial a dhesion molecules that facilitate invasion of tbe allograft by circula ting leukocytes. To define the role of endothelial HLA class II antige n and adhesion molecule expression in lung allograft rejection, we pro spectively analyzed endothelial expression of HLA class II, E-selectin , and intercellular adhesion molecule-1 (ICAM-1) antigens in 52 transb ronchial biopsy specimens from 24 lung allograft recipients as compare d to normal control subjects. Thirty-one of 52 specimens showed histol ogic rejection and 8 of 24, patients developed histologic obliterative bronchiolitis (OB) by the end of the study period. Increased expressi on of HLA class II antigen was seen in 32 of 52 (62%) lung allograft s pecimens, but increased expression did not correlate with acute reject ion or OB. In contrast, E-selectin expression was seen in 30 of 52 (58 %) biopsy specimens and was associated with acute rejection (p<0.005) and with the development of OB (p<0.05). Increased expression of ICAM- 1 was seen in only 18 of 52 (35%) biopsy specimens and did not correla te with acute rejection or OB, These data suggest that E-selectin expr ession may be a tissue marker of acute and chronic lung rejection poss ibly by promoting leukocyte adhesion to the allograft endothelium. The high levels of endothelial HLA class II expression may reflect long-t erm antigenic stimulation of the allograft even in the absence of reje ction.