“…Despite the lack of classic GVHD histopathology, it is not unreasonable to suggest that pulmonary epithelial and endothelial cells can be potential targets for activated donor T cells after allo SCT. First, the lung is a rich source of major and minor histocompatibility (HC) antigens and professional antigen-presenting cells (62,63) and is the site of complex immunologic networks, the proper balance of which allows for infectious surveillance and maintenance of structural integrity, whereas dysregulation of such networks can result in tissue injury and scarring (64). Furthermore, the inflammatory mediators TNF-a andLPS, which are believed to playa part in GVHD (52,54,65), have also been implicated as contributors to pulmonary dysfunction in several experimental systems and clinical syndromes, including adult respiratory distress syndrome (ARDS), lung allograft rejection, and pneumonitis after toxin exposure (32-36,39,66--69).…”