XXXX colony formation by treatment of mice with monoclonal antibodies to pulmonary capillary endothelial cells.

@entity19 @entity5 @entity4 @entity2 @entity189 @entity320
Two rat monoclonal antibodies, 34A and 201B, have been isolated and shown to bind preferentially to capillary endothelial cells in the lung. Administration of these antibodies to @entity19 increases the number of lung colonies derived from i.v. injection of @entity5 cells. The antibodies increase lung colonization in C57BL/6 @entity19 following i.v. injection of @entity19 @entity320 cells and in BALB/c @entity19 following injection of line 1 @entity2 cells. Neither 34A nor 201B monoclonal antibody binds to B16 @entity320 or line 1 @entity189 and so must exert its effect by interaction with endothelial cells. Antibodies injected i.v., s.c., or i.p. are active from 1 h to 1 wk if injected before cell injection. The effect is optimal when 0.1 ml of ascites fluid containing 120 micrograms of antigen binding capacity of both MoAbs 34A and 201B is injected. Significant damage to endothelial cells could not be documented by histopathological examination at the light microscope level or by protein leakage into the air space as measured by lung lavage. However, electron micrographs taken 3 h after monoclonal antibody injection show minor damage to endothelial cell membranes throughout the lung with some areas of mild @entity4 . The increased colonization may be mediated by this subtle damage to endothelial cells, or antibody interactions with endothelial cells may trigger secondary reactions such as altered expression of growth factors.
