Abstract: Leukocytes are believed to access sites of inflammation via cell adhesion molecule (CAM) mediated adhesion, activation and transmigration through the vascular endothelium. However, little is known about the mechanisms by which immune effector cells gain access to transplanted organ. The objective of this work was to evaluate a simple experimental model to characterize the migration of T lymphocytes to vascular tissue following transplantation. Brown Norway aortic allografts were transplanted orthotopically into Lewis recipients (n = 10). T cells were isolated from naïve or allo-exposed (activated) Lewis spleens using nylon wool columns. Cr⁵¹ labeled naïve T cells and In¹¹¹ labeled activated T cells (15x10⁶ of each) were injected into animals, 9 days after transplantation with or without anti- 4/ 2_monoclonal antibody (n = 5/group). All animals were then sacrificed on day 10 and evaluated by histology and counts. All allografts had significant infiltration of the adventitia by mononuclear cells at day 10 as compared to control aorta. There was an average of 220+33 Cr⁵¹ cpm and 224 + 30. In¹¹¹ cpm as compared to control aorta (p<0.0001). Anti 4/ 2 mAb treatment resulted in significant reduction in labeled T cell infiltration with a 89% reduction in Cr⁵¹ cpm and 73% reduction in In¹¹¹ cpm both approaching control levels. We have demonstrated that T lymphocytes infiltrate vascular tissue early after transplantation and appears to be mediated via 4/ 2 integrin mechanism. This represents direct evidence of the role of CAM in trafficking of T cells in transplanted allografts and the characterization of a model to evaluate this trafficking.