Selective expression of the vascular addressin recognized by MECA-79 on endothelia in endocardial infiltrates of human heart allografts

Tissue-specific cell-cell adhesion between lymphocytes and endothelia may be pivotal in the development of subsequent immune recognition phenomena and in the exit of lymphocytes from the vascular system. The monoclonal antiody MECA-79 stains the peripheral lymph node addressin, an endothelial cell adhesion molecule for lymphocytes found on high endothelial venules in murine and human peripheral lymph nodes, and reflects site-specific and tissue-selective reactivity. Utilizing avidin-biotin complex immunoperoxidase, we studied areas of endocardial infiltrate with MECA-79 in 168 formalin-fixed, paraffin-embedded endomyocardial biopsy specimens from human heart allograft recipients. Staining in these specimens was compared to that in transmural left ventricular sections of failed heart allografts with or without rejection present, sections from hearts with fatal myocarditis, and sections from hearts with myocardial infarcts. Of the 168 endomyocardial biopsy specimens, 41 (23%) had typical vascularized endocardial mononuclear cell infiltrates (Quilty effects). Of these 41 specimens, 29 (64%) had high endothelial venule positivity with MECA-79. In contrast, staining of small blood vessels was positive in only a single vessel in the deep myocardium of 15 large transmural allograft sections and in none of 18 myocarditis or 4 infarct sections. The selective and striking MECA-79 staining in endocardial infiltrates suggests that lymphocyte homing to this location can involve mechanisms distinct from areas of myocardial rejection.