Lucididade na educação infantil

507

CONCISE COMMUNICATION

Pathogenic Mechanisms in Rheumatic Carditis: Focus on Valvular Endothelium
Suzanne Roberts,1,a,b Stanley Kosanke,2,a S. Terrence Dunn,2 David Jankelow,3 Carlos M. G. Duran,4 and Madeleine W. Cunningham1
Departments of 1Microbiology and Immunology and 2Pathology, University of Oklahoma Health Sciences Center, Oklahoma City; 3 Department of Medicine, Division of Cardiology, University of Witwatersrand, Johannesburg, South Africa; 4Cardiovascular Sciences Division, University of Montana and International Heart Institute, Missoula

To clarify immune-mediated mechanisms in rheumatic heart disease caused by group A streptococcal infection, valve tissues from rheumatic patients with valvular heart disease who required valve replacement were studied for reactivity with monoclonal anti-CD4 or antiCD8 monoclonal antibodies or anti–vascular cell adhesion molecule–1 (VCAM-1). At the valve surface, CD4+ and CD8+ T lymphocytes were adherent to valve endothelium and penetrated through the subendothelial layer. T cell extravasation into the valve through the surface valvular endothelium appeared to be an important event in the development of rheumatic heart disease. VCAM-1 was expressed on the valvular endothelium in rheumatic valves. Evidence suggested that the pathogenesis of rheumatic heart disease involved the activation of surface valvular endothelium with the expression of VCAM-1 and the extravasation of CD4+ and CD8+ lymphocytes through the activated endothelium into the valve. Lymphocytic infiltration through the valve surface endothelium has not been appreciated as a potential initiating step in disease pathogenesis.

Group A streptococci are important human pathogens that cause a number of suppurative infections in humans, including pharyngitis, which can lead to acute rheumatic fever (ARF) in a susceptible host [1]. ARF is a leading cause of heart disease in children worldwide [1], and since 1985 there has been a resurgence of ARF in