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(Circulation. 1995;92:281-282.)
© 1995 American Heart Association, Inc.

Articles

T-Cells and T-Cell Clones in Rheumatic Fever Valvulitis

Getting to the Heart of the Matter?

John B. Zabriskie, MD

From the Laboratory of Clinical Microbiology/Immunology, The Rockefeller University, New York, N.Y.

Correspondence to John B. Zabriskie, MD, Head of the Laboratory of Clinical Microbiology/Immunology, Rockefeller University, New York, NY 10021-6399.

	Introduction

 
In spite of almost sixty years of intensive investigation, the pathogenic mechanisms underlying the initiation of the disease rheumatic fever remain elusive. This is not to say we have not made any progress. The identification of the organism as a group A Streptococcus by Rebecca Lancefield,¹ the pioneering work of the association of Group A streptococci with rheumatic fever by Collis,² and Coburn,³ and the primary prevention of rheumatic fever by judicious use of penicillin by Rammelkemp and associates⁴ all represent milestones in our understanding of this host-parasite relationship.

What is missing is our understanding of the exact sequence of events starting with a preceding streptococcal pharyngitis, often so mild as to go unnoticed, through a clearly defined latent period and ending with one or more clinical manifestations of disease involving different organ systems.

Among the many hypotheses entertained to explain this sequence of events has been the concept that rheumatic fever is a streptococcal-induced autoimmune disease. Thus, there is an abnormal immune response (both at a humoral and cellular level) on the part of the host to those streptococcal antigens cross reactive with relevant mammalian antigens. Implicit in this concept is that the abnormal immune response on the part of the host is genetically programmed.

While still speculative, a mounting body of evidence is emerging to support this concept. At the humoral level, heart reactive antibodies are seen in ARF patients during the acute stages, decline over time after the attack, and are invariably seen in recurrences.⁵ The streptococcal-induced . . . [Full Text of this Article]

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