Rheumatic fever and rheumatic heart disease are considered to result from abnormal immune responses after Group A streptococcal pharyngitis. Production of interleukin 1 (IL-1), tumor necrosis factor-alpha (TNF), interleukin 2 (IL-2) and immunoglobulin (Ig) by blood and tonsillar mononuclear cells from rheumatic or healthy children was measured after stimulation in vitro by pokeweed mitogen (PWM) or the streptococcal extracellular product, blastogen A (BLA). Tonsillar cells from patients with rheumatic heart disease produced significantly less IL-1, TNF, IL-2, and Ig than control tonsillar cells. In contrast, blood mononuclear cell cultures from rheumatic children produced more TNF and IL-2 than controls. Our findings suggest that abnormal regulation of cytokine and Ig production may contribute to the pathogenesis of acute rheumatic fever and rheumatic heart disease.
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