Summary: Cell-mediated immunity (CMI) was examined in 74 children with acute rheumatic fever (ARF) grouped as with or without carditis and inactive disease with valvular lesions and 26 healthy controls of the same age.Absolute lymphocyte count, skin tests with PPD, Candida, and streptokinase streptodornase (SK-SD) antigens were employed. The lymphocyte transformation test was performed by using phytohemagglutinin (PHA), SK-SD, Candida, and cardiac antigens, and incorporation of tritiated thymidine into DNA was measured.Absolute lymphocyte counts in all groups were not significantly different than those of controls. Skin test responses to PPD, Candida, and SK-SD antigens were significantly decreased in patients with rheumatic activity. In contrast, inactive rheumatic patients with valvular lesions showed higher percentages of positive reactions which were not significantly different than those of the healthy controls. The in vitro response to PHA was decreased in active rheumatic fever (RF) patients, whereas patients with inactive RF with valvular lesions showed a hyperactivity to this mitogen. Patients with inactive RF with valvular lesions also exhibited an exaggerated cellular reactivity to SK-SD antigen, but the patients in active groups showed more of a decreased reactivity than did the controls. Patients with evidence of rheumatic carditis exhibited the same degree of cellular reactivity to these antigens and mitogen as did patients without clinical evidence of rheumatic heart disease. Candida did not cause significant stimulation of blastic transformation in any of the study groups. The blastic transformation response to heart homogenates was present in 25% of the cases with active rheumatic carditis, in 15% without carditis, and in 46% of the patients with inactive valvular lesions.Plasma from the patients with active RF caused inhibition of the in vitro response of the normal lymphocytes to PHA.In the last few years, it has become increasingly apparent that, in addition to the well documented alterations in humoral immunity, ARF is also accompanied by abnormalities in cell-mediated immunity (CMI) where the precise significance in pathogenesis of rheumatic carditis remains controversial.Speculation: Patients with active rheumatic fever may have depressed cellular immune responses both in vivo and in vitro to PHA and specific antigens. Observations on the responses to SK-SD and heart homogenate in inactive rheumatic fever patients suggest that patients with rheumatic carditis build up a cellular immune response to the heart.Our findings also suggest that the possibility of lymphocyte sensitization by heart tissue antigens might play a part in the pathogenesis of rheumatic carditis. But the reason for hyporeactivity and the exact link if any between lymphocyte abnormalities and tissue lesions of rheumatic carditis remain to be elucidated.
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