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Abstract

ABSTRUCT: BACKGROUND: CD4+CD25+ regulatory T cells are known to suppress the immune response in general, these cells were studied in the presence of streptococcal M protein which has an important role in the pathogenesis of rheumatic heart disease. OBJECTIVE: The purpose of this study was to determine the role of streptococcal M protein in naturally occurring CD4+CD25+ regulatory T cells (nTregs) function and development in rheumatic heart disease Iraqi patients. METHODS: Streptococcus pyogenes was isolated for subsequent M protein extraction. Also, peripheral blood nTregs and CD4+ T cells were isolated by using Magnetic Cell Separation System (MACS). Tissue culture system for isolated cells was performed in the presence and absence of M protein stimulation. Cell count was performed, also, TNF-α, and IL-4 were determined in culture supernatant using ELISA system. RESULTS: It was found a highly significant positive association between the number of the cellular proliferation for both nTregs and CD4+ T cells with or without streptococcal M protein stimulation in isolated cell culture systems (p < 0.01), but, there found a highly significant negative correlation between the mean number of nTregs and CD4+ T cells in mixed culture system in the absence of M protein (r = -0.995). whereas, in the presence of M protein, there was a positive non-significant association between the mean number of both nTregs and CD4+ T cells (r = 0.353) (p > 0.05). Results obtained from ELISA test revealed that M protein-stimulated CD4+ T cells produced IL-4 in very little amounts (< 4 pg/ml) in all cultures of samples and there was no significant difference among them. Whereas, TNF-α was produced in higher concentrations in the culture supernatants when compared with IL-4. CONCLUSION: Streptococcal M protein has an important role in increasing the proliferation of both CD4+CD25+ regulatory T cells and CD4+ T cells, but the newer generation of CD4+CD25+ regulatory T cells in the presence of M protein has lower suppressive activity against CD4+ T cells.

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