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.