The number and activity of CD3TCR Vα7.2CD161 cells are increased in children with acute rheumatic fever.

BACKGROUND

Acute rheumatic fever (ARF) is an autoimmune disease caused by group A β-hemolytic streptococci (GAS) and may develop into rheumatic heart disease (RHD). The pathogenesis of ARF and RHD involves molecular mimicry and antibody-mediated mechanisms. T cell involvement is described in various stages of the disease. Mucosal associated invariant T (MAIT) cells are enriched at the mucosa and are present in the blood and may be activated by GAS.

METHODS

In this study, we investigated the quantity and activity of CD3TCRVα7.2CD161 cells in the active and recovered ARF patients and healthy controls. Twenty newly diagnosed, 20 recovered-ARF children, and 20 healthy controls were enrolled in the study. Peripheral blood (PB) mononuclear cells were isolated by Ficoll-Paque density gradient. CD4, CD4 subsets of CD3CD161TCRVα7.2 cells and IFN-γ and TNF-α production were quantified by Flow cytometry.

RESULTS

Acute and recovered ARF patients had significantly elevated the number of CD3TCRVα7.2CD161 cells in their PB. Both CD4 and CD4 subsets were increased. Moreover, total CD3TCRVα7.2CD161 cell numbers were significantly higher in the recovered patients' PB compared with active ARF patients. In addition, CD3TCRVα7.2CD161 cells in both acute and recovered patients produced significantly more IFN-γ and TNF-α. Non-MAIT total CD3 T cell, CD4 and CD4 T cell subsets were also increased in active and recovered ARF patients and they also produced more IFN-γ and TNF-α.

CONCLUSION

Our data reveal that CD3TCRVα7.2CD161 cells are elevated and actively producing IFN-γ and TNF-α in acute and recovered ARF patients and may contribute to ARF pathology.