Background Treg cells play an important role in the maintenance of peripheral immunological self-tolerance through suppression of self-reactive T cells. Changes of the proportion of Treg cells within T cells as well as that of Treg subpopulations such as CD45RA+FoxP3lo resting Treg (rTreg) and CD45RA-FoxP3hi activated Treg (aTreg) in peripheral blood have been reported in several autoimmune diseases, but results have been variable.
Objectives We investigated the proportion of Treg cell and its subpopulations in peripheral blood from patients with three autoimmune diseases, SLE, RA and BD. Then we intended to find possible relationships between changes of Treg cells and autoimmune mechanisms in such disease.
Methods Peripheral blood samples were obtained from 42 rheumatoid arthritis (RA), 13 systemic lupus sclerosis (SLE), 7 Behcet’s disease (BD) and 22 healthy controls. In flow cytometric analysis, CD4+CD25highFoxP3+ population was analyzed as Treg cells. The CD4+CD25++CD45RA+ and CD4+CD25+++CD45RA- cell populations were gated as rTreg and aTreg, respectively.
Results The proportion of CD4+CD25highFoxP3+ Treg was significantly lower in RA patients (P<0.001) and BD patients (P<0.01) compared to healthy controls. SLE patients also showed lower proportion of CD4+CD25highFoxP3+ Treg cells than controls, but it was not statistically significant. The proportion of rTreg and non-suppressive T cells were similar among RA, SLE and BD patients and healthy controls. However, the proportion of aTreg was significantly lower in RA patients (P<0.01) and BD patients (P<0.05) compared to healthy controls. Comparison of the ratio of aTreg to rTreg revealed a significantly decreased ratio in RA patients compared to healthy controls (P<0.01). SLE and BD patients did not show statistically significant changes of the ratio of aTreg to rTreg compared to controls.
Conclusions The decrement of Treg population was significant in RA and BD patients than SLE, and these findings likely resulted from the decrement of the aTreg subpopulation fraction. Although a variety of studies has evaluated Treg in autoimmune diseases, we suggest that the distinction and evaluation of the proportions of Treg subpopulation, especially aTreg, would be more informative in assessing the dynamics of Treg cells as well as understanding the mechanism of autoimmune diseases.
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Disclosure of Interest None Declared