Objective: To investigate the expression of CD(4)(+) CD(25)(+) regulatory T cells (Tregs) in the peripheral blood and salivary gland of patients with primary Sjögren's syndrome (pSS).
Methods: Samples of peripheral venous blood were collected from 57 newly diagnosed pSS patients, 1 male and 56 females, aged 47 (20 approximately 76), and 46 healthy controls. The levels of CD(4)(+) CD(25)(+) T regulatory cells and CD(4)(+) CD(25)(high) T regulatory cells in the peripheral blood were measured by flow-cytometric assay. Biopsy specimens of labial gland were collected from the 57 patients and 6 healthy person or patients with labial gland cyst. Pathological examination was conducted by light microscopy. Immunohistochemistry was conducted, by using monoclonal mouse anti-human to detect the expression of CD25, CD4, CD8, and CD68. Western blotting was used to detect the levels of IgG, IgM, and IgA. The salivary flow rate was measured. Schirmer's test was used to measure the tear flow rate.
Results: The level of CD(4)(+) CD(25)(+) Tregs in the blood of pSS patients was 6.9% (2.84% - 13.50%), significantly lower than that of the healthy controls [10.9% (5.77% - 15.3%), P < 0.001). The level of CD(4)(+) CD(25)(high) Tregs the blood of pSS patients was 0.6% (0.001% - 1.83%), significantly lower than that of the healthy controls [1.1% (0.13% - 2.45%), P < 0.001]. Immunohistochemistry showed that most of the infiltrating lymphocytes in the labial gland of the pSS patients were CD(4)(+) T cells, and there was no CD(25)(+) T cell in both groups. The numbers of peripheral CD(4)(+) CD(25)(+) T cells and CD(4)(+) CD(25)(high) Tregs in the pSS patients were not correlated with the tear flow rate, salivary flow rate, anti-SS-A/SS-B antibodies, and immunoglobulin level.
Conclusion: The pSS patients show an absence of CD(4)(+) CD(25)(+) T cell in the labial gland of pSS patients, and reduction of the numbers of CD(4)(+) CD(25)(+) and CD(4)(+) CD(25)(high) Tregs in the peripheral blood, which suggests that Tregs play an important role in the pathogenesis of salivary gland destruction in SS.