Abstract
This study analyzed the expression of membrane OX40 and OX40L (mOX40 and mOX40L) and levels of soluble OX40 and OX40L (sOX40 and sOX40L) in T1D patients to determine their clinical significance. Peripheral blood (PB) was collected from patients with T1D and healthy control participants. Expression of mOX40 and mOX40L on immune cells was detected by flow cytometry. Levels of sOX40 and sOX40L in sera were measured by ELISA. We demonstrated for the first time enhanced sOX40 and sOX40L expression and reduced mOX40 and mOX40L levels in T1D patients which correlated with the clinical characteristics and inflammatory factors. These results suggest that OX40/OX40L signal may be promising biomarkers and associated with the pathogenesis of T1D.
Highlights
Type 1 diabetes (T1D) is a chronic and organ-specific autoimmune disease, is influenced by inherited or environmental factors, is increasing in all age groups, especially examined in children, and leads to the loss of insulin production in beta cells when immune cells invade the pancreatic islets [1,2,3]
To characterize OX40 and OX40L expression and determine the role of OX40/OX40L signal in the development and pathogenesis of T1D, we evaluated the expression of sOX40 and sOX40L in the peripheral blood mononuclear cell (PBMC) and sera of patients with T1D and healthy controls (HCs) and analyzed the correlation with clinical and inflammatory indicators
Flow cytometry analyses demonstrated that OX40 expression on CD3+, CD4+, and CD8+ T cells in PBMC samples was less frequent in patients with T1D than HCs (14 34 ± 1 02% vs. 22 47 ± 1 87%, p = 0 003; 18 78 ± 1 31% vs. 24 85 ± 1 87%, p = 0 093; and 7 94 ± 0 66% vs. 15 9 ± 1 87%, p < 0 001; respectively) (Figures 1(a) and 1(b))
Summary
Type 1 diabetes (T1D) is a chronic and organ-specific autoimmune disease, is influenced by inherited or environmental factors, is increasing in all age groups, especially examined in children, and leads to the loss of insulin production in beta cells when immune cells invade the pancreatic islets [1,2,3]. The activation of T cells is mediated by antigen stimulation through T cell receptors and some costimulatory molecules. It has been suggested that CTLA-4 and PD-1 contribute to the development of T1D [4,5,6]. Multiple clinical immune intervention trials have been provided for the treatment of T1D such as blocking the costimulation of T cells [7,8,9]. The contributions of OX40 and OX40L to the development of T1D remain to be studied. OX40/OX40L is a pair of important positive costimulatory signal molecules in the second signal system of T cells
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