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B7-H4 deficiency in salivary gland of patients with primary Sjögren's syndrome impairs the regulatory effect on T cells.
International Journal of Rheumatic Diseases 2017 April
AIM: Our previous study confirmed the defect of B7-H4 expression in peripheral blood and salivary glands of patients with primary Sjögren's syndrome (pSS). The aim of this study was to analyze the effect of the deficit expression of B7-H4 on CD4+ T cells.
METHODS: CD4+ T cells were purified by magnetic-activated cell sorting MACS. The proliferation and cytokine production of CD4+ T cells co-cultured with purified salivary gland epithelial cells (SGECs) from pSS or non-SS sicca syndrome were detected.
RESULTS: By co-culturing the gland cells with CD4+ T cells, we found the proliferation of CD4+ T cells was significantly suppressed. The effect was weaker when SGECs from pSS patients were used compared to that from non-pSS sicca syndrome controls. Simultaneously, the productions of cytokines interleukin (IL)-5, IL-13, IL-17A, IL-6 in supernatant were reduced and also SGECs from pSS patients decreased them less than that from non-SS controls.
CONCLUSIONS: The decrease of B7-H4 expression in salivary glands of SS patients contributes to the defect of negatively regulating the inflammation caused by CD4+ T cells, thereby providing new insights into the role of B7-H4 in the inflammatory process of salivary glands in SS.
METHODS: CD4+ T cells were purified by magnetic-activated cell sorting MACS. The proliferation and cytokine production of CD4+ T cells co-cultured with purified salivary gland epithelial cells (SGECs) from pSS or non-SS sicca syndrome were detected.
RESULTS: By co-culturing the gland cells with CD4+ T cells, we found the proliferation of CD4+ T cells was significantly suppressed. The effect was weaker when SGECs from pSS patients were used compared to that from non-pSS sicca syndrome controls. Simultaneously, the productions of cytokines interleukin (IL)-5, IL-13, IL-17A, IL-6 in supernatant were reduced and also SGECs from pSS patients decreased them less than that from non-SS controls.
CONCLUSIONS: The decrease of B7-H4 expression in salivary glands of SS patients contributes to the defect of negatively regulating the inflammation caused by CD4+ T cells, thereby providing new insights into the role of B7-H4 in the inflammatory process of salivary glands in SS.
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