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display heightened levels of circulating inflammatory markers such as tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), IL-1β, and monocyte chemoattractant protein 1 (MCP-1), as well as decreased plasma levels of anti-inflammatory cytokines
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expression of cytokines and cellular adhesion molecules important for the migration and homing of LCs has been described ( 9 ). On the other hand, the infiltration of organs by a monoclonal cell population and the discovery of v-Raf murine sarcoma viral
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transcription and release of a broad range of pro- and anti-inflammatory cytokines, e.g. TNF-α ( 11 , 12 ). Furthermore, the same mechanism leads to shedding of sCD163, which can be measured in the circulation as a robust marker of macrophage activation ( 13
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inflammatory disorder characterized by chronic low-grade inflammation and excessive production of pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). Experimental and clinical evidence suggests that chronic
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Institute of Oncology, The Affiliated Hospital of Jiangsu University, Zhenjiang, China
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, 13 ), the pathogenesis of HT remains unclear. During HT pathogenesis, the cytokine IL-1 has been reported to stimulate thyroid follicular cell (TFC) proliferation and produce other pro-inflammatory cytokines, such as IL-6 and IL-8, which in turn
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Clinical Research Centre, Medical University of Bialystok, Bialystok, Poland
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proinflammatory cytokines such as interleukin-6 (IL6), IL12, or IL17 ( 8 , 9 ). Specific chemokines that are also related to the pathogenesis of this disease include C-X-C motif chemokine ligand 9 (CXCL9), CXCL10, CXCL11, and their receptor chemokine receptor
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tumor tissues ( 6 ). IL-6 belongs to the main member of the IL-6 cytokine family and regulates multitudinous functions related to biological metabolism and immunity ( 7 ). Abnormal IL-6 cytokine expression and its aberrant downstream signaling activation
Shanghai National Clinical Research Center for Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of the National Health Commission of the PR China, Shanghai National Center for Translational Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China
Guangdong Geriatric Institute, Guangdong Provincial People’s Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China
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Shanghai National Clinical Research Center for Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of the National Health Commission of the PR China, Shanghai National Center for Translational Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China
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Shanghai National Clinical Research Center for Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of the National Health Commission of the PR China, Shanghai National Center for Translational Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China
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Reproductive Medicine Center, Guangdong Provincial People’s Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China
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Shanghai National Clinical Research Center for Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of the National Health Commission of the PR China, Shanghai National Center for Translational Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China
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Division of Endocrinology, Department of Internal Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China
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Shanghai National Clinical Research Center for Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of the National Health Commission of the PR China, Shanghai National Center for Translational Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China
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related diseases. As indispensable components of immunity, CD4+ T lymphocytes play vital roles during the course of GD. The infiltration of T lymphocytes leads to the destruction of thyroid tissues, which synthesize proinflammatory cytokines to maintain
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(MCP1 (CCL2)) and plasminogen activator inhibitor (PAI1 (SERPINE1)), as well as proinflammatory cytokines, such as tumor necrosis factor alpha (TNFα (TNF)), interleukin 1 (IL1 (IL1A)), IL6, and IL8 (CXCL8) (37, 38) . Differences in the production of
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-grade inflammatory disease characterized by increased circulating concentrations of inflammatory cytokines and the recruitment of immune cells, including macrophages and T cells, to metabolic tissues ( 2 ). Myeloid-derived suppressor cells (MDSCs) represent a group