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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Background And Purpose: The CD4+CD25+ regulatory T (Treg) cells exert immunoregulatory functions in various autoimmune diseases, in part through transforming growth factor-beta1 (TGF-beta1), and can be expanded by TGF-beta1 stimulation in normal subjects. This study aimed to examine intrinsic TGF-beta1 expression and the response to TGF-beta1 stimulation of this CD4+CD25+ subset in patients with systemic lupus erythematosus (SLE).
Methods: Flow cytometry with multicolor staining of CD4+, CD25+, and TGF-beta1 was used to quantify the percentage of CD4+CD25+ T cells in fresh peripheral blood and TGF-beta1-stimulated peripheral blood mononuclear cell (PBMC) cultures, and their corresponding intracellular TGF-beta1 expression.
Results: In fresh peripheral blood, we found that decreased percentages of CD4+CD25+/CD4+ in SLE patients were associated with disease activity and renal involvement. Intracellular TGF-beta1 expression of CD4+CD25+ cells was significantly elevated in SLE compared with matched controls (p<0.001). In addition, there was significant negative correlation between TGF-beta1 expression and percentage of CD4+CD25+ cells present (r = -0.432, p=0.004). Nevertheless, in ex vivo unstimulated PBMC cultures, the percentage and intracellular TGF-beta1 expression of CD4+CD25+ cells of SLE were normalized to the levels of the control group. In TGF-beta1-stimulated PBMC cultures, CD4+CD25+ cells and their intracellular TGF-beta1 expression were significantly increased (p<0.001), both in SLE and controls. Moreover, the increments in the percentage of CD4+CD25+ cells and intracellular TGF-beta1 expression by TGF-beta1 stimulation were comparable in SLE and controls, and were not significantly influenced by disease activity or renal involvement in SLE.
Conclusions: CD4+CD25+ cells were deficient in peripheral blood but not impaired either in intrinsic TGF-beta1 expression or in response to TGF-beta1 stimulation in patients with SLE. This study suggests that TGF-beta1, by inducing CD4+CD25+ cells, has potential clinical application in treating SLE.
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Microb Pathog
December 2024
Center of Molecular Metabolism, Nanjing University of Science and Technology, 200 Xiaolingwei Street, Nanjing, 210094, China.. Electronic address:
Sepsis remains a life-threatening condition with high mortality rates despite current therapeutic approaches. While Huang-Lian-Jie-Du Decoction (HLJDD), a traditional Chinese medicine formula, has been historically used to treat inflammatory conditions, its therapeutic potential in sepsis and underlying mechanisms remain unexplored. This study investigated HLJDD's comprehensive effects on sepsis pathophysiology using a rat cecal ligation and puncture (CLP) model.
View Article and Find Full Text PDFInt Immunopharmacol
December 2024
Department of Immunology, Tarbiat Modares University, Tehran, Iran.
Sulfur mustard (SM) induced pulmonary disorder is a heterogeneous disease characterized by uncontrolled inflammatory immune responses. In this cross-sectional study carried out in Isfahan-Iran, our objective was to thoroughly evaluate the clinical health and peripheral blood leukocyte profiles of adult veterans exposed to SM 25-30 years. In total, 361 people were studied in two groups, 287 chemical veterans with pulmonary complications and 64 healthy individuals as a control group.
View Article and Find Full Text PDFClin Transl Med
December 2024
Andalusian Center of Molecular Biology and Regenerative Medicine-CABIMER, Junta de Andalucía-University of Pablo de Olavide-University of Seville-CSIC, Seville, Spain.
Background: The complex aetiology of type 1 diabetes (T1D), characterised by a detrimental cross-talk between the immune system and insulin-producing beta cells, has hindered the development of effective disease-modifying therapies. The discovery that the pharmacological activation of LRH-1/NR5A2 can reverse hyperglycaemia in mouse models of T1D by attenuating the autoimmune attack coupled to beta cell survival/regeneration prompted us to investigate whether immune tolerisation could be translated to individuals with T1D by LRH-1/NR5A2 activation and improve islet survival.
Methods: Peripheral blood mononuclear cells (PBMCs) were isolated from individuals with and without T1D and derived into various immune cells, including macrophages and dendritic cells.
Background: Allergen-specific immunotherapy (AIT) is so far the only disease-modifying therapy for allergy, resulting in a long-lasting tolerance. However, the existing safety concerns and the need for more efficacious alternatives that shorten the duration of treatment have stimulated research into the development of novel alternatives. Some of these novel alternatives involve modifying allergens with molecules that target innate immunomodulatory receptors to suppress the immune activity of immune cells.
View Article and Find Full Text PDFTransl Androl Urol
November 2024
Department of Urology, Xijing Hospital, Air Force Medical University, Xi'an, China.
Background: Previous studies have investigated the association between immune inflammation, metabolism and erectile dysfunction (ED). However, these studies are limited by biases, confounding factors, and reverse causality, failing to establish causality. We conducted a two-sample Mendelian randomization (MR) study to elucidate the causal relationships between immune cells, inflammatory cytokines, plasma metabolites, and the risk of ED.
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