The influence of UV-light (240-390 nm) at the dozes of 151 and 755 J/m2 on the maintenance of membrane markers of lymphocytes: CD3, CD19, CD4, CD8, CD25, CD95 using the method of flow cytometry was investigated. It was demonstrated that UV-irradiation of lymphocytes induced the decrease in the number of CD3, CD4 and CD19 markers together with a simultaneous increase of the amount of CD8, CD25 receptors during the daily incubation of cells in a nutrient medium without plasma. When autologous plasma is used during incubation of both native and UV-irradiated lymphocytes, the percentage of cells with the specified markers is not different from the corresponding values in the cells immediately after their purification. This finding points at the important role of antioxidants of the blood plasma and growth factors for the maintenance of the sub-population structure of lymphocytes. However, the level of expression of CD95, one of the markers of apoptosis, increases in the photomodified cells incubated both in the presence and in the absence of plasma. This increase was revealed to be caused mainly by the synthesis of the protein de novo under the influence of apoptosis-inducing factors.
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Immunopharmacol Immunotoxicol
February 2025
Nursing Department, College of Nursing and Health Sciences, Jazan University, Jazan, Saudi Arabia.
Background: One of the common findings in systemic sclerosis (SSc) patients has been long-term exposure to environmental toxins such as pesticides. However, the data available shows an equivocal association between pesticide exposure and autoimmunity in SSc.
Methods: We investigated the levels of organochlorine pesticides (OCPs) in blood of 20 SSc patients and 17 healthy controls, and also studied their effect on T lymphocytes and their functional responses.
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 PDFJCI Insight
December 2024
Department of Microbiology and Immunology, McGill University, Montreal, Quebec, Canada.
Deficits in IL-2 signaling can precipitate autoimmunity by altering the function and survival of FoxP3+ regulatory T cells (Tregs) while high concentrations of IL-2 fuel inflammatory responses. Recently, we showed that the non-beta IL-2 SYNTHORIN molecule SAR444336 (SAR'336) can bypass the induction of autoimmune and inflammatory responses by increasing its reliance on IL-2 receptor α chain subunit (CD25) to provide a bona fide IL-2 signal selectively to Tregs, making it an attractive approach for the control of autoimmunity. In this report, we further demonstrate that SAR'336 can support non-beta IL-2 signaling in murine Tregs and limit NK and CD8+ T cells' proliferation and function.
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.
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