Pathogenic mechanisms underlying the development of systemic lupus erythematosus (SLE) are very complex and not yet entirely clarified. However, the pivotal role of T lymphocytes in the induction and perpetuation of aberrant immune response is well established. Among T cells, IL-17 producing T helper (Th17) cells and regulatory T (Treg) cells represent an intriguing issue to be addressed in SLE pathogenesis, since an imbalance between the two subsets has been observed in the course of the disease. Treg cells appear to be impaired and therefore unable to counteract autoreactive T lymphocytes. Conversely, Th17 cells accumulate in target organs contributing to local IL-17 production and eventually tissue damage. In this setting, targeting Treg/Th17 balance for therapeutic purposes may represent an intriguing and useful tool for SLE treatment in the next future. In this paper, the current knowledge about Treg and Th17 cells interplay in SLE will be discussed.
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http://dx.doi.org/10.1155/2012/823085 | DOI Listing |
Pharmaceuticals (Basel)
January 2025
School of Life and Health Sciences, Hainan Province Key Laboratory of One Health, Collaborative Innovation Center of One Health, Hainan University, No. 58 Renmin Avenue, Haikou 570228, China.
Inflammatory bowel disease (IBD) is a persistent inflammatory condition affecting the gastrointestinal tract, distinguished by the impairment of the intestinal epithelial barrier, dysregulation of the gut microbiota, and abnormal immune responses. (L.) , traditionally used in Chinese herbal medicine for gastrointestinal issues such as bleeding and dysentery, has garnered attention for its potential therapeutic benefits.
View Article and Find Full Text PDFJ Clin Med
January 2025
Department of Prosthodontics, School of Dentistry, Rio de Janeiro State University, Rio de Janeiro 20551-030, Brazil.
: Cytokines related to the Th17 response have been associated with peri-implant diseases; however, the effect of peri-implant therapy on their modulation remains underexplored. To evaluate the effect of peri-implant therapy on the expression of cytokines related to the Th17 response in the peri-implant crevicular fluid (PICF) (GM-CSF, IFN-γ, IL-1β, IL-4, IL-6, IL-10, IL-12 (p70), IL-17A, IL-21, IL-23, and TNF-α) of partially edentulous patients with peri-implant disease (PID). : Thirty-seven systemically healthy individuals presenting with peri-implant mucositis (PIM) (n = 20) or peri-implantitis (PI) (n = 17) were treated and evaluated at baseline (T0) and three months after therapy (T1).
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Department of Medical Surgical Disciplines, Faculty of Medicine, Titu Maiorescu University of Bucharest, 031593 Bucharest, Romania.
In approximately half of the recurrent spontaneous abortion (RSA) cases, the underlying cause is unknown. However, most unexplained miscarriages are thought to be linked to immune dysfunction. This review summarizes the current evidence regarding the immunological evaluations of patients with RSA, with potential implications for clinical research.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Centro Nacional de Microbiología, Instituto de Salud Carlos III (ISCIII), Majadahonda, 28220 Madrid, Spain.
Class IA PI3K p110δ and p110α subunits participate in TCR and costimulatory receptor signals involved in T cell-mediated immunity, but the role of p110α is not completely understood. Here, we analyzed a mouse model of the Cre-dependent functional inactivation of p110α (kinase dead) in T lymphocytes (p110αKD-T, KD). KD mice showed increased cellularity in thymus and spleen and altered T cell differentiation with increased number of CD4CD8 DP thymocytes, enhanced proportion of CD4 SP lymphocytes linked to altered apoptosis, lower Treg cells, and increased AKT and ERK phosphorylation in activated thymocytes.
View Article and Find Full Text PDFMicroorganisms
January 2025
Intensive Care Unit, Sismanogleio General Hospital, 37 Sismanogleiou Str., 15126 Marousi, Greece.
Metabolic disorders, including type 2 diabetes mellitus (T2DM), obesity, and metabolic syndrome, are systemic conditions that profoundly impact the skin microbiota, a dynamic community of bacteria, fungi, viruses, and mites essential for cutaneous health. Dysbiosis caused by metabolic dysfunction contributes to skin barrier disruption, immune dysregulation, and increased susceptibility to inflammatory skin diseases, including psoriasis, atopic dermatitis, and acne. For instance, hyperglycemia in T2DM leads to the formation of advanced glycation end products (AGEs), which bind to the receptor for AGEs (RAGE) on keratinocytes and immune cells, promoting oxidative stress and inflammation while facilitating Staphylococcus aureus colonization in atopic dermatitis.
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