Immune-mediated inflammatory diseases are various groups of conditions that result in immune system disorders and increased cancer risk. Despite the identification of causative cytokines and pathways, current clinical treatment for immune-mediated inflammatory diseases is limited. In addition, immune-mediated inflammatory disease treatment can increase the risk of cancer. Several previous studies have demonstrated that Toxoplasma gondii manipulates the immune response by inhibiting or stimulating cytokines, suggesting the potential for controlling and maintaining a balanced immune system. Additionally, T. gondii also has the unique characteristic of being a so-called "Trojan horse" bacterium that can be used as a drug delivery system to treat regions that have been resistant to previous drug delivery therapies. In this study, we reviewed the potential of T. gondii in drug development and as a delivery system through current research on inflammation-regulating mechanisms in immune-mediated inflammatory diseases.
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http://dx.doi.org/10.1038/s12276-024-01165-7 | DOI Listing |
Adv Healthc Mater
January 2025
State Key Laboratory of Oral Diseases, National Center for Stomatology, National Clinical Research Center for Oral Diseases, Department of Orthodontics, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041, China.
Immune-mediated bone regeneration driven by bone biomaterials offers a therapeutic strategy for repairing bone defects. Among 2D nanomaterials, TiCT MXenes have garnered substantial attention for their potential in tissue regeneration. This investigation concentrates on the role of MXene nanocomposites in modulating the immune microenvironment within bone defects to facilitate bone tissue restoration.
View Article and Find Full Text PDFInflamm Res
January 2025
Departments of Oral Medicine, Stomatological Hospital, School of Stomatology, Southern Medical University, Guangzhou, Guangdong Province, China.
Mucosal-associated invariant T (MAIT) cells, a type of T lymphocytes with innate-like characteristics, are crucial in bridging innate and adaptive immunity. When activated, MAIT cells release various inflammatory molecules and swiftly respond to antigens. Notably, numerous studies highlight the significant impact of MAIT cells on tumors and various immune disorders by influencing the immune microenvironment.
View Article and Find Full Text PDFNPJ Digit Med
January 2025
Department of Neurology, University Hospital Schleswig-Holstein Campus Kiel, Kiel University, Kiel, Germany.
Fatigue is prevalent in immune-mediated inflammatory and neurodegenerative diseases, yet its assessment relies largely on patient-reported outcomes, which capture perception but not fluctuations over time. Wearable sensors, like inertial measurement units (IMUs), offer a way to monitor daily activities and evaluate functional capacity. This study investigates the relationship between sit-to-stand and stand-to-sit transitions and self-reported physical and mental fatigue in participants with Parkinson's, Huntington's, rheumatoid arthritis, systemic lupus erythematosus, primary Sjögren's syndrome and inflammatory bowel disease.
View Article and Find Full Text PDFImmun Inflamm Dis
January 2025
IBD Unit, IRCCS Sacro Cuore Don Calabria, Negrar, Italy.
Background: Immune-mediated inflammatory diseases (IMIDs) are a group of chronic conditions characterized by dysregulated immune responses and persistent inflammation. Rheumatoid arthritis (RA), spondyloarthritis (SpA), and ulcerative colitis (UC) exemplify prominent IMIDs, each presenting unique challenges for their management, that impact patient's quality of life (QoL). Obesity, marked by persistent low-grade inflammation, influences the progression, response to treatment, and clinical management of patients with RA, SpA, and UC.
View Article and Find Full Text PDFFASEB J
January 2025
School of Pharmacy, Anhui Medical University, Hefei, China.
The activation of acid-sensing ion channel 1a (ASIC1a) in response to extracellular acidification leads to an increase in extracellular calcium influx, thereby exacerbating the degeneration of articular chondrocytes in rheumatoid arthritis (RA). It has been suggested that the inhibition of extracellular calcium influx could potentially impede chondrocyte ferroptosis. The cystine transporter, solute carrier family 7 member 11 (SLC7A11), is recognized as a key regulator of ferroptosis.
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