apyrase and Colitis--Ulcerative

apyrase has been researched along with Colitis--Ulcerative* in 2 studies

Other Studies

2 other study(ies) available for apyrase and Colitis--Ulcerative

ArticleYear
CD39/CD73/A2a Adenosine Metabolic Pathway: Targets for Moxibustion in Treating DSS-Induced Ulcerative Colitis.
    The American journal of Chinese medicine, 2021, Volume: 49, Issue:3

    Ulcerative Colitis (UC) is a chronic inflammation disease, and the incidence of UC is increasing recently. Both clinical trials and animal experiments show that moxibustion is a complementary and alternative treatment for UC. Previous studies showed that moxibustion can improve UC by regulating the balance of Tregs and Th17 (Sun

    Topics: 5'-Nucleotidase; Animals; Antigens, CD; Apyrase; Cell Survival; Colitis, Ulcerative; Colon; Dextran Sulfate; Disease Models, Animal; Epithelial Cells; Interleukin-6; Mice; Moxibustion; Receptor, Adenosine A2A; Signal Transduction; Tumor Necrosis Factor-alpha

2021
Heightened Expression of CD39 by Regulatory T Lymphocytes Is Associated with Therapeutic Remission in Inflammatory Bowel Disease.
    Inflammatory bowel diseases, 2015, Volume: 21, Issue:12

    To evaluate whether changes in expression of CD39 by regulatory T lymphocytes (Treg) impact treatment response in inflammatory bowel disease. To then define the biological role of expression of CD39 on Treg in an animal model of colitis.. A prospective study of consecutive patients commencing anti-tumor necrosis factor therapy with infliximab (IFX) or adalimumab (ADA), who were then followed for 12 months. Treatment responses were defined both symptomatically and by endoscopy showing mucosal healing. Peripheral blood Tregs were quantified by flow cytometry. Functional importance of CD39 expression by Treg was determined in an adoptive T-cell transfer model of colitis.. Forty-seven patients (ulcerative colitis, n = 22; Crohn's disease, n = 25) were recruited; 16 patients were complete responders and 13 nonresponders to anti-tumor necrosis factor. CD39 expression by Treg was lower in active inflammatory bowel disease and increased significantly after treatment in responders (CD39Treg/total Treg; 8% at baseline to 22.5% at late time point, P < 0.001). Responders were more likely to have therapeutic drug levels and in multivariate analysis therapeutic drug levels were associated with higher expression of CD39 by FoxP3 Treg and lower frequencies of interleukin 17A expressing cells. Tregs with genetic deletion of CD39 exhibit decrements in potential to suppress intestinal inflammation in a murine (CD45RB) T-cell transfer model of colitis in vivo, when compared with wild-type Treg.. Increased expression of CD39 by peripheral blood Treg is observed in the setting of clinical and endoscopic remission in inflammatory bowel disease. Deficiency of CD39 expression by Treg can be linked to inability to suppress experimental colitis.

    Topics: Adalimumab; Adult; Animals; Anti-Inflammatory Agents; Antibodies, Monoclonal; Antigens, CD; Apyrase; Colitis, Ulcerative; Crohn Disease; Female; Gastrointestinal Agents; Humans; Immunologic Factors; Infliximab; Interleukin-17; Male; Mice; Middle Aged; Prospective Studies; Remission Induction; T-Lymphocytes, Regulatory; Tumor Necrosis Factor-alpha; Young Adult

2015