Doganay, Fulya (2021) Effector T cells in celiac disease: Comprehensive study on their interaction in chronic inflammation and autoimmunity. Master's Research Project 2, Biomedical Sciences.
|
Text
FDoganaySecondResearchPAugust21.pdf Download (1MB) | Preview |
|
Text
toestemming.pdf Restricted to Registered users only Download (162kB) |
Abstract
Celiac disease (CeD) is a common autoimmune disease, mainly mediated by T cells. It involves CD4+ T cell-mediated gluten recognition, and effector T cells, including CD8+ and γδ T cell subsets. Gliadin-derived peptides, derived from gluten, activate lamina propria gliadin-specific CD4+ T cells in a TCR dependent manner, which leads to the release of cytokines. A non-circulating subset of effector T cells called tissue residency memory T cells (TRM) play a crucial role in the pathogenesis of CeD. These effector T cell subsets produce pro-inflammatory cytokines and cause inflammation and further injury in the intestine. CeD pathogenesis is also linked to resistance to Treg suppression by the potent cytotoxicity of IL (Interlukin)-15. Furthermore, such resistance may play a role in the development of autoimmune disease.Effector T lymphocytes from active CeD become resistant to suppression by Treg. This resistance might cause a loss of tolerance to gluten. This role for TRM cells in intestinal autoimmunity raises the possibility for therapeutics directed at resident T cell populations. In this review, we sought to examine the putative novel treatment to restore anti-inflammatory cytokines and optimal manipulation of Treg suppression and mitigate the inflammatory role of Teff (T effector) cells.
Item Type: | Thesis (Master's Research Project 2) |
---|---|
Supervisor name: | Jonkers, I.H. |
Degree programme: | Biomedical Sciences |
Thesis type: | Master's Research Project 2 |
Language: | English |
Date Deposited: | 11 Feb 2022 09:46 |
Last Modified: | 11 Feb 2022 09:46 |
URI: | https://fse.studenttheses.ub.rug.nl/id/eprint/26588 |
Actions (login required)
View Item |