Contribution of gamma delta t-cell and dendritic cell subset in experimental DSS-induced colitis

• Main Author: Ricky Abdi Gunawan Koean
• Other Authors: Ruedl Christiane
• Format: Final Year Project
• Language: English
• Published: 2014
• Subjects: DRNTU::Science
• Online Access: http://hdl.handle.net/10356/60735
• Institution: Nanyang Technological University

The ability of our gastrointestinal tract to maintain balance between its commensal and host immune response through a structured mucosal barrier is very delicate. Therefore, impairment in the structure mucosal barrier would lead to development of inflammatory bowel disease. In this dissertation, we investigated the contribution of a subset of T cell, the Gamma Delta-T cells as well different DCs subsets found in lamina propria in an acute colitis model. In order to achieve this, the Gamma Delta-T cells deficient mice were back crossed with two distinct mice phenotypes which carry Diphtheria toxin receptor (DTR) on their dendritic cells (DCs). Clec9a-DTR mice express DTR on their CD11c+CD103+CD11b- DC population while Clec4a4-DTR mice express DTR on CD11c+CD103+CD11b+ DCs. Thus upon injection of Diptheria toxin (DT), we are able to ablate these specific population of DCs. Through the characterization of the intestinal Gamma Delta-T cells we have found a higher population ratio of IL-17 producing Vgamma4 Gamma Delta-T cell in the distal part of the colon. We also seemed to observe that the Gamma Delta-T cell number including Vgamma4 Gamma Delta-T cell is controlled by CD11c+CD103+CD11b- DCs during steady state and inflammation. Furthermore, in our acute Dextran Sulphate Sodium (DSS)-induced colitis model, Gamma Delta-T cells are likely to play regulatory functions. In the absence of Gamma Delta-T cells, the disease progression accelerated even in the presence or absence of CD11c+CD103+CD11b- DCs.