Contribution of gamma delta t-cell and dendritic cell subset in experimental DSS-induced colitis
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...
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| Format: | Final Year Project (FYP) |
| Language: | English |
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2014
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| Online Access: | http://hdl.handle.net/10356/60735 |
| _version_ | 1826121866556735488 |
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| author | Ricky Abdi Gunawan Koean |
| author2 | Ruedl Christiane |
| author_facet | Ruedl Christiane Ricky Abdi Gunawan Koean |
| author_sort | Ricky Abdi Gunawan Koean |
| collection | NTU |
| description | 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. |
| first_indexed | 2024-10-01T05:39:31Z |
| format | Final Year Project (FYP) |
| id | ntu-10356/60735 |
| institution | Nanyang Technological University |
| language | English |
| last_indexed | 2024-10-01T05:39:31Z |
| publishDate | 2014 |
| record_format | dspace |
| spelling | ntu-10356/607352023-02-28T18:00:45Z Contribution of gamma delta t-cell and dendritic cell subset in experimental DSS-induced colitis Ricky Abdi Gunawan Koean Ruedl Christiane School of Biological Sciences DRNTU::Science 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. Bachelor of Science in Biological Sciences 2014-05-29T08:01:17Z 2014-05-29T08:01:17Z 2014 2014 Final Year Project (FYP) http://hdl.handle.net/10356/60735 en Nanyang Technological University 38 p. application/pdf |
| spellingShingle | DRNTU::Science Ricky Abdi Gunawan Koean Contribution of gamma delta t-cell and dendritic cell subset in experimental DSS-induced colitis |
| title | Contribution of gamma delta t-cell and dendritic cell subset in experimental DSS-induced colitis |
| title_full | Contribution of gamma delta t-cell and dendritic cell subset in experimental DSS-induced colitis |
| title_fullStr | Contribution of gamma delta t-cell and dendritic cell subset in experimental DSS-induced colitis |
| title_full_unstemmed | Contribution of gamma delta t-cell and dendritic cell subset in experimental DSS-induced colitis |
| title_short | Contribution of gamma delta t-cell and dendritic cell subset in experimental DSS-induced colitis |
| title_sort | contribution of gamma delta t cell and dendritic cell subset in experimental dss induced colitis |
| topic | DRNTU::Science |
| url | http://hdl.handle.net/10356/60735 |
| work_keys_str_mv | AT rickyabdigunawankoean contributionofgammadeltatcellanddendriticcellsubsetinexperimentaldssinducedcolitis |