In healthy individuals, the interaction between intestinal epithelial cells and lamina propria lymphocytes (LPL) gives rise to a population of CD8 + T cells with suppressor function (Ts). Loss of this homeostasis can result in mucosal inflammation. Ts lines were generated from the LP of normal and Ulcerative Colitis patients and were able to suppress CD4 + T cell proliferation in a contact dependent fashion. In contrast, Ts lines generated from Crohn’s disease (CD) patients had a markedly decreased capacity to mediate suppression. Expression of neither surface/intracytoplasmic markers nor secreted cytokines could explain this difference. Microarray analysis of the RNA from these lines showed differential expression in multiple genes regulated by TGF-β. CD tissue cultures produced high levels of TGF-β compared to controls. Interestingly, introducing TGF-β or supernatants from CD tissue cultures, into the suppressor assay, resulted in reduced suppressor activity in a dose dependent fashion. This could explain the defect in suppression in CD.
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|Advisor:||Mayer, Lloyd, Berin, Cecilia|
|Commitee:||Blander, Julie M., Braun, Jonathan, Cortes, Patricia, Merad, Miriam|
|School:||Mount Sinai School of Medicine|
|School Location:||United States -- New York|
|Source:||DAI-B 73/05, Dissertation Abstracts International|
|Subjects:||Cellular biology, Immunology|
|Keywords:||CD8+ T cells, Crohn's disease, Intestines, Suppression, TGF-beta|
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