Mechanisms of Host Viral Interactions Leading to Loss of Oral Tolerance in Celiac Disease Patients
Session Number
C32
Advisor(s)
Romain Bouziat, University of Chicago Reinhard Hinterleitner, University of Chicago Bana Jabri, University of Chicago
Location
B-131 Grainger
Start Date
28-4-2016 2:00 PM
End Date
28-4-2016 2:25 PM
Abstract
Celiac disease is a complex autoimmune disorder induced by the ingestion of gluten that causes inflammation and mucosal damage in the small intestine due to a loss of tolerance to gluten. Past studies have suggested that virus infections play a role in the development of celiac disease. In this investigation, we aimed to study how infection by reovirus T1L affects the gene expression of IL-27 and IL-12, important for oral tolerance, in type-1 interferon knockout mice and interferon regulatory factor 1 (IRF1) knockout mice. Through real time polymerase chain reaction (qPCR) and flow cytometry (FACS staining), we gathered results showing that IRF1 KO mice had no significant increase in gene expression of IL-27 or IL-12 when infected by T1L, indicating that removal of the IRF1 gene can restore oral tolerance. Looking forward, we will continue studying the mechanisms that lead to oral tolerance by looking at other genes such as IL-12 and BATF3 expressed in certain dendritic cell subsets important to maintain oral tolerance.
Mechanisms of Host Viral Interactions Leading to Loss of Oral Tolerance in Celiac Disease Patients
B-131 Grainger
Celiac disease is a complex autoimmune disorder induced by the ingestion of gluten that causes inflammation and mucosal damage in the small intestine due to a loss of tolerance to gluten. Past studies have suggested that virus infections play a role in the development of celiac disease. In this investigation, we aimed to study how infection by reovirus T1L affects the gene expression of IL-27 and IL-12, important for oral tolerance, in type-1 interferon knockout mice and interferon regulatory factor 1 (IRF1) knockout mice. Through real time polymerase chain reaction (qPCR) and flow cytometry (FACS staining), we gathered results showing that IRF1 KO mice had no significant increase in gene expression of IL-27 or IL-12 when infected by T1L, indicating that removal of the IRF1 gene can restore oral tolerance. Looking forward, we will continue studying the mechanisms that lead to oral tolerance by looking at other genes such as IL-12 and BATF3 expressed in certain dendritic cell subsets important to maintain oral tolerance.