Session 2F: Mechanisms of Host Viral Interactions Leading to Loss of Oral Tolerance in Celiac Disease Patients
Session Number
Session 2F:3rd Presentation
Advisor(s)
Bana Jabri, University of Chicago
Location
Room A115
Start Date
28-4-2017 10:00 AM
End Date
28-4-2017 11:15 AM
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 shown that virus infections also play a role in the development of celiac disease by stimulating an immune response, such as upregulating type-1 interferon expression, and inducing inflammation in the gut. In this investigation, we aimed to study how infection by reovirus T1L affects the gene expression of IL-27 and IL-12 in type-1 interferon knockout mice and interferon regulatory factor 1 (IR-F1) knockout mice. Through real time polymerase chain reaction (qPCR) and flow cytometry (FACS staining), we gathered results showing that IR-F1 KO mice had no significant increase in gene expression of IL-27 or IL-12 when infected by T1L, indicating that removal of the IR-F1 gene can increase oral tolerance. Mice that were knockout for type-1 interferon actually died because of a decrease in immune protection. Looking forward, we will continue studying the mechanisms that lead to oral tolerance by looking at other genes such as IL-12 and BATF3.
Session 2F: Mechanisms of Host Viral Interactions Leading to Loss of Oral Tolerance in Celiac Disease Patients
Room A115
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 shown that virus infections also play a role in the development of celiac disease by stimulating an immune response, such as upregulating type-1 interferon expression, and inducing inflammation in the gut. In this investigation, we aimed to study how infection by reovirus T1L affects the gene expression of IL-27 and IL-12 in type-1 interferon knockout mice and interferon regulatory factor 1 (IR-F1) knockout mice. Through real time polymerase chain reaction (qPCR) and flow cytometry (FACS staining), we gathered results showing that IR-F1 KO mice had no significant increase in gene expression of IL-27 or IL-12 when infected by T1L, indicating that removal of the IR-F1 gene can increase oral tolerance. Mice that were knockout for type-1 interferon actually died because of a decrease in immune protection. Looking forward, we will continue studying the mechanisms that lead to oral tolerance by looking at other genes such as IL-12 and BATF3.
Comments
Additional team members: Dr. Reinhard Hinterleitner and Dr. Romain Bouziat