Event Title

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

Disciplines

Biology

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.


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Apr 28th, 2:00 PM Apr 28th, 2:25 PM

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.