Celiac Disease: Gliadin Peptides Activate Immune System through CXCR3-dependent binding, FPR1 binding, and p38 MAPK Pathway Upregulation
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Authors
Chacko, Steven J.
Issue Date
2018
Type
Thesis
Language
en_US
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Abstract
Chapter 1 of this paper is an overview of celiac disease (CD) that covers the clinical features of the disease including pathophysiology, symptoms, risk factors, treatment, etc. The condition is caused by ingestion of gluten to genetically predisposed individuals. A fragment of gluten, gliadin, initiates multiple immune responses which result in the intestinal damage and a multitude of intestinal and extra-intestinal symptoms.
Chapter 2 takes an in-depth examination of a specific fragment, gliadin. Several laboratory studies have been completed which evaluate the mechanisms behind how gliadin triggers immunological responses such as through cytokine production, neutrophil migration, and T-cell maturation. Multiple experiments via rats have been used to discover the proteins, including CXCR3 and FPR1, and the pathways, p38 MAPK, which are used by gliadin fragments to induce inflammatory responses. Research that is focused on these gliadin-induced pathways can be potentially used reduce the risk and symptoms of CD development.
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In Copyright