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Published on: December 15, 2011
Immunology in Celiac Disease
Eric Marietta1, Rok Seon Choung1, Alberto Rubio-Tapia2
1Division of Gastroenterology and Hepatology, Mayo Clinic, Guggenheim 10-02, 200 1st Street Southwest, Rochester, MN 55905, USA.
Celiac disease (CeD) diagnosis is definitively ruled out by the absence of human leukocyte antigen DQ2 and DQ8. These HLA variants influence immune responses to gliadin peptides, impacting CeD risk.
Area of Science:
- Immunology
- Genetics
Background:
- Celiac disease (CeD) is an autoimmune disorder strongly linked to human leukocyte antigen (HLA) DQ2 and DQ8.
- The presence of HLA-DQ2 or HLA-DQ8 is essential for CeD development, while their absence excludes the diagnosis.
- Specific suballeles of HLA-DQ2 and HLA-DQ8 influence the risk and presentation of CeD.
Purpose of the Study:
- To elucidate the role of human leukocyte antigen (HLA) DQ2 and DQ8 in celiac disease (CeD) pathogenesis.
- To highlight the immunogenic gliadin peptides influenced by HLA-DQ2 and DQ8.
- To identify key immune cells involved in CeD.
Main Methods:
- Review of recent publications focusing on CeD pathogenesis.
- Analysis of the association between HLA-DQ2/DQ8 and gliadin peptide immunogenicity.
- Identification of immune cell involvement, including T cells, antigen-presenting cells (APCs), B cells, and epithelial cells.
Main Results:
- The absence of HLA-DQ2 and/or DQ8 definitively rules out CeD diagnosis.
- HLA-DQ2 and DQ8 dictate the immunogenicity of specific gliadin peptides.
- Key immune players in CeD pathogenesis include T cells, APCs, B cells, and epithelial cells.
Conclusions:
- HLA-DQ2 and DQ8 are critical determinants in celiac disease susceptibility.
- Understanding the interaction between gliadin peptides and HLA variants is key to CeD pathogenesis.
- Further research is exploring the roles of specific immune cells like γδ T cells, mast cells, and eosinophils in CeD.
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