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Celiac disease: mechanisms and emerging therapeutics
Harrison A Besser1, Chaitan Khosla2
1Department of Chemistry, Stanford University, Stanford, CA 94305, USA; Stanford Medical Scientist Training Program, Stanford University School of Medicine, Stanford, CA 94305, USA.
Celiac disease (CeD) is an autoimmune disorder caused by gluten. Research is exploring non-dietary treatments by targeting the molecular interactions involved in CeD pathogenesis for therapeutic development.
Area of Science:
- Immunology
- Gastroenterology
- Autoimmune Diseases
Background:
- Celiac disease (CeD) is a prevalent autoimmune disorder triggered by gluten ingestion.
- Currently, no medicinal therapies exist for CeD, leaving dietary changes as the only management option.
- Understanding the molecular basis of CeD is crucial for developing alternative treatments.
Purpose of the Study:
- To review the current understanding of celiac disease pathogenesis.
- To explore how this knowledge can be applied to therapeutic design and development for non-dietary treatments.
Main Methods:
- Review of existing scientific literature on celiac disease.
- Analysis of the molecular and cellular mechanisms underlying CeD.
- Examination of potential therapeutic targets within the identified pathogenic pathways.
Main Results:
- A model of CeD pathogenesis involving interactions between MHC class II proteins, deamidated gluten peptides, and T cell receptors (TCRs) has been established.
- This pathogenic axis presents a viable target for pharmacological intervention.
- Additional host and environmental factors contributing to disease initiation and progression have been identified.
Conclusions:
- Targeting the key molecular interactions in CeD pathogenesis offers a promising strategy for developing non-dietary therapies.
- Further research into host and environmental factors may reveal additional therapeutic avenues.
- The development of medicinal treatments for CeD is an active and evolving area of research.
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