Celiac Disease Potential Cure Research Proposal

Celiac disease (CD) is a chronic autoimmune disorder triggered by an aberrant immune response to gluten proteins, primarily associated with HLA-DQ2 and HLA-DQ8 genetic variants. These human leukocyte antigen (HLA) molecules present deamidated gluten peptides to CD4+ T cells, leading to immune activation, chronic inflammation, and intestinal damage. Current treatments rely solely on strict gluten avoidance, necessitating the development of novel therapeutic strategies. This research explores the potential of CRISPR gene-editing technology to correct pathogenic HLA variants, thereby preventing the initiation of the autoimmune response. By restoring wild-type alleles at the HLA-DQ2.5 and HLA-DQ8 loci, CRISPR-based interventions could eliminate the genetic predisposition to CD. Additionally, therapeutic apheresis is proposed as a method to selectively remove memory T cells created by the disease, reducing ongoing immunological damage. Integrating gene editing with immunomodulatory approaches offers a promising pathway toward a cure for CD. This study aims to establish a framework for these interventions, potentially transforming CD treatment and providing insights applicable to other autoimmune diseases.

Publication Details

Journal
Stanford Digital Repository
Published
2025-03-05
DOI
https://doi.org/10.25740/dm927rk3421
Primary Topic
Celiac Disease Research and Management
Type
article
Field-Weighted Citation Impact
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Celiac Disease Potential Cure Research Proposal

Stanford Digital Repository
Celiac Disease Research and Management
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Celiac Disease Potential Cure Research Proposal

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Abstract

Celiac disease (CD) is a chronic autoimmune disorder triggered by an aberrant immune response to gluten proteins, primarily associated with HLA-DQ2 and HLA-DQ8 genetic variants. These human leukocyte antigen (HLA) molecules present deamidated gluten peptides to CD4+ T cells, leading to immune activation, chronic inflammation, and intestinal damage. Current treatments rely solely on strict gluten avoidance, necessitating the development of novel therapeutic strategies. This research explores the potential of CRISPR gene-editing technology to correct pathogenic HLA variants, thereby preventing the initiation of the autoimmune response. By restoring wild-type alleles at the HLA-DQ2.5 and HLA-DQ8 loci, CRISPR-based interventions could eliminate the genetic predisposition to CD. Additionally, therapeutic apheresis is proposed as a method to selectively remove memory T cells created by the disease, reducing ongoing immunological damage. Integrating gene editing with immunomodulatory approaches offers a promising pathway toward a cure for CD. This study aims to establish a framework for these interventions, potentially transforming CD treatment and providing insights applicable to other autoimmune diseases.

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Celiac Disease Research and Management
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