Beyond gluten-free diet: Novel therapeutic frontiers in celiac disease armamentarium

Figure 1 Immunopathogenesis of celiac disease. Schematic representation summarizing the key steps from gluten ingestion to immune activation and enterocyte injury. IFN-γ: Interferon-γ; IL-21: Interleukin-21; TNF-α: Tumor necrosis factor-α; tTG: Tissue transglutaminase; HLA-DQ: Human leukocyte antigen-DQ; APCs: Antigen-presenting cells; NK: Natural killer; Th: T helper.

Figure 2 Limitations of the gluten-free diet. GFD: Gluten-free diet.

Figure 3 Gluten-free diet adherence monitoring tools. Illustration comparing various methods for assessing gluten-free diet adherence, arranged from least accurate to most accurate (inner to outer rings). GIP: Gluten immunogenic peptide.

Figure 4 Treatment targets and strategies in celiac disease. This schematic figure illustrates the pathophysiological steps of gluten-induced intestinal injury and highlights corresponding therapeutic intervention points. Strategies include: (1) removal of toxic gluten peptides; (2) enhancement of epithelial barrier integrity through permeability inhibitors; (3) inhibition of tissue transglutaminase 2-mediated deamination; (4) blockade of HLA-DQ2/DQ8 antigen presentation; (5) immune-modulating therapies targeting both innate and adaptive pathways; (6) microbiome-directed approaches; and (7) miscellaneous emerging modalities. Together, these targeted strategies aim to prevent gluten peptide entry, modify immune activation, restore epithelial integrity, and ultimately reduce enterocyte damage in celiac disease. FN-γ: Interferon-γ; IL-21: Interleukin-21; TNF-α: Tumor necrosis factor-α; tTG: Tissue transglutaminase; HLA-DQ: Human leukocyte antigen-DQ.

Figure 5  Potential benefits of probiotics in celiac disease.