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Figure 1: Novel drug targets for Celiac disease: (1) Endopeptidases/glutenases break down immunogenic gliadin peptide; (2) CXCR3 inhibitors prevents receptor-gliadin complex formation thereby inhibit zonulin secretion; (3) probiotics ameliorate gliadin induced dysbiosis; (4) tight junction modulator inhibit zonulin production which prevents gliadin induced compromised gut permeability; (5) gluten tolerization provide gluten tolerance; (6) TG2 inhibitor prevents deamidation of gliadin peptide; (7) DQ2/DQ8 blocking peptide inhibit gliadin-HLA complex formation and activation of T-cells; (8) cathepsin S inhibitor inhibits the proteolyses of MHC Class II invariant chain (9) anti interferon-γ/anti tumor necrosis factor-alpha prevent inflammation; (10) anti interleukin-15 inhibits IEL production. CXCR3 = Chemokine receptor, IELs = Intraepithelial lymphocytes, TG2 = Tissue transglutaminase, HLA = Human leukocyte antigen, DC = Dendritic cells

Figure 1: Novel drug targets for Celiac disease: (1) Endopeptidases/glutenases break down immunogenic gliadin peptide; (2) CXCR3 inhibitors prevents receptor-gliadin complex formation thereby inhibit zonulin secretion; (3) probiotics ameliorate gliadin induced dysbiosis; (4) tight junction modulator inhibit zonulin production which prevents gliadin induced compromised gut permeability; (5) gluten tolerization provide gluten tolerance; (6) TG2 inhibitor prevents deamidation of gliadin peptide; (7) DQ2/DQ8 blocking peptide inhibit gliadin-HLA complex formation and activation of T-cells; (8) cathepsin S inhibitor inhibits the proteolyses of MHC Class II invariant chain (9) anti interferon-γ/anti tumor necrosis factor-alpha prevent inflammation; (10) anti interleukin-15 inhibits IEL production. CXCR3 = Chemokine receptor, IELs = Intraepithelial lymphocytes, TG2 = Tissue transglutaminase, HLA = Human leukocyte antigen, DC = Dendritic cells