Celiac Disease—Sandwiched between Innate and Adaptive Immunity

Emerging patterns of risk factor make‐up enable subclassification of rheumatoid arthritis

“…Nonetheless, the intestinal lesions in patients with celiac disease are generated by gluten-reactive T cells and not by anti-tissue transglutaminase antibodies. Production of these bystander autoantibodies is likely to be initiated due to the ability of tissue transglutaminase to crosslink itself to deaminated gluten peptides and the subsequent uptake and presentation of these complexes by tissue transglutaminase-specific B cells to glutenspecific T cells that provide help for antibody production (17). However, regardless of whether or not ACPAs are pathogenic, studies investigating the ACPA response have revealed important novel insights into the contribution of genetic risk factors to the phenotype of RA.…”

DNAM-1 Mediates Epithelial Cell-Specific Cytotoxicity of Aberrant Intraepithelial Lymphocyte Lines from Refractory Celiac Disease Type II Patients

“…This is presumably linked to the adaptive gluten-specific T cell response in the lamina propria as the damage is restored upon withdrawal of gluten in the diet (23). In contrast, RCD II and the successive state of overt lymphoma are characterized by gluten-independent tissue damage and a monoclonal expansion of aberrant sTCR-CD3 2 IELs (24).…”

Sensitive detection of cereal fractions that are toxic to celiac disease patients by using monoclonal antibodies to a main immunogenic gluten peptide

“…Oral administration of glutamine-and proline-specific proteases (i.e., glutenases) is a potential therapeutic alternative (or adjunct) to a gluten-free diet (Stepniak & Koning, 2006;Cerf-Bensussan et al, 2007). However, validation of the efficacy of these enzymes at detoxifying gluten in vitro must precede clinical testing, and such validation currently relies on low-throughput, technically challenging cell-culture-based assays (Siegel et al, 2006;Gass et al, 2007;Stepniak & Koning, 2006) or on polyclonal anti-gliadin-antibody-based ELISA assays that are only grossly quantitative (Gass et al, 2007).…”