SEARCH RESULTS FOR: Dermatitis-herpetiformis

Dermatitis herpetiformis

Dermatitis Herpetiformis: Pathogenesis and clinical findings Genetic predisposition, HLA-DQ2 and HLA-DQ8 Long term exposure to gliadin, a component of gluten, via dietary gluten ingestion Tissue transglutaminase (TTG) in gut lumen is cross linked to gliadin HLA-DQ2 on antigen presenting cells recognizes gliadin antigen Gliadin antigen is presented to sensitized T helper cells and epitope spreading occurs Authors: Elise Hansen Reviewers: Sunawer Aujla Jori Hardin* * MD at time of publication Type 1 T helper cells and plasma cells produce IgA antibody with gliadin antigen Type 1 T helper cells and plasma cells produce IgA antibody with gliadin crosslinked to TTG Type 1 T helper cells and plasma cells produce IgA antibody with gliadin crosslinked to epidermal transglutaminase 3 (TG3) IgA anti-TTG and IgA anti-TG3 circulate in bloodstream IgA anti-TG3 antibodies reach dermis TG3-IgA complex forms and deposits in papillary dermis TG3-IgA complex and Interleukin 8 stimulate neutrophil chemotaxis Neutrophils infiltrate papillary dermis Neutrophils produce proteases Proteases destroy the basement membrane of the dermis Epidermis no longer adheres to dermis Epidermal transglutaminase 3 (TG3) is released from superficial keratinocytes Vesicles filled with IgA deposits and neutrophils Epidermal layer Destruction of dermal papillae/ basement membrane Dermal layer Y Grouped vesicles on extensor surfaces Pruritus TG3-IgA complex Grouped excoriations on extensor surfaces Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published August 25, 2023 on www.thecalgaryguide.com