Presented at the 13th International Congress on Autoimmunity in Athens, Greece

Speaker: Aaron Lerner

Key Takeaways:

  • Gluten is proinflammatory, oxidative, increases intestinal permeability, and compromises immune functions
  • Cross-reactivity and sequence homology exist between gluten and brain antigens
  • Neurotransmitters, tight junction functions, tryptophan metabolism, HPA endocrine axis, and dysbiomic mobilome are involved in the process
  • Intestinal originated gluten-selected T cells, inflammatory cytokines, protein complexes, dysbiotic mobilome, and antibodies can reach the brain via blood and lymph vessels, neural and endocrine pathways
  • Many neurodegenerative conditions might benefit from gluten withdrawal



  • Is immunogenic (produces an immune response) and cytotoxic (toxic to cells)
  • Stimulates Th17 (cells that play a role in host defense against extracellular pathogens, particularly at the mucosal and epithelial barriers, but aberrant activation has been linked to the pathogenesis of various autoimmune diseases)
  • Increases intestinal permeability/inflammation
  • Causes microbial dysbiosis (a disruption to the gut microbiota homeostasis caused by an imbalance in the microflora, changes in their functional composition and metabolic activities, or a shift in their local distribution)

A gluten-free diet can improve non-celiac autoimmune diseases.

This is discussed by Lerner and his team in their publication in Cells, titled “Let Food Be Thy Medicine: Gluten and Potential Role in Neurodegeneration.”