Fig 4. Proposed involvement of memory T cells in the pathogenesis of AIP.

Autoantigens from acinar cells and pancreatic duct epithelium trigger activation of T cells, which may differentiate into T effector cells or memory T cells. The first population mediates destruction of pancreatic tissue, whereas the latter type of T cells perpetuates and enhances autoimmune reactions upon antigen re-exposure. Relative frequencies of splenic leukocyte subsets, development of AIP (pancreatic damage) and possibly expression/processing of autoantigens are controlled by QTLs. Overlapping QTLs for certain immune cell phenotypes and AIP suggest the existence of pathogenetic links.