The etiology and pathogenesis of type 1 diabetes (T1D) – one of the most frequent chronic, life-debilitating, autoimmune diseases in humans – have long fascinated endocrinologists, pathologists and biologists alike. Currently conventional wisdom portrays T1D as T-cell mediated autoimmune disease that leads to the specific destruction of pancreatic insulin-producing beta-cells.
In recent years, the immunological perspective of several autoimmune diseases (e.g., systemic lupus erythematosus, psoriasis, vasculitis) has changed significantly. In contrast, the immunological view of T1D that was delineated in the 1970s continues to prevail, more or less unchanged, today. I am convinced that our focus has been overly narrow and that the T-cell– and beta-cell–centered view in T1D pathogenesis needs reinvigoration. Said mechanisms likely represent only one aspect of the much more complex immune response that affects T1D patients. This is indeed what distinguishes the immune system from other “organs”: it hosts a complex interaction between several “players”, each with its own specific role, that act collectively to win “the game” (which, in T1D, is pancreas destruction).
Accordingly, we are now attempting to widen our view by studying immune subsets thus far - more or less - neglected in T1D and trying to understand whether T1D is a pancreas-specific disease - in which the beta-islets are the more affected - rather than a eta-cell specific.