IL-6 is a pro-inflammatory cytokine upregulated in some autoimmune diseases. The 
role of IL-6 in the development of type 1 diabetes (T1D) is unclear. Clinical 
studies are investigating whether tocilizumab (anti-IL-6 receptor) can help 
preserve beta cell function in patients recently diagnosed with T1D. However, in 
some rodent models and isolated human islets, IL-6 has been found to have a 
protective role for beta cells by reducing oxidative stress. Hence, we 
systematically investigated local tissue expression of IL-6 in human pancreas 
from non-diabetic, auto-antibody positive donors and donors with T1D and T2D. 
IL-6 was constitutively expressed by beta and alpha cells regardless of the 
disease state. However, expression of IL-6 was highly reduced in 
insulin-deficient islets of donors with T1D, and the expression was then mostly 
restricted to alpha cells. Our findings suggest that the implication of IL-6 in 
T1D pathogenesis might be more complex than previously assumed.