The hypothesis that viruses could play a key role in the pathogenesis of type 1 diabetes (T1D) has a long history and several viruses seem to trigger pancreatic islet autoimmunity through several mechanisms, including direct destruction of pancreatic β-cells, bystander activation of autoreactive T-cells, molecular mimicry and viral persistence. Moreover, although the presence and involvement of CD8+ autoreactive T cells has been confirmed and associated to T1D pathogenesis, increasing attention is now being directed toward the role of innate immunity and of non-specific inflammation as contributing factors to the pathogenesis of this complex disease. A picture is emerging in which beta cells, innate and adaptive immune systems are engaged in intrinsic conversations ultimately determining the fate of beta cells with the contribution of innate immune cells and inflammatory molecules.
As we know, inflammation is a biological response that is triggered by infections, tissue injury, stress or malfunction, and its adequate control is essential for the preservation of tissue integrity; however, excessive, or defective inflammatory signaling may have adverse consequences and increase the risk of developing autoimmune diseases. In T1D, if viruses could trigger the primary insult to pancreatic islets, they may lead to the initiation and amplification of an innate immune response and inflammation. We can hypothesize a scenario in which viruses could infect pancreatic β-cells; after internalization, viruses could trigger inflammatory signaling cascades, leading to the production of pro-inflammatory chemokines and cytokines, Although local inflammation and activation of antiviral defenses, should eradicate the viral infection, in some genetically susceptible individuals these cellular attempts to neutralize the invading virus might be characterized by exaggerated inflammatory response, defective triggering of intracellular anti-inflammatory or defective anti-apoptotic responses, then inducing progressive inflammation and β-cell loss.
That said, the rationale for this Research Topic arises because we believe there are still many aspects to be clarified regarding the contribution of environmental factors (in particular viruses), as well as the contribution of the immune system in particular (innate immune system) and inflammation in the pathogenesis of T1D.
We welcome the submission of original research, reviews/mini-reviews, perspectives, and opinion articles on the contribution of viruses, innate immune system and inflammation in T1D pathogenesis. We accept contributions related to, but not limited to, the following themes:
- Role of environmental factors in T1D, the role of viruses and of the anti-viral host response in T1D.
- Contribution of innate immunity and inflammation in T1D
- Dialogue between innate and adaptive immune systems in T1D
- Possible intervention and prevention therapies in T1D
- Viruses and innate immunity system in other autoimmune diseases besides T1D