Besides insulin injections, one treatment strategy being used today is to transplant pancreatic islets into diabetes patients to replace their defective islets. This way, the newly transplanted islets can produce natural insulin and help manage the disease naturally. As with all transplants, however, islet allotransplants can be rejected by the host immune system, and immunosuppressants to reduce rejection can lead to its own set of problems. By finding a way to make transplanted islets more resistant to host rejection without the complications from immunosuppression, patients can have a more permanent solution to diabetes with less need for regular insulin treatments. This is the impetus behind our customer's research as they reported a novel use of a seemingly unrelated cell type to deliver insulin within a mouse model.
I'm sure doctors and other researchers know far more about this than I, so it won't be as unusual for them, but when I think about diabetes, I think about the pancreas and islets, not about some testicular cell. As Washburn et al. outline in their manuscript, the so-called Sertoli cells have been shown to survive long-term in new hosts without the need for immunosuppressive treatments. In normal physiology, Sertoli cells are testicular cells that serve to not only help sperm develop properly, but also have the capacity to regulate immune function. For their experiments, Washburn et al. used the unique features of these Sertoli cells to deliver functional insulin through a lentiviral system. In their study, it was observed that this insulin-producing engineered murine Sertoli cell line could survive long term as allografts in a mouse diabetes model.
In the manuscript, there were several very promising results that showed the utility of this strategy in future therapeutic development. Initially, the engineered Sertoli cells (termed MSC1) survived complement exposure as was previously reported for this cell type. The MSC1 cells could produce detectable insulin and displayed over 75% survival over a 50-day trial, with very little IgM and IgG infiltration as well as low complement marker staining to suggest a lower immune response to the graft. Conversely, complement inhibitory proteins were markedly increased in the engineered MSC1 cells, suggesting another survival mechanism to maintain the grafts in the new host mice. While there needs to be more study of Sertoli cells to determine the exact mechanisms they might use to modify the immune response to improve survival, this study shows the possibility of using insulin-producing immune-resistant cells as a permanent solution for diabetes patients.
With over 16,000 catalog antibody products and custom services available to generate reagents to unique markers, ABclonal is equipped to deal with myriad experimental approaches, including the study from our customer outlined in this article. In their study, Washburn et al. took advantage of our high-quality antibodies to Complement Factor B, Complement C4A, Complement C3, and Complement C9 to study the behavior of the complement-mediated immune response in their mouse model. Please read their article to enjoy their beautiful immunohistochemistry data using ABclonal antibodies, and contact us at service@abclonal.com to see how we can help you get published too!