A recent independent study cited using whole blood collected from HemCare donors to carry out research into how lung cancer suppresses the immune system. 
Scientists at a Boston-based pharmaceutical company have been trying to puzzle out exactly how lung cancer cells are able to suppress the immune system, and prevent it from launching an effective response. While previous research has exposed cancer-associated fibroblasts (CAFs) as the primary culprits in this process, there is still little real knowledge of how these cells are able to interfere with immune cell function.
Non-small cell lung cancer is the leading cause of cancer-related deaths worldwide. The disease is enormously difficult to treat, in part because only 20% of cases respond to available immunotherapies. New knowledge on the mechanisms by which lung tumors are able to “re-program” immune cells is therefore crucial.
With this study, the Boston-based group seems to have made a breakthrough. Key to their research was the capacity to access the right tissue donors for their study; specifically, HemaCare-procured tissues from non-small cell lung cancer and colorectal cancer patients who were willing to grant permission for their donated cells to be used in cancer research.
In an elegant series of experiments, the authors were able to reveal more about the lung tumor microenvironment than scientists have ever uncovered before. Through in-depth analysis of lung cancer data sets, they identified a positive correlation between donor-derived CAFs and monocytic immune suppressor cell abundance. This data was validated using specialized cell imaging technology that tracks spatial interactions between cells.
Next, the group used chemotaxis assays to show that CAFs recruited monocytes by secreting a chemoattractant protein known as CCL2. Once the two cell types were in close proximity, CAFs were able to induce the monocytes to differentiate into a suppressor cell subtype. The new suppressor cells would then rigorously suppress cytotoxic T-cell proliferation.
The authors went on to demonstrate that CAF induced suppressor cell activation could be disrupted by blocking CCL2, while monocytic suppressor cell activity could be abrogated by reducing the amount of reactive oxygen species (ROS) the immune cells generated. Thus, not only did the authors reveal a new immune suppression mechanism, they also illustrated new potential therapeutic pathways.
Studies like these are changing the way we view medicine. The more we understand about our own biology, the more we can use it as an ally in fighting disease. But while the scope of cell-based therapies is growing daily, these medicines will only ever be as good as the building blocks they are made from. Donor recruitment and access, quality oversight, and cell handling procedures are all critical parameters in assuring high-quality medicines, and ultimately, the ability to successfully treat more patients.
- Xiang H., et al. Cancer-associated fibroblasts promote immunosuppression by inducing ROS-generating monocytic MDSCs in lung squamous cell carcinoma. Cancer Immunol Res. Feb 2020.