New research led by Kip Connor, PhD, finds that microglia—the primary immune cells of the central nervous system, including the retina—play a vital role in regulating neuroinflammation in autoimmune uveitis. The study, published in Proceedings of the National Academy of Sciences and featured on eyewire News, may one day lead to better treatment targets for the disease.
In the preclinical model of autoimmune uveitis, the researchers describe, for the first time, a role for microglia in directing the initiation of autoimmune uveitis by orchestrating the inflammatory response within the retina. In reaction to disease induction, microglia closely associate with the retinal vasculature and facilitate inflammatory immune cell entry past the blood brain, or ocular, barrier into the retina. When the researchers depleted microglia in this model, they observed that the disease was completely blocked.
“Normally, the blood brain barrier serves as an impediment and prevents the immune response from going into tissues of the central nervous system, including the retina. However, our results provide clear evidence, that in the context of uveitis, microglia can facilitate entry of inflammatory immune cells into the retina, and enable the host immune responses to attack cells that are not normally recognized by the immune system,” said Dr. Connor.
“Until now, the role of microglia in retinal disease has not been fully understood, but our research shows—for the first time—that these cells serve as gatekeepers from the immune system to the central nervous system. This gateway not only has implications for treating uveitis, but may provide future avenues for drug delivery across the blood brain barrier for other diseases of the central nervous system.”