We had a chance to collaborate with Dr. Luc Vallières and his team at the Université Laval in a study that was recently published in the Journal of Clinical Investigation Insight. In the paper, Hawkins et. al. shows that during central nervous system (CNS) autoimmunity, a population of neutrophils gains access to the inflamed CNS. Interestingly, these CNS neutrophils acquire a very un-neutrophil like property: the ability to acquire and present antigens to T and B cells – something normally performed by very different kinds of immune cells.
We contributed to this study through our ongoing work to develop and characterize mouse models of CNS autoimmunity that incorporate B cells in the disease process. We found extensive neutrophil invasion of the CNS in one of these B cell-dependent models of CNS autoimmunity induced using a modified MOG protein that we developed. By using this B cell-dependent model, Hawkins et. al. showed that deletion of a protease (ASPRV1), which is highly expressed in CNS neutrophils, leads to a significant decrease in the severity of CNS autoimmunity.
Overall this has been, and will continue to be, a productive collaboration that has taught us a great deal about how neutrophils contribute to CNS autoimmunity but also identifies a novel role for neutrophils in the immune response that remains unstudied.