The main effector function of Th17 cells is the recruitment of neutrophils. Once activated, neutrophils can extrude their chromatin, generating neutrophil extracellular traps (NETs). NETs, despite having antimicrobial activity, can also induce life-threatening immunopathology.

In this project, we exploit our recent finding that blocking NETs can inhibit the autoimmune disease experimental autoimmune encephalomyelitis (EAE), a model of the autoimmune component of MS. We are interested in whether:

• NETs play a pivotal role in initiating CNS inflammation in EAE by enhancing the ability of Th17 cells to respond to the MOG auto-antigen
• This heightened Th17 response results in enhanced NET production, platelet activation and a resultant vicious pathological cycle of CNS injury

We  investigate these hypotheses using different EAE models as well as in vitro assays and analysis of blood samples from a large MS-patient cohort.

This project is carried out in close collaboration with The Parish Group at JCSMR.