To examine the longitudinal expression of IL-33 in MS patients following relapse.

We showed previously that IL-33 levels were increased in peripheral blood mononuclear cells (PBMC) of RRMS when compared to controls. IL-33 is thought to regulate tissue modelling and repair, and the protective effect of IL-33 has been described in animals following experimental injury to the CNS.  We therefore explored the expression of IL-33 in PBMC after relapse in patients with RRMS.

Patients recruited for the study were designated to have a relapse either clinically or by MRI changes. Blood for the studies were drawn at month 0 and between months 5-7, 8-11, and 12-15 after a confirmed relapse. PBMC was subjected to flow cytometry and the IL-33 and IL-33 regulated  genes analysed. There were 12 patients in the group with 7 on beta interferon and 8 on Tecfidera.

Expression of IL-33 was found to fall into three epochs. Four patients had the highest levels of IL-33 soon after the relapse and prior to receiving steroids. A second group 4 patients showed highest level of L-33 when their blood was drawn between months 5-7 after attack and a third group showed maximal expression of IL-33 after month 12. In all three groups there was a greater than 5 fold increase in the expression of IL-33 in the CD14+ cell subset when compared to base line and in stable RRMS patients. The was no correlation between patients receiving Tecfidera or Beta Interferon and  IL-33 expression. 

In MS patients the period following relapse is associated with tremendous but transient spikes in IL-33. The heightened levels of expression is not seen in either stable MS or OND controls. Given the known

neuroreparative function of  IL-33 are known the role of IL-33 in promoting repair and recovery in MS needs further study.