Role of CD5 signalling for pro-inflammatory Th17 response in multiple sclerosis

This study aimed to assess the role of the CD5-CK2-STAT3 signalling axis in human pro-inflammatory Th17 cells. Blockade of CD5 reduced production of IL-17A, IFN-γ and GM-CSF by Th17-polarised cells without affecting proliferation. In comparison, blockade of its intracellular interaction partner CK2 exerted partly similar effects with a decrease in IL-17A and GM-CSF production but also impaired T cell proliferation. Both blocking agents resulted in a decreased phosphorylation of the downstream signalling molecule STAT3. The CD5 targeting treatment was able to abolish cytotoxic effects caused by Th17-polarised cells. Transcriptomic and proteomic analysis showed that CD5 expression correlates with an inflammatory immune profile in MS in serum as well as CSF. Single cell analysis from Csf of RRMS and NIND patients