A group from University of Glasgow, UK, etc. has reported a detailed studies on the relationship between glycosylation of Synovial fibroblasts(SFs) and arthritis inflammation.
https://www.nature.com/articles/s41467-021-22365-z
It is well known that glycosylation of IgG changes to agalacto types, and the expression of TNFα increases in arthritis. Authors evaluated changes in glycosylation of SFs with using lectins and MS, and confirmed that sialylation decreased in both N-glycans and O-glycans. The decrease in sialylation was observed in α-3Sia but not α-3Sia. Furthermore, levels of sialylation correlated with disease stages. And, it was shown that the decrease in sialylation seems to be induced by TNF, in contrast with IL-1 or IL-17 that had no effect.
It is so important to establish whether desialylation plays a leading role in SFs activation, or on the contrary, it is a more indirect consequence of ongoing inflammation. Authors demonstrated that α2-6Sia blocking by ST6GAL1 mRNA silencing upregulates IL-6 and CcL2. This would be a really meaningful thing relating to the therapeutic strategies.
In a figure below, CIA means Collagen-induced arthritis.
