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However, persistently elevated interferons and receptor activation of the MNK1/MNK2eIF4E signaling pathway at all disease phases caused sensorymotor dysfunction and pain by inducing hyperexcitability and sensitization of a GFRA3 + C-fiber subtype of joint-innervating sensory neurons

IL-6 appears to influence dramatically the nature of the immune response by dictating the recruitment, activation and apoptotic clearance of individual leucocyte subpopulations (e.g

The SERCA2b is downregulated but more active due to glutathionylation of the redox-sensitive cysteine