Deep Insight into the Role of MIF in Spondyloarthritis.
Brian WuAkihiro NakamuraPublished in: Current rheumatology reports (2022)
MIF and its cognate receptor CD74 are extensively involved in the pathogenesis of SpA including inflammation in the spine, joint, eyes, skin, and gut. The majority of the current evidence has consistently shown that MIF drives the inflammation in these distinct anatomical sites. In preclinical models, genetic deletion or blockade of MIF reduces the severity of inflammation. Although MIF is generally an upstream cytokine which regulates downstream effector cytokines, MIF also intensifies type 3 immunity by promoting helper T 17 (Th17) plasticity. MIF- or CD74-targeted therapies have also reported to be well tolerated in clinical trials for other diseases. Recent findings suggest that MIF-CD74 axis is a new therapeutic target for SpA to improve various clinical features. Clinical trials for MIF- or CD74-targeted therapies for SpA patients are warranted.
Keyphrases
- clinical trial
- oxidative stress
- ejection fraction
- regulatory t cells
- dendritic cells
- newly diagnosed
- stem cells
- nk cells
- rheumatoid arthritis
- multidrug resistant
- ankylosing spondylitis
- optical coherence tomography
- systemic lupus erythematosus
- phase ii
- study protocol
- heat shock
- cell therapy
- patient reported outcomes
- heat stress