Shift in perspective: autoimmunity protecting against rheumatoid arthritis.
Yibo HeMike AounZhongwei XuRickard HolmdahlPublished in: Annals of the rheumatic diseases (2024)
A hallmark of rheumatoid arthritis (RA) is the increased levels of autoantibodies preceding the onset and contributing to the classification of the disease. These autoantibodies, mainly anti-citrullinated protein antibody (ACPA) and rheumatoid factor, have been assumed to be pathogenic and many attempts have been made to link them to the development of bone erosion, pain and arthritis. We and others have recently discovered that most cloned ACPA protect against experimental arthritis in the mouse. In addition, we have identified suppressor B cells in healthy individuals, selected in response to collagen type II, and these cells decrease in numbers in RA. These findings provide a new angle on how to explain the development of RA and maybe also other complex autoimmune diseases preceded by an increased autoimmune response.
Keyphrases
- rheumatoid arthritis
- disease activity
- systemic lupus erythematosus
- ankylosing spondylitis
- interstitial lung disease
- rheumatoid arthritis patients
- induced apoptosis
- machine learning
- chronic pain
- deep learning
- multiple sclerosis
- cell cycle arrest
- high resolution
- pain management
- bone mineral density
- neuropathic pain
- oxidative stress
- drug induced
- signaling pathway
- spinal cord
- spinal cord injury
- systemic sclerosis
- cell death
- binding protein
- tissue engineering