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An Autoimmune Basis for Raynaud's Phenomenon: Murine Model and Human Disease
D P Ascherman1, Y Zang2, I Fernandez2
1Miami VA Medical Center and University of Miami Miller School of Medicine, Miami, Florida.
Arthritis & Rheumatology (Hoboken, N.J.)
|March 24, 2018
Summary
Autoimmune antibodies targeting cytokeratin 10 (K10) can cause Raynaud's phenomenon (RP)-like symptoms. This study identifies anti-K10 antibodies as a key factor in RP pathogenesis in patients with anti-RNP autoimmunity.
Area of Science:
- Rheumatology
- Immunology
- Vascular Biology
Background:
- Raynaud's phenomenon (RP) is frequently observed in patients with anti-RNP-positive rheumatic diseases.
- The autoimmune basis for RP in these patients has not been fully elucidated.
Purpose of the Study:
- To investigate autoantibodies potentially mediating RP pathogenesis.
- To identify specific autoantigens involved in RP development.
Main Methods:
- Screening of patient and murine sera for autoantibodies capable of inducing RP-like ischemia and endothelial cell apoptosis.
- Proteomic analysis to identify candidate autoantigens.
- Utilizing murine models and in vitro systems for functional assays.
- Investigating the role of cytokeratin 10 (K10) and anti-K10 antibodies.
Main Results:
- RNP-positive sera induced RP-like tissue ischemia and endothelial cell apoptosis.
- Cytokeratin 10 (K10) was identified as a key autoantigen.
- Monoclonal anti-K10 antibodies replicated RP-like pathology; K10 knockout or anti-K10 depletion conferred protection.
- Cold exposure exacerbated K10 expression and tissue damage.
Conclusions:
- Anti-K10 antibodies are sufficient to induce RP-like ischemia.
- These antibodies play a significant role in the pathogenesis of RP in anti-RNP-positive patients.
