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Updated: Feb 10, 2026

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Published on: July 4, 2007
Annexin A1 and Autoimmunity: From Basic Science to Clinical Applications
Maurizio Bruschi1, Andrea Petretto2, Augusto Vaglio3
1Laboratory of Molecular Nephrology, Istituto Giannina Gaslini, Largo Gaslini n 5, 16147 Genoa, Italy. mauriziobruschi@gaslini.org.
High levels of Annexin A1 protein and anti-Annexin A1 autoantibodies are linked to systemic lupus erythematosus (SLE). This review explores Annexin A1
Area of Science:
- Immunology
- Autoimmunity
- Molecular Biology
Background:
- Annexin A1 is a key regulator of inflammation and immunity.
- Autoantibodies against Annexin A1 are found in systemic lupus erythematosus (SLE).
- The precise role of Annexin A1 in human autoimmune diseases requires further investigation.
Purpose of the Study:
- To review the association between anti-Annexin A1 autoantibodies and SLE manifestations, particularly lupus nephritis.
- To explore potential mechanisms, such as post-translational modifications within neutrophil extracellular traps (NETs), that may render Annexin A1 immunogenic in SLE.
Main Methods:
- Literature review of existing studies on Annexin A1, autoantibodies, and SLE.
- Analysis of data correlating serum Annexin A1 levels with SLE and lupus nephritis.
- Hypothesis formulation regarding Annexin A1 modification in NETs and its role in autoimmunity.
Main Results:
- Elevated serum Annexin A1 levels are observed in SLE patients with renal complications.
- Increased Annexin A1 levels do not correlate with circulating anti-Annexin A1 autoantibodies.
- Post-translational modifications, like citrullination within NETs, are hypothesized to be crucial for Annexin A1 immunogenicity.
Conclusions:
- While Annexin A1 is implicated in SLE, its direct role in autoantibody development is complex.
- Modified Annexin A1 within NETs, particularly citrullinated Annexin A1, presents a plausible mechanism for triggering autoimmunity in SLE.
- Further experimental validation is needed to confirm Annexin A1 modification as a driver of autoimmunity in human diseases.
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