Name: Isabelle AUGER
Adress: INSERM UMR639, Parc Scientifique de Luminy, case 939, 163 Avenue de Luminy, 13288 Marseille cedex 09, France. Tel: + 33 4 91 82 87 50. Fax: + 33 4 91 83 09 26. Email: firstname.lastname@example.org
Personal: Date of birth: August, 20, 1970. Place of birth: Marseille, France. Citizenship: French. Languages: French, English.
Current position: INSERM Researcher, INSERM UMR639, Immunogenetics of rheumatoid arthritis, Marseille, France.
Education: Luminy Science University, Marseille, France, (PhD, 1997).
Qualifications: HDR, 2005 (Immunology, University Medical School, Marseille, France). PhD, 1997 (Immunology, Luminy Science University, Marseille, France).
Research Experience: Post doctoral position, INSERM U463, Institut de Biologie, Nantes, France (1998-1999). Post doctoral position, INSERM U639, Marseille, France (1997-1998).
Patent applications: 2010: WO2010115745A3. Biomarkers, Methods and Kits for the diagnosis of rheumatoid arthritis. 2009: EP09306063.0. Methods for diagnosing rheumatoid arthritis. 2009: EP09305266.0. Serological Methods and Kits for the diagnosis of rheumatoid arthritis. 2008: WO2009138408A3. Methods and Kits for the diagnosis of rheumatoid arthritis.
Rheumatoid arthritis (RA) is a chronic inflammatory joint disease causing articular cartilage and bone destruction. Its worldwide prevalence is 1%, its cause is unknown.
RA is an autoantibody mediated disease. Among the various autoantibodies known in RA, autoantibodies to citrullinated proteins (ACPA) are highly specific. Citrulline is generated by post translational conversion of arginine residues. This process is catalyzed by a group of enzymes called calcium dependent peptidyl arginine deiminases, PAD. ACPA recognize citrulline on different proteins like filaggrin, vimentin or fibrin. ACPAs are detected by a commercial enzyme-linked immunoabsorbent assay containing a synthetic cyclic citrullinated peptide (anti CCP). Anti CCP antibodies identify 60% of RA patients. However, a negative result in anti-CCP antibody testing does not exclude RA.
Therefore, there is a great need for new biological markers of RA to permit early intervention to potentially prevent inflammation and joint destruction. In particular, biomarkers that would allow reliable diagnosis in CCP negative patients and biomarkers that would allow reliable diagnosis and monitoring of the early stages of the disease.
In the past 5 years, we have identified new autoantibodies associated with RA, mapped epitopes and studied the functional role of these autoantibodies. These autoantibodies could bring new understanding of the development of RA and be the basis for diagnosis in early arthritis.