Thursday May 3 @ 3 pm CEST (9 am EDT)
Join our webinar to:
- Learn about pain in rheumatoid arthritis and mouse models of arthritis-associated pain.
- Gain knowledge on how autoantibodies can increase neuronal excitability through multiple mechanisms.
- Gain insight into how “reverse translational” approaches can generate new insights to disease and pain pathology.
Camilla Svensson, Associate Professor and research group leader for Molecular Pain research at the Department of Physiology and Pharmacology, Karolinska Institutet.
Disease-relevant models of chronic pain are essential for developing new therapeutics and overcome poor translation between animal studies and the clinical setting. In this webinar, we will describe the translational potential of using patient-derived autoantibodies in basic research models and how this approach can be applied to gain new insights to pain mechanisms and drug targets.
Today, approximately 1% of the population in the EU and US are diagnosed with rheumatoid arthritis (RA) and pain is one of the most problematic symptoms for these patients. The cause of pain in RA has traditionally been attributed to the inflammatory process in the joint, but it is becoming increasingly clear that other mechanisms are also at play. For example, joint pain frequently precedes joint inflammation in RA, indicating that non-inflammatory pronociceptive (pain) processes are activated already at early stages of the disease characterized by presence of antibodies and absence of joint inflammation. Furthermore, despite the success with new disease-modifying drugs in RA that target the pro-inflammatory cascades, up to 40% of the RA patients are dissatisfied with their pain level even though disease activity is under medical control. The mechanisms driving pain prior to, and subsequent to, disease flares in RA are underexplored.
We have addressed the possibility that anti-citrullinated protein antibodies (ACPA), present in a major subset of patients with RA and used clinically as a serological marker for the diagnosis of RA, may be directly responsible for the induction of pain. We found that mice injected with either human ACPA IgG purified from RA patients, or monoclonal ACPA generated from synovial B-cells from RA patients, developed long-lasting pronounced evoked and spontaneous pain-like behavior in the absence of visual and histological signs of inflammation. Non-ACPA IgG from RA patients, IgG from healthy controls and control monoclonal IgG were without pronociceptive effect.
This webinar will highlight the role of autoantibodies and antibody receptors in arthritis-induced pain and focus on the mechanisms by which ACPA activates sensory neurons. The identification of novel contributions of autoantibodies to persistent pain may aid in the development of new treatment strategies, not only for pain in RA, but also for pain in other diseases associated with autoantibody production.
Camilla I Svensson, PhD, Associate professor and group leader at the Karolinska Institutet
Dr. Svensson started her laboratory at the Karolinska Institutet, Department of Physiology and Pharmacology in 2008, where she today is leading a research team exploring pain mechanisms in rheumatic disease, with a specific focus on the role of autoantibodies and associated inflammatory and non-inflammatory processes. Camilla is funded by the Swedish Research Council and is a Wallenberg Academy Fellow and Ragnar Söderberg Fellow in Medicine. Prior to her appointment at the Karolinska Institutet, Camilla was a Postdoctoral Fellow at the Department of Medicine, Division of Rheumatology at the University of California, San Diego (UCSD), USA, studying inhibitory regulation of intracellular signal transmission in rheumatoid arthritis. Camilla earned her PhD in Molecular Pathology at UCSD in 2005, with work focused on spinal mechanisms of pain signal transmission.