Camilla Svensson

Chronic pain is a major burden on the life of sufferers and society as a whole. While our understanding of the condition is progressing, adequate therapies are still lacking and millions of people are living with persistent debilitating pain that has no discernable function.

One promising avenue in pain research in recent years has been the role of neuroinflammation in the peripheral and the central nervous system, where the communication between immune cells and neurons now is known to be a vital driver of chronic pain. However, while these new insights bring us closer to potential new drug treatments, the field is currently lacking the answers to a few vital questions. We are addressing some of those by focusing our work on pain mechanisms in conditions with joint inflammation and autoimmunity, such as rheumatoid arthritis. We are asking if autoantibodies and B-cells directly activate pain neurons. Does long-term inflammation located in the joint have “nerve damaging” effects? When focusing on the central nervous system we are exploring how microglia and astrocytes respond in different pain states. Do they mediate both pro- and anti-inflammatory cascades? And are they able to maintain molecular memory of previous insults, which might then affect their responses during a chronic pain state? Be decipher these types of questions we hope to advance our understanding of how chronic pain is mediated and identify novel targets for pain relief.

I was the Chair of the Young Academy of Sweden 2016–2017.