Katalin Sándor

This study identifies SEMA4D and OSM as mediators of neutrophil-neuron communication in arthritis-induced pain, showing their role in neuronal sprouting and hypersensitivity.

This study examines skin neuroimmune changes in fibromyalgia patients, identifying novel dermal alterations and correlations between immune cell populations and nerve fiber density.

The paper examines lipid metabolism and anti-satellite glial cell IgG antibodies in fibromyalgia patients, finding associations between lipid concentrations, symptom severity, and autoantibody levels.

The paper examines bile acid and short-chain fatty acid levels in fibromyalgia patients and healthy controls, finding higher bile acid levels in patients and associations with autoantibodies and mental well-being.

This study shows that fibromyalgia pain is caused by IgG autoantibodies that sensitize sensory neurons in mice, suggesting potential treatment through reducing IgG levels.