Nilesh M. Agalave

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 shows that TLR4+ dermal fibroblasts induce acute and transitional pain states in mice through inflammatory and calcium signaling mechanisms.

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.

This study shows osteoclasts contribute to pain in arthritis by affecting bone vascularization and innervation, and inhibitors can reverse this pain.