Interleukin-31 Receptor and neurogenic inflammation

• Applicant: Dr. Ferda Cevikbas
• Subject Area: Dermatology
• Term: from 2008 to 2011
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 72250917

The mechanisms how nerve cells communicate with immune cells during inflammation, inflammatory pain or pruritus are only poorly understood. One of the skin diseases in which the neurogenic aspect plays an essential role for the mediation of inflammation (erythematic, vasodilatation, recruitment of inflammatory cells to the site of inflammation) and itching is atopic dermatitis (AD). The underlying molecular and cellular mechanisms how the nervous system communicates with the immune system in atopic dermatitis, however, are poorly investigated. Therefore, identifying mediators and receptors responsible for mediating neuroimmune communication is promising for the development of better therapies and to improve the quality of life in atopic dermatitis patients. Recently, interleukin (1L)-31 has been demonstrated to be up-regulated in atopic dermatitis by activating the oncostatin M receptor (OSMR) and IL-31 receptor A (IL-31 RA) complex. With others, we found that IL-31 RA is expressed by murine and human sensory neurons and may thus be involved in neurogenic inflammation, pain and/ or pruritus. However, the biological function of this novel neuroimmune pathway, especially with respect to communication with other neuronal receptors (Protease-activated receptors (PARs), TRPV channels neuropeptide receptors) is completely unknown. Therefore, the aim of this project will be to investigate the relevance of IL-31 and its receptor complex in neurogenic inflammation and pain, and to analyse the communication with PARs and TRPV channels or/and neuropeptide receptors, and to define the crucial signaling cascade mediating these effects.

• DFG Programme: Research Fellowships
• International Connection: USA
• Host: Professor Dr. Nigel Bunnett