Participation of interleukin 17A in neuroimmune interactions

• Published in: Brain, behavior, and immunity behavior, and immunity, 2014-10, Vol.41, p.1-9
• Main Authors: Moynes, Derek M, Vanner, Stephen J, Lomax, Alan E
• Format: Article
• Language: English
• Subjects: Allergy and Immunology; Animals; Arthritis, Rheumatoid - immunology; Arthritis, Rheumatoid - physiopathology; Autoimmune Diseases - immunology; Autoimmune Diseases - physiopathology; Autoimmunity; Central Nervous System - immunology; Central Nervous System - physiology; Disease Models, Animal; Electrophysiology; Epilepsy - immunology; Epilepsy - physiopathology; Ganglia, Spinal - cytology; Ganglia, Spinal - physiology; Humans; Inflammation - immunology; Inflammation - physiopathology; Interleukin-17 - physiology; Lymphocyte Subsets - immunology; Lymphocyte Subsets - metabolism; Mice; Nerve Degeneration - immunology; Nerve Degeneration - metabolism; Neuralgia - immunology; Neuralgia - physiopathology; Neurite sprouting; Neuroglia - metabolism; Neuroimmunomodulation - physiology; Neurons - metabolism; Neuropathology; Pain Perception - physiology; Plasticity; Psychiatry; Rats; Receptors, Interleukin-17 - physiology; Th17 Cells - immunology
• ISSN: 0889-1591; 1090-2139
• DOI: 10.1016/j.bbi.2014.03.004

Abstract Inflammation involving the helper T cell 17 (Th17) subset of lymphocytes has been implicated in a number of diseases that affect the nervous system. As the canonical cytokine of Th17 cells, interleukin 17A (IL-17A) is thought to contribute to these neuroimmune interactions. The main receptor for IL-17A is expressed in many neural tissues. IL-17A has direct effects on neurons but can also impact neural function via signaling to satellite cells and immune cells. In the central nervous system, IL-17A has been associated with neuropathology in multiple sclerosis, epilepsy syndromes and ischemic brain injury. Effects of IL-17A at the level of dorsal root ganglia and the spinal cord may contribute to enhanced nociception during neuropathic and inflammatory pain. Finally, IL-17A plays a role in sympathetic axon growth and regeneration of damaged axons that innervate the cornea. Given the widespread effects of IL-17A on neural tissues, it will be important to determine whether selectively mitigating the damaging effects of this cytokine while augmenting its beneficial effects is a possible strategy to treat inflammatory damage to the nervous system.