免疫镇痛（英文）.pdfVIP

Arch. Immunol. Ther. Exp. (2011) 59:11–24 DOI 10.1007/s00005-010-0106-x REVIEW Dual Peripheral Actions of Immune Cells in Neuropathic Pain Halina Machelska Received: 16 March 2010 / Accepted: 13 September 2010 / Published online: 14 January 2011 L. Hirszfeld Institute of Immunology and Experimental Therapy, Wroclaw, Poland 2011 Abstract Ability to perceive physiological pain is Abbreviations essential in protecting the individual from tissue destruc- CCI Chronic constriction injury tion. In contrast, pathological chronic pain is an expression CFA Complete Freund’s adjuvant of maladaptive alterations outlasting its biological useful- CGRP Calcitonin gene-related peptide ness. In such conditions even eating, speaking or wearing CNS Central nervous system clothes might be painful, as in neuropathic pain. Such pain CRF Corticotropin-releasing factor is caused by diseases or injuries affecting nerves (e.g. CXCL1 Chemokine (C-X-C motif) ligand 1 diabetes, trigeminal neuralgia or amputation). Neuropathic (keratinocyte-derived chemokine) pain is not an exclusive neuronal phenomenon but also CXCL2/3 Chemokine (C-X-C motif) ligand 2 involves immune responses. Damaged peripheral nerves (macrophage inflammatory protein-2) are infiltrated by mast cells, granulocytes, macrophages CXCR2 CXC chemokine receptor 2 and T lymphocytes. It is widely emphasized that these DRG Dorsal root ganglion cells, via secretion of inflammatory mediators (e.g. proin- ICAM-1 Intercellular adhesion molecule-1 flammatory cytokines, chemokines), contribute to the IL Interleukin generation of neuropathic pain. However, l