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GLIA: A NOVEL DRUG DISCOVERY TARGET FOR CLINICAL PAIN

GLIA: A NOVEL DRUG DISCOVERY TARGET FOR CLINICAL PAIN

GLIA: A NOVEL DRUG DISCOVERY TARGET FOR CLINICAL PAIN

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REVIEWS107. Cronstein, B. N., Naime, D. & Ostad, E. The antiinflammatoryeffects of methotrexate are mediated byadenosine. Adv. Exp. Med. Biol. 370, 411–416 (1994).108. Montesinos, M. C. et al. Reversal of the antiinflammatoryeffects of methotrexate by the nonselective adenosinereceptor antagonists theophylline and caffeine: evidencethat the antiinflammatory effects of methotrexate aremediated via multiple adenosine receptors in rat adjuvantarthritis. Arthritis Rheum. 43, 656–663 (2000).109. Neurath, M. F. et al. Methotrexate specifically modulatescytokine production by T cells and macrophages in murinecollagen-induced arthritis (CIA): a mechanism formethotrexate-mediated immunosuppression. Clin. Exp.Immunol. 115, 42–55 (1999).110. Hayem, G., Domarle, O., Thuong-Guyot, M., Pocidalo, J. J.& Meyer, O. Effects of methotrexate on the oxidativemetabolism of cultured rabbit articular chondrocytes.J. Rheumatol. 27, 1117–1120 (2000).111. Rudwaleit, M. et al. Response to methotrexate in earlyrheumatoid arthritis is associated with a decrease of T cellderived tumour necrosis factor-α, increase of interleukin-10,and predicted by the initial concentration of interleukin-4.Ann. Rheum. Dis. 59, 311–314 (2000).112. Brody, M., Bohm, I. & Bauer, R. Mechanism of action ofmethotrexate: experimental evidence that methotrexateblocks the binding of interleukin-1β to the interleukin-1receptor on target cells. Eur. J. Clin. Chem. Clin. Biochem.31, 667–674 (1993).113. Segal, R., Mozes, E., Yaron, M. & Tartakovsky, B. The effectsof methotrexate on the production and activity of interleukin-1.Arthritis Rheum. 32, 370–377 (1989).114. Segal, R., Yaron, M. & Tartakovsky, B. Rescue ofinterleukin-1 activity by leucovorin following inhibition bymethotrexate in a murine in vitro system. Arthritis Rheum.33, 1745–1748 (1990).115. Gregorios, J. B. et al. Morphologic alterations in rat brainfollowing systemic and intraventricular methotrexateinjection: light and electron microscopic studies.J. Neuropathol. Exp. Neurol. 48, 33–47 (1989).116. Hommes, D. et al. Inhibition of stress-activated MAP kinasesinduces clinical improvement in moderate to severe Crohn’sdisease. Gastroenterology 122, 7–14 (2002).117. Lali, F. V., Hunt, A. E., Turner, S. J. & Foxwell, B. M. Thepyridinyl imidazole inhibitor SF203580 blocksphosphoinositide-dependent protein kinase activity, proteinkinase B phosphorylation, and retinoblastomahyperphosphorylation in interleukin-2-stimulated T cellsindependently of p38 mitogen-activated protein kinase.J. Biol. Chem. 275, 7395–7402 (2000).118. Dunn, S. L., Young, E. A., Hall, M. D. & McNulty, S. Activationof astrocyte intracellular signaling pathways by interleukin-1 inrat primary striatal cultures. Glia 37, 31–42 (2002).119. Jeohn, G. H. et al. Go6976 inhibits LPS-induced microglialTNF-α release by suppressing p38 MAP kinase activation.Neuroscience 114, 689–697 (2002).120. Jin, S. X., Zhaung, Z. Y., Woolf, C. J. & Ji, R. R. p38 MAPK isactivated after a spinal nerve ligation first in spinal cordmicroglia and then in DRG neurons and contributes to thegeneration of neuropathic pain. J. Neurosci. 23, 4017–4022(2003).121. Kim, S. Y. et al. Activation of p38 MAP kinase in the rat dorsalroot ganglia and spinal cord following peripheral inflammationand nerve injury. Neuroreport 13, 2483–2486 (2002).122. Hamilton, T. A., Ohmori, Y., Tebo, J. M. & Kishore, R.Regulation of macropahge gene expression by pro- and antiinflammatorycytokines. Pathobiology 67, 241–244 (1999).123. Kontoyiannis, D. et al. Interleukin-10 targets p38 MAPK tomodulate ARE-dependent TNF mRNA translation and limitintestinal pathology. EMBO J. 20, 3760–3770 (2001).124. Donnelly, R. P., Dickensheets, H. & Finbloom, D. S. Theinterleukin-10 signal transduction pathway and regulation ofgene expression in mononuclear phagocytes. J. InterferonCytokine Res. 19, 563–573 (1999).125. Sawada, M., Suzumura, A., Hosoya, H., Marunouchi, T. &Nagatsu, T. Interleukin-10 inhibits both production ofcytokines and expression of cytokine receptors in microglia.J. Neurochem. 72, 1466–1471 (1999).126. Foey, A. D. et al. Regulation of monocyte IL-10 synthesis byendogenous IL-1 and TNF-α: role of the p38 and p42/44mitogen-activated protein kinases. J. Immunol. 160,920–928 (1998).127. Huber, T. S. et al. Anticytokine therapies for acuteinflammation and the systemic inflammatory responsesyndrome: IL-10 and ischemia/reperfusion injury. Shock13, 425–434 (2000).128. Bachis, A. et al. Interleukin-10 prevents glutamate-mediatedcerebellar granule cell death by blocking caspase-3-likeactivity. J. Neurosci. 21, 3104–3112 (2001).129. Milligan, E. D. et al. Inflammatory and chronic constrictioninjury-induced pain states are controlled by spinal deliveryof viral and non-viral vectors encoding the antiinflammatorygene, interleukin-10 (IL10). Proc. Soc.Neurosci. 29 (in the press).130. Kastin, A. J., Akerstrom, V. & Pan, W. Interleukin-10 as aCNS therapeutic: the obstacle of theblood–brain/blood–spinal cord barrier. Brain Res. Mol.Brain Res. 114, 168–171 (2003).131. Davidson, B. L. & Breakefield, X. O. Viral vectors for genedelivery to the nervous system. Nature Rev. Neurosci. 4,353–364 (2003).This review article focuses on the promise of genetherapy for the resolution of a variety of clinical targets.132. Xu, Z. L., Mizuguchi, H., Mayumi, T. & Hayakawa, T.Regulated gene expression from adenovirus vectors: asystematic comparison of various inducible systems.Gene 309, 145–151 (2003).133. Wiesler-Frank, J., Milligan, E. D., Maier, S. F. & Watkins, L. R.in Encyclopedic Reference of Pam (eds Schmidt, R. &Willis, W. D.) (Springer, Berlin, in the press).134. Volterra, A. & Bezzi, P. in The Tripartite Synapse (edsVolterra, A., Magistretti, P. J. & Hayden, P. G.) 164–182(Oxford Univ. Press, Oxford, 2002).AcknowledgementsOur laboratory is supported by grants from the National Institute onDrug Abuse, National Institute of Neurological Diseases and Stroke,and National Institute of Mental Health.Competing interest statementThe authors declare competing financial interests: see Web versionfor details.Online linksDATABASESThe following terms in this article are linked online to:LocusLink: http://www.ncbi.nlm.nih.gov/LocusLink/CX3CR1 | fractalkineOnline Mendelian Inheritance in Man:http://www.ncbi.nlm.nih.gov/Omim/Alzheimer’s disease | Crohn’s disease | rheumatoid arthritisAccess to this interactive links box is free online.NATURE REVIEWS | <strong>DRUG</strong> <strong>DISCOVERY</strong> VOLUME 2 | DECEMBER 2003 | 985

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