[1] Walker LC, Jucker M. Neurodegenerative diseases: expanding the prion concept. Annu Rev Neurosci, 2015; 38, 87−103. doi:  10.1146/annurev-neuro-071714-033828
[2] Chen C, Dong XP. Epidemiological characteristics of human prion diseases. Infect Dis Poverty, 2016; 5, 47. doi:  10.1186/s40249-016-0143-8
[3] Aguzzi A, Nuvolone M, Zhu CH. The immunobiology of prion diseases. Nat Rev Immunol, 2013; 13, 888−902. doi:  10.1038/nri3553
[4] Gasque P, Dean YD, McGreal EP, et al. Complement components of the innate immune system in health and disease in the CNS. Immunopharmacology, 2000; 49, 171−86. doi:  10.1016/S0162-3109(00)80302-1
[5] Boshtam M, Asgary S, Kouhpayeh S, et al. Aptamers against pro- and anti-inflammatory cytokines: a review. Inflammation, 2017; 40, 340−9. doi:  10.1007/s10753-016-0477-1
[6] Tribouillard-Tanvier D, Striebel JF, Peterson KE, et al. Analysis of protein levels of 24 cytokines in scrapie agent-infected brain and glial cell cultures from mice differing in prion protein expression levels. J Virol, 2009; 83, 11244−53. doi:  10.1128/JVI.01413-09
[7] Xie WL, Shi Q, Zhang J, et al. Abnormal activation of microglia accompanied with disrupted CX3CR1/CX3CL1 pathway in the brains of the hamsters infected with scrapie agent 263K. J Mol Neurosci, 2013; 51, 919−32. doi:  10.1007/s12031-013-0002-z
[8] Felton LM, Cunningham C, Rankine EL, et al. MCP-1 and murine prion disease: separation of early behavioural dysfunction from overt clinical disease. Neurobiol Dis, 2005; 20, 283−95. doi:  10.1016/j.nbd.2005.03.008
[9] Saas P, Boucraut J, Quiquerez AL, et al. CD95 (Fas/Apo-1) as a receptor governing astrocyte apoptotic or inflammatory responses: a key role in brain inflammation? J Immunol, 1999; 162, 2326-33.
[10] Gossner A, Hunter N, Hopkins J. Role of lymph-borne cells in the early stages of scrapie agent dissemination from the skin. Vet Immunol Immunopathol, 2006; 109, 267−78. doi:  10.1016/j.vetimm.2005.08.021
[11] Schultz J, Schwarz A, Neidhold S, et al. Role of interleukin-1 in prion disease-associated astrocyte activation. Am J Pathol, 2004; 165, 671−8. doi:  10.1016/S0002-9440(10)63331-7
[12] Rossi D, Zlotnik A. The biology of chemokines and their receptors. Annu Rev Immunol, 2000; 18, 217−42. doi:  10.1146/annurev.immunol.18.1.217
[13] Belperio JA, Keane MP, Arenberg DA, et al. CXC chemokines in angiogenesis. J Leukoc Biol, 2000; 68, 1−8. doi:  10.1189/jlb.68.1.1
[14] Wightman SC, Uppal A, Pitroda SP, et al. Oncogenic CXCL10 signalling drives metastasis development and poor clinical outcome. Br J Cancer, 2015; 113, 327−35. doi:  10.1038/bjc.2015.193
[15] Banquet S, Delannoy E, Agouni A, et al. Role of Gi/o-Src kinase-PI3K/Akt pathway and caveolin-1 in β2-adrenoceptor coupling to endothelial NO synthase in mouse pulmonary artery. Cell Signalling, 2011; 23, 1136−43. doi:  10.1016/j.cellsig.2011.02.008
[16] Chou CH, Wei LH, Kuo ML, et al. Up-regulation of interleukin-6 in human ovarian cancer cell via a Gi/PI3K-Akt/NF-κB pathway by lysophosphatidic acid, an ovarian cancer-activating factor. Carcinogenesis, 2005; 26, 45−52.
[17] Ding Q, Lu PP, Xia YJ, et al. CXCL9: evidence and contradictions for its role in tumor progression. Cancer Med, 2016; 5, 3246−59. doi:  10.1002/cam4.934
[18] Hsieh MJ, Tsai TL, Hsieh YS, et al. Dioscin-induced autophagy mitigates cell apoptosis through modulation of PI3K/Akt and ERK and JNK signaling pathways in human lung cancer cell lines. Arch Toxicol, 2013; 87, 1927−37. doi:  10.1007/s00204-013-1047-z
[19] Hueso L, Ortega R, Selles F, et al. Upregulation of angiostatic chemokines IP-10/CXCL10 and I-TAC/CXCL11 in human obesity and their implication for adipose tissue angiogenesis. Int J Obes, 2018; 42, 1406−17. doi:  10.1038/s41366-018-0102-5
[20] Kouroumalis A, Nibbs RJ, Aptel H, et al. The chemokines CXCL9, CXCL10, and CXCL11 differentially stimulate Gαi-independent signaling and actin responses in human intestinal myofibroblasts. J Immunol, 2005; 175, 5403−11. doi:  10.4049/jimmunol.175.8.5403
[21] Nash CA, Séverin S, Dawood BB, et al. Src family kinases are essential for primary aggregation by Gi-coupled receptors. J Thromb Haemostasis, 2010; 8, 2273−82. doi:  10.1111/j.1538-7836.2010.03992.x
[22] Fang JX, Wang C, Shen C, et al. The expression of CXCL10/CXCR3 and effect of the axis on the function of T lymphocyte involved in oral lichen planus. Inflammation, 2019; 42, 799−810. doi:  10.1007/s10753-018-0934-0
[23] Li JH, Ge ML, Lu SH, et al. Pro-inflammatory effects of the Th1 chemokine CXCL10 in acquired aplastic anaemia. Cytokine, 2017; 94, 45−51. doi:  10.1016/j.cyto.2017.04.010
[24] Trotta T, Costantini S, Colonna G. Modelling of the membrane receptor CXCR3 and its complexes with CXCL9, CXCL10 and CXCL11 chemokines: putative target for new drug design. Mol Immunol, 2009; 47, 332−9. doi:  10.1016/j.molimm.2009.09.013
[25] Chen J, Chen C, Hu C, et al. IP10, KC and M-CSF are remarkably increased in the brains from the various strains of experimental mice infected with different scrapie agents. Virol Sin, 2020; 35, 614−25. doi:  10.1007/s12250-020-00216-3
[26] Xiao K, Zhang BY, Zhang XM, et al. Re-infection of the prion from the scrapie-infected cell line SMB-S15 in three strains of mice, CD1, C57BL/6 and Balb/c. Int J Mol Med, 2016; 37, 716−26. doi:  10.3892/ijmm.2016.2465
[27] Shi Q, Zhang BY, Gao C, et al. Mouse-adapted scrapie strains 139A and ME7 overcome species barrier to induce experimental scrapie in hamsters and changed their pathogenic features. Virol J, 2012; 9, 63. doi:  10.1186/1743-422X-9-63
[28] Clarke MC, Haig DA. Multiplication of scrapie agent in mouse spleen. Res Vet Sci, 1971; 12(2), 195-7.
[29] Birkett CR, Hennion RM, Bembridge DA, et al. Scrapie strains maintain biological phenotypes on propagation in a cell line in culture. EMBO J, 2001; 20, 3351−8. doi:  10.1093/emboj/20.13.3351
[30] Niu PH, Zhang SY, Zhou PP, et al. Ultrapotent human neutralizing antibody repertoires against middle east respiratory syndrome coronavirus from a recovered patient. J Infect Dis, 2018; 218, 1249−60. doi:  10.1093/infdis/jiy311
[31] Wang J, Zhang BY, Zhang J, et al. Treatment of SMB-S15 cells with resveratrol efficiently removes the PrPSc accumulation in vitro and prion infectivity in vivo. Mol Neurobiol, 2016; 53, 5367−76. doi:  10.1007/s12035-015-9464-z
[32] Prasad KN, Bondy SC. Oxidative and inflammatory events in prion diseases: can they be therapeutic targets? Curr Aging Sci, 2019; 11, 216-25.
[33] Lv Y, Chen C, Zhang BY, et al. Remarkable activation of the complement system and aberrant neuronal localization of the membrane attack complex in the brain tissues of scrapie-infected rodents. Mol Neurobiol, 2015; 52, 1165−79. doi:  10.1007/s12035-014-8915-2
[34] Chen C, Lv Y, Hu C, et al. Alternative complement pathway is activated in the brains of scrapie-infected rodents. Med Microbiol Immunol, 2020; 209, 81−94. doi:  10.1007/s00430-019-00641-6
[35] Ma Y, Shi Q, Wang J, et al. Reduction of NF-κB (p65) in scrapie-infected cultured cells and in the brains of scrapie-infected rodents. ACS Chem Neurosci, 2017; 8, 2535−48. doi:  10.1021/acschemneuro.7b00273
[36] Ma Y, Shi Q, Xiao K, et al. Stimulations of the culture medium of activated microglia and TNF-alpha on a scrapie-infected cell line decrease the cell viability and induce marked necroptosis that also occurs in the brains from the patients of human prion diseases. ACS Chem Neurosci, 2019; 10, 1273−83. doi:  10.1021/acschemneuro.8b00354
[37] Salvesen Ø, Tatzelt J, Tranulis MA. The prion protein in neuroimmune crosstalk. Neurochem Int, 2019; 130, 104335. doi:  10.1016/j.neuint.2018.11.010
[38] Shen Q, Zhang R, Bhat NR. MAP kinase regulation of IP10/CXCL10 chemokine gene expression in microglial cells. Brain Res, 2006; 1086, 9−16. doi:  10.1016/j.brainres.2006.02.116
[39] Sui Y, Potula R, Dhillon N, et al. Neuronal apoptosis is mediated by CXCL10 overexpression in simian human immunodeficiency virus encephalitis. Am J Pathol, 2004; 164, 1557−66. doi:  10.1016/S0002-9440(10)63714-5
[40] Lang S, Li LB, Wang XN, et al. CXCL10/IP-10 neutralization can ameliorate lipopolysaccharide-induced acute respiratory distress syndrome in rats. PLoS One, 2017; 12, e0169100. doi:  10.1371/journal.pone.0169100
[41] Rocha NP, Scalzo PL, Barbosa IG, et al. Cognitive status correlates with CXCL10/IP-10 levels in Parkinson’s disease. Parkinson’s Dis, 2014; 2014, 903796.
[42] Duan RS, Yang X, Chen ZG, et al. Decreased fractalkine and increased IP-10 expression in aged brain of APPswe transgenic mice. Neurochem Res, 2008; 33, 1085−9. doi:  10.1007/s11064-007-9554-z
[43] Bettcher BM, Johnson SC, Fitch R, et al. Cerebrospinal fluid and plasma levels of inflammation differentially relate to CNS markers of Alzheimer’s disease pathology and neuronal damage. J Alzheimer’s Dis, 2018; 62, 385−97. doi:  10.3233/JAD-170602
[44] Mohd Hasni DS, Lim SM, Chin AV, et al. Peripheral cytokines, C-X-C motif ligand10 and interleukin-13, are associated with Malaysian Alzheimer's disease. Geriatr Gerontol Int, 2017; 17, 839−46. doi:  10.1111/ggi.12783
[45] Hirsch EC, Vyas S, Hunot S. Neuroinflammation in Parkinson's disease. Parkinsonism Relat Disord, 2012; 18, S210−2.
[46] Simpson JE, Newcombe J, Cuzner ML, et al. Expression of the interferon-γ-inducible chemokines IP-10 and Mig and their receptor, CXCR3, in multiple sclerosis lesions. Neuropathol Appl Neurobiol, 2000; 26, 133−42. doi:  10.1046/j.1365-2990.2000.026002133.x
[47] Krauthausen M, Saxe S, Zimmermann J, et al. CXCR3 modulates glial accumulation and activation in cuprizone-induced demyelination of the central nervous system. J Neuroinflammation, 2014; 11, 109. doi:  10.1186/1742-2094-11-109
[48] Zhou YQ, Liu DQ, Chen SP, et al. The role of CXCR3 in neurological diseases. Curr Neuropharmacol, 2019; 17, 142−50. doi:  10.2174/1570159X15666171109161140
[49] Xia MQ, Bacskai BJ, Knowles RB, et al. Expression of the chemokine receptor CXCR3 on neurons and the elevated expression of its ligand IP-10 in reactive astrocytes: in vitro ERK1/2 activation and role in Alzheimer’s disease. J Neuroimmunology, 2000; 108, 227−35. doi:  10.1016/S0165-5728(00)00285-X
[50] Balashov KE, Rottman JB, Weiner HL, et al. CCR5+ and CXCR3+ T cells are increased in multiple sclerosis and their ligands MIP-1αand IP-10 are expressed in demyelinating brain lesions. Proc Natl Acad Sci USA, 1999; 96, 6873−8. doi:  10.1073/pnas.96.12.6873
[51] van Wanrooij EJ, de Jager SC, van Es T, et al. CXCR3 antagonist NBI-74330 attenuates atherosclerotic plaque formation in LDL receptor-deficient mice. Arterioscler Thromb Vasc Biol, 2008; 28, 251−7. doi:  10.1161/ATVBAHA.107.147827
[52] Zernecke A, Shagdarsuren E, Weber C. Chemokines in atherosclerosis: an update. Arterioscler Thromb Vasc Biol, 2008; 28, 1897−908. doi:  10.1161/ATVBAHA.107.161174
[53] Ferrari SM, Ruffilli I, Colaci M, et al. CXCL10 in psoriasis. Adv Med Sci, 2015; 60, 349−54. doi:  10.1016/j.advms.2015.07.011
[54] Krauthausen M, Kummer MP, Zimmermann J, et al. CXCR3 promotes plaque formation and behavioral deficits in an Alzheimer'’s disease model. J Clin Invest, 2015; 125, 365−78. doi:  10.1172/JCI66771
[55] Riemer C, Schultz J, Burwinkel M, et al. Accelerated prion replication in, but prolonged survival times of, prion-infected CXCR3-/- mice. J Virol, 2008; 82, 12464−71. doi:  10.1128/JVI.01371-08
[56] Guedes JR, Lao TT, Cardoso AL, et al. Roles of microglial and monocyte chemokines and their receptors in regulating Alzheimer’s disease-associated amyloid-β and tau pathologies. Front Neurol, 2018; 9, 549. doi:  10.3389/fneur.2018.00549
[57] Sui Y, Stehno-Bittel L, Li SP, et al. CXCL10-induced cell death in neurons: role of calcium dysregulation. Eur J Neurosci, 2006; 23, 957−64. doi:  10.1111/j.1460-9568.2006.04631.x
[58] Peggion C, Bertoli A, Sorgato MC. Possible role for Ca2+ in the pathophysiology of the prion protein? BioFactors, 2011; 37, 241-9.
[59] De Mario A, Peggion C, Massimino ML, et al. The link of the prion protein with Ca2+ metabolism and ROS production, and the possible implication in aβ toxicity. Int J Mol Sci, 2019; 20, 4640. doi:  10.3390/ijms20184640