279
Views
17
CrossRef citations to date
0
Altmetric
Research Articles

Variants of autophagy-related gene 5 are associated with neuromyelitis optica in the Southern Han Chinese population

, , , , , & show all
Pages 563-566 | Received 08 Mar 2014, Accepted 25 May 2014, Published online: 23 Jun 2014

References

  • Compston, and A., A. Coles. 2008. Multiple sclerosis. Lancet 372: 1502–1517
  • Mitsdoerffer, M., V. Kuchroo, and T. Korn. 2013. Immunology of neuromyelitis optica: a T cell-B cell collaboration. Ann. N. Y. Acad. Sci. 1283: 57–66
  • de Seze, J. 2003. Neuromyelitis optica. Arch. Neurol. 60: 1336–1338
  • Matsuoka, T., T. Matsushita, Y. Kawano, et al. 2007. Heterogeneity of aquaporin-4 autoimmunity and spinal cord lesions in multiple sclerosis in Japanese. Brain 130: 1206–1223
  • Lennon, V. A., D. M. Wingerchuk, T. J. Kryzer, et al. 2004. A serum autoantibody marker of neuromyelitis optica: distinction from multiple sclerosis. Lancet 364: 2106–2112
  • Jarius, S., F. Paul, D. Franciotta, et al. 2007. Revised diagnostic criteria for neuromyelitis optica – incorporation of NMO-IgG status. Nat. Clin. Pract. Neurol. 3: E1. doi:10.1038/ncpneuro0501
  • Papadopoulos, M. C., and A. S. Verkman. 2012. Aquaporin 4 and neuromyelitis optica. Lancet Neurol. 11: 535–544
  • Jarius, S., and B. Wildemann. 2010. AQP4 antibodies in neuromyelitis optica: diagnostic and pathogenetic relevance. Nat. Rev. Neurol. 6: 383–392
  • Fujihara, K. 2011. Neuromyelitis optica and astrocytic damage in its pathogenesis. J. Neurol. Sci. 306: 183–187
  • Vincent, T., P. Saikali, R. Cayrol, et al. 2008. Functional consequences of neuromyelitis optica-IgG astrocyte interactions on blood-brain barrier permeability and granulocyte recruitment. J. Immunol. 181: 5730–5737
  • Takano, R., T. Misu, T. Takahashi, et al. 2010. Astrocytic damage is far more severe than demyelination in NMO: a clinical CSF biomarker study. Neurology 75: 208–216
  • Irani, S., and B. Lang. 2008. Autoantibody-mediated disorders of the central nervous system. Autoimmunity 41: 55–65
  • Alirezaei, M., H. S. Fox, C. T. Flynn, et al. 2009. Elevated ATG5 expression in autoimmune demyelination and multiple sclerosis. Autophagy 5: 152–158
  • Miller, B. C., Z. Zhao, L. M. Stephenson, et al. 2008. The autophagy gene ATG5 plays an essential role in B lymphocyte development. Autophagy 4: 309–314
  • Conway, K. L., P. Kuballa, B. Khor, et al. 2013. ATG5 regulates plasma cell differentiation. Autophagy 9: 528–537
  • Bhattacharya, A., and N. T. Eissa. 2013. Autophagy and autoimmunity crosstalks. Front. Immunol. 4: 88. doi: 10.3389/fimmu.2013.00088
  • Levine, B., N. Mizushima, and H. W. Virgin. 2011. Autophagy in immunity and inflammation. Nature 469: 323–335
  • Zhou, X. J., and H. Zhang. 2012. Autophagy in immunity: implications in etiology of autoimmune/autoinflammatory diseases. Autophagy 8: 1286–1299
  • Pua, H. H., and Y. W. He. 2007. Maintaining T lymphocyte homeostasis: another duty of autophagy. Autophagy 3: 266–267
  • Pua, H. H., I. Dzhagalov, M. Chuck, et al. 2007. A critical role for the autophagy gene Atg5 in T cell survival and proliferation. J. Exp. Med. 204: 25–31
  • , International Consortium for Systemic Lupus ErythematosusJ. B. Harley, M. E. Alarcon-Riquelme, et al. 2008. Genome-wide association scan in women with systemic lupus erythematosus identifies susceptibility variants in ITGAM, PXK, KIAA1542 and other loci. Nat. Genet. 40: 204–210
  • Gateva, V., J. K. Sandling, G. Hom, et al. 2009. A large-scale replication study identifies TNIP1, PRDM1, JAZF1, UHRF1BP1 and IL10 as risk loci for systemic lupus erythematosus. Nat. Genet. 41: 1228–1233
  • Zhou, X. J., X. L. Lu, J. C. Lv, et al. 2011. Genetic association of PRDM1-ATG5 intergenic region and autophagy with systemic lupus erythematosus in a Chinese population. Ann. Rheum. Dis. 70: 1330–1337
  • Han, J. W., H. F. Zheng, Y. Cui, et al. 2009. Genome-wide association study in a Chinese Han population identifies nine new susceptibility loci for systemic lupus erythematosus. Nat. Genet. 41: 1234–1237
  • Wellcome Trust Case Control Consortium. 2007. Genome-wide association study of 14,000 cases of seven common diseases and 3,000 shared controls. Nature 447: 661–678
  • Gregersen, P. K., C. I. Amos, A. T. Lee, et al. 2009. REL, encoding a member of the NF-kappaB family of transcription factors, is a newly defined risk locus for rheumatoid arthritis. Nat. Genet. 41: 820–823
  • Kochi, Y., Y. Okada, A. Suzuki, et al. 2010. A regulatory variant in CCR6 is associated with rheumatoid arthritis susceptibility. Nat. Genet. 42: 515–519
  • Barrett, J. C., S. Hansoul, D. L. Nicolae, et al. 2008. Genome-wide association defines more than 30 distinct susceptibility loci for Crohn's disease. Nat. Genet 40: 955–962
  • Wingerchuk, D. M., V. A. Lennon, S. J. Pittock, et al. 2006. Revised diagnostic criteria for neuromyelitis optica. Neurology 66: 1485–1489
  • Polman, C. H., S. C. Reingold, B. Banwell, et al. 2011. Diagnostic criteria for multiple sclerosis: 2010 revisions to the McDonald criteria. Ann. Neurol. 69: 292–302
  • Zhao, G. X., Y. Liu, Z. X. Li, et al. 2013. Variants in the promoter region of CYP7A1 are associated with neuromyelitis optica but not with multiple sclerosis in the Han Chinese population. Neurosci. Bull. 29: 525–530
  • Lee, H. K., J. M. Lund, B. Ramanathan, et al. 2007. Autophagy-dependent viral recognition by plasmacytoid dendritic cells. Science 315: 1398–1401
  • Shi, C. S., and J. H. Kehrl. 2010. TRAF6 and A20 regulate lysine 63-linked ubiquitination of Beclin-1 to control TLR4-induced autophagy. Sci. Signal. 3: ra42. doi: 10.1126/scisignal.2000751
  • Blanchet, F. P., and V. Piguet. 2010. Immunoamphisomes in dendritic cells amplify TLR signaling and enhance exogenous antigen presentation on MHC-II. Autophagy 6: 816–818
  • Latiano, A., O. Palmieri, S. Cucchiara, et al. 2009. Polymorphism of the IRGM gene might predispose to fistulizing behavior in Crohn's disease. Am. J. Gastroenterol. 104: 110–116
  • Watanabe, K., S. Ichinose, K. Hayashizaki, and T. Tsubata. 2008. Induction of autophagy by B cell antigen receptor stimulation and its inhibition by costimulation. Biochem. Biophys. Res. Commun. 374: 274–281
  • Pua, H. H., and Y. W. He. 2009. Autophagy and lymphocyte homeostasis. Curr. Top. Microbiol. Immunol. 335: 85–105
  • Lu, X. L., X. J. Zhou, J. P. Guo, et al. 2011. Rs548234 polymorphism at PRDM1-ATG5 region susceptible to rheumatoid arthritis in Caucasians is not associated with rheumatoid arthritis in Chinese Han population. Chin. Med. J. 124: 2863–2867
  • Raychaudhuri, S., B. P. Thomson, E. F. Remmers, et al. 2009. Genetic variants at CD28, PRDM1 and CD2/CD58 are associated with rheumatoid arthritis risk. Nat. Genet. 41: 1313–1318
  • Wang, H., Y. Dai, W. Qiu, et al. 2011. HLA-DPB1 0501 is associated with susceptibility to anti-aquaporin-4 antibodies positive neuromyelitis optica in southern Han Chinese. J. Neuroimmunol. 233: 181–184
  • Wang, H., X. Zhong, K. Wang, et al. 2012. Interleukin 17 gene polymorphism is associated with anti-aquaporin 4 antibody-positive neuromyelitis optica in the Southern Han Chinese – a case control study. J. Neurol. Sci. 314: 26–28
  • Takahashi, T., K. Fujihara, I. Nakashima, et al. 2007. Anti-aquaporin-4 antibody is involved in the pathogenesis of NMO: a study on antibody titre. Brain 130: 1235–1243
  • Lu, Z., W. Qiu, Y. Zou, et al. 2010. Characteristic linear lesions and longitudinally extensive spinal cord lesions in Chinese patients with neuromyelitis optica. J. Neurol. Sci. 293: 92–96

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.