Interleukin-17 gene polymorphism is associated with Vogt–Koyanagi–Harada syndrome but not with Behçet's disease in a Chinese Han population

Shu, Qinmeng; Yang, Peizeng; Hou, Shengping; Li, Fuzhen; Chen, Yuanyuan; Du, Liping; Jiang, Zhengxuan

doi:10.1016/j.humimm.2010.06.020

Cited by 67 publications

(48 citation statements)

References 62 publications

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“…IL-17 was found to stimulate fibroblasts to produce IL-6, IL-11, IL-8 (Mo et al, 2001;Ran et al, 2012). Majority of analyzes about genetic polymorphism of IL-17 were focus on a range of cancers, including breast cancer, gastric cancer and cervical cancer (Quan et al, 2005;Shibata et al, 2009;Shu et al, 2010;Wang et al, 2012). But no analysis about the relationship between IL-17 polymorphisms and silicosis has been reported.…”

Section: Discussionmentioning

confidence: 99%

Association between Polymorphisms of Interleukin-17A and Interleukin-17F Genes and Silicosis Susceptibility in Chinese Han People

Chen

Fan²,

Jin³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Section: Discussionmentioning

confidence: 99%

Association between Polymorphisms of Interleukin-17A and Interleukin-17F Genes and Silicosis Susceptibility in Chinese Han People

Chen

Fan²,

Jin³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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“…Our previous studies have shown that polymorphisms of genes encoding interleukin (IL)-17, STAT4, and IL-23R are associated with the susceptibility to VKH syndrome. [14][15][16] These findings indicate that genetic factors may play an important role in the development of VKH syndrome. Janus kinase 1 (JAK1), Janus kinase 2 (JAK2), and signal transducer and activator of transcription 3 (STAT3) axis have been reported to be critical for Th1 and Th17 cell differentiation.…”

mentioning

confidence: 82%

JAK1, but NotJAK2andSTAT3, Confers Susceptibility to Vogt–Koyanagi–Harada (VKH) Syndrome in a Han Chinese Population

Hou

et al. 2013

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. Janus kinase 1 (JAK1), JAK2, and signal transducer and activator of transcription 3 (STAT3) play an important role in Th1 and Th17 differentiation and gene polymorphisms of these factors have been demonstrated to be associated with certain autoimmune diseases. The present study was performed to assess the association between JAK1, JAK2, and STAT3 polymorphisms and Vogt-Koyanagi-Harada (VKH) syndrome in a Han Chinese population. METHODS.A case-control study was performed in 737 Chinese VKH syndrome patients and 809 healthy controls from a Han Chinese population. The genotypes of three singlenucleotide polymorphisms (SNPs) (rs310230, rs310236, rs310241) in JAK1 were performed using an SNP genotyping system. Three SNPs (rs10758669, rs7857730, rs10119004) in JAK2 and four SNPs (rs6503695, rs744166, rs2293152, and rs12948909) in STAT3 were analyzed using polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP). Hardy-Weinberg equilibrium (HWE) was tested using the v 2 test. Genotype frequencies were estimated through direct counting. Allele and genotype frequencies were compared between patients and controls using the v 2 test.RESULTS. There was no deviation from the HWE in all controls tested. Three SNPs, including rs310230, rs310236, and rs310241, in JAK1 were significantly associated with VKH syndrome (Pc ¼ 0.008, 0.005, 0.001, respectively). None of the tested SNPs of JAK2 and STAT3 was associated with VKH syndrome. Stratification analysis according to headache, dysacusis, alopecia, poliosis, and vitiligo for VKH syndrome did not reveal an association.CONCLUSIONS. These results suggest that JAK1 genetic polymorphisms, but not JAK2 and STAT3, are associated with the susceptibility to VKH syndrome.

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“…Vogt -Koyanagi -Harada disease is a bilateral, chronic, diffuse granulomatous uveitis with poliosis, vitiligo, central nervous system, and auditory signs. Many researchers, especially Yang's group, have investigated the gene polymorphisms of many factors including IL-17 that are associated with Vogt -Koyanagi -Harada disease in a Chinese Han population (Shu et al 2010) since Yakura et al first reported the HLA-D locus linkage (Yakura et al 1976 (Heyn et al 2013). …”

Section: Acquired Hypopigmentation Disordersmentioning

confidence: 99%

Melanocytes and Their Diseases

Yamaguchi

Hearing

2014

Cold Spring Harbor Perspectives in Medicine

167

103

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Human melanocytes are distributed not only in the epidermis and in hair follicles but also in mucosa, cochlea (ear), iris (eye), and mesencephalon (brain) among other tissues. Melanocytes, which are derived from the neural crest, are unique in that they produce eu-/pheomelanin pigments in unique membrane-bound organelles termed melanosomes, which can be divided into four stages depending on their degree of maturation. Pigmentation production is determined by three distinct elements: enzymes involved in melanin synthesis, proteins required for melanosome structure, and proteins required for their trafficking and distribution. Many genes are involved in regulating pigmentation at various levels, and mutations in many of them cause pigmentary disorders, which can be classified into three types: hyperpigmentation (including melasma), hypopigmentation (including oculocutaneous albinism [OCA]), and mixed hyper-/hypopigmentation (including dyschromatosis symmetrica hereditaria). We briefly review vitiligo as a representative of an acquired hypopigmentation disorder.

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Interleukin-17 gene polymorphism is associated with Vogt–Koyanagi–Harada syndrome but not with Behçet's disease in a Chinese Han population

Cited by 67 publications

References 62 publications

Association between Polymorphisms of Interleukin-17A and Interleukin-17F Genes and Silicosis Susceptibility in Chinese Han People

Association between Polymorphisms of Interleukin-17A and Interleukin-17F Genes and Silicosis Susceptibility in Chinese Han People

JAK1, but NotJAK2andSTAT3, Confers Susceptibility to Vogt–Koyanagi–Harada (VKH) Syndrome in a Han Chinese Population

Melanocytes and Their Diseases

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