| Peer-Reviewed

Correlation Analysis of Th17/Treg Cells and PTPN22 Gene Polymorphism in HT Patients with Different Iodine Nutritional Status

Received: 8 March 2021    Accepted:     Published: 26 April 2021
Views:       Downloads:
Abstract

Background: The incidence of Hashimoto's thyroiditis (HT) may be related to environmental, immune, and genetic factors. Different iodine nutritional status can affect thyroid function. Th17/Treg cell imbalance is involved in the pathogenesis of autoimmune thyroid diseases, and PTPN22 is an important susceptibility gene related to autoimmune diseases. To study the relationship between Th17/Treg cells and cytokines and PTPN22 gene polymorphism in HT patients with different iodine nutritional status is to determine the role of immune and genetic factors in the pathogenesis of HT. Objective: To investigate the correlation between Th17/Treg cells and factors protein tyrosine phosphatase non-receptor type 22 (PTPN22) gene-1123G>C site (rs2488457) polymorphism in peripheral blood mononuclear cells (PBMC) of Hashimoto's thyroiditis (HT) patients with different iodine nutritional status. Methods: 100 HT patients and 60 healthy subjects in Cang Zhou are selected from 2019 to 2020. Flow cytometry and real-time fluorescent quantitative PCR are used to detecting the proportion and ratio of Th17 and Treg cells in PBMC, as well as retinoic acid-related orphan receptor-γt (ROR-γt) and fork head/winged spiral transcription factor 3 (Foxp3) mRNA expression levels. Single allele-specific primer-polymerase chain reaction (SASP-PCR) technology is taken to sequence PTPN gene promoter-1123SNP leading to calculate the gene Type and allele frequency. Results: Th17 and Treg cells and factors in the PBMC of HT patients have a certain correlation with the-1123G>C locus of PTPN22 gene (rs2488457). The distribution frequency of rs2488457 genotype is consistent with Hardy Weinberg's law of genetic equilibrium. The distribution frequencies of various genotypes and alleles are significantly different between HT patients and the control group (P<0.05). PTPN22 gene-1123G>C site C/G, C/C genotype can increase of the risk of HT, while G/G genotype can decrease of the risk of HT. In Conclusion: The polymorphism of rs2488457 is related to susceptibility to HT. Carrying C/G and C/C genotypes may be risk factors for HT, and G/G genotypes may be protective factors for HT, but it has nothing to do with iodine nutrition status.

Published in Science Journal of Public Health (Volume 9, Issue 2)
DOI 10.11648/j.sjph.20210902.15
Page(s) 64-71
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

Iodine Nutritional Status, Hashimoto's Thyroiditis, Th17/Treg Cells and Factors, PTPN22, Gene Polymorphism

References
[1] Tang QL, Xue YM. Hashimoto's thyroiditis related gene research progress [J]. Drug Research, 2013, 10 (15): 42-46.
[2] Thomas Heiberg Brix and Laszlo Hegedus. twin studies as a model for exploring the aetiology of autoimmune thyroid disease [J]. Clinical Endocrinology, 2012, 76: 457-464.
[3] Shi Y, Wang H, Su Z, et al. Differentiation imbalance of Th1/Th17 in peripheral blood mononuclear cells might contribute to pathogenesis of Hashimoto's thyroiditis [J]. Scand J Immunol. 2010, 72 (3): 250-255.
[4] Wang S, Baidoo SE, Liu Y, et al. T cell-derived leptin contributes to increased frequency of T helper type 17 cells in female patients with Hashimoto's thyroiditis [J]. Clin Exp Immunol. 2013, 171 (1): 63-68.
[5] XieXY, Xi' erNY, Guo T, et al. TheAlterationoftheTh1, Th2, Th17, Treg Cells in the Peripheral Blood in Patients with Grave' s Disease (GD) and Hashimoto'ds Thyroiditis with Hypothyroidism. J Radioimmunology, 2011, 24 (3): 290-293.
[6] Glick AB, WodzinskiA, FuP, et al. Impairment of regulatory T cell function in autoimmune thyroid disease [J]. Thyroid, 2013, 23 (7): 871-878.
[7] Marazuela M, García-López MA, Figueroa-Vega N, et al. Regulatory T cells in human autoimmunethyroiddisease [J]. Clin Endocrinol Metab. 2006, 91 (9): 3639-3646.
[8] Chen MH, DaiB. Relationship between protein tyrosine phosphatase nonreceptor type 22 and rheumatoid arthritis [J]. Foreign Medicals Ciences Ection of Medgeography, 2014, 35 (3): 252-255.
[9] Li Sheng Dong. Analysis of association between PTPN22 and transcription factor FOXP3 gene polymorphisms and genetic susceptibility to systemic lupus erythematosus [J]. Chin Mode Doct, 2017, 55 (5): 1-4.
[10] Su Y. Association Study between PTPN22 Gene Polymorphism and Myasthenia Gravis [D]. Master's thesis of shandong university, 2019.
[11] Xu QH, Wu J, Chen ZT. Advances in the Research of the SPNs of PTPN22 Gene and Autoimmune Related Diseaes [J]. Med J Wuhan Unive, 2017, 38 (5): 844-849.
[12] Chinese Medical Association Endocrine Credits “China thyroid disease treatment guidelines” Writing Group. China thyroid disease treatment guidelines-Thyroiditis [J]. Chin J inter Med, 2008, 47 (9): 784-788.
[13] Chinese Medical Association Endocrine Credits “China thyroid disease treatment guidelines” Writing Group. China thyroid disease treatment guidelines-iodine deficiencydisorders [J]. Journal of Internal Medicine, 2008, 47 (8): 689-690.
[14] Kleinewietfeld M, Hafler DA. The plasticity of human Treg and Th17 cells and its role in autoimmunity [J]. Semin Immunol. 2013, 25 (4): 305-312.
[15] SinghB, SchwartzJA, SandrockC, et al. Modulation of autoimmune diseases by interleukin (IL)-17 producing regulatory T helper (Th17) cells [J]. Indian J Med Res, 2013, 138 (5): 591-594.
[16] Uqba Khan, Ghazanfar H. T Lymphocytes and Autoimmunity [J]. Int Rev Cell Mol Biol. 2018, 341: 125-168.
[17] Chang HH, Tai TS, Lu B, et al. ChristinePTPN22.6, a dominant negative isoform of PTPN22 and potential biomarker of rheumatoid arthritis [J]. PLoS One. 2012, 7 (3): e33067.
[18] Zheng K, Zhang J, Zhang P. et al. PTPN22 and CTLA-4 gene polymorphisms in resected thymomas and thymus for myasthenia gravis [J]. Thorac Cancer. 2012, 3 (4): 307-312.
[19] Liu J, Chen M, Li R, et al. Biochemical and functional studies of lymphoid-specific tyrosine phosphatase (Lyp) variants S201F and R266W [J]. PLoS One. 2012, 7 (8): e43631.
[20] Xuan C, Lun LM, Zhao JX, et al. PTPN22 gene polymorphism (C1858T) is associated with susceptibility to type 1 diabetes: a meta-analysis of 19, 495 cases and 25, 341 controls [J]. Ann Hum Genet, 2013, 77 (3): 191-203.
[21] Lavrikova EIu, Nikitin AG, Seregin IA, et al. Association of the C1858T polymorphism of the PTPN22 gene with type 1 diabetes [J]. MolBiol (Mosk), 2009, 43 (6): 1040-1043.
[22] Wang L, Zhang L, Xiao H, et al. Interference of protein tyrosine phosphatase non-receptor type 22 inhibits NLRP3 inflammasome activation to alleviate inflammation after cerebral hemorrhage in rats [J]. J Third Milit Med Univ, 2019, 41 (24): 2409-2416.
[23] Kawasaki E, Awata T, Ikegami H, et al. Systematic search for single nucleotide polymorphisms in a lymphoid tyrosine phosphatase gene (PTPN22): association between a promoter polymorphism and type 1 diabetes in Asian populations [J]. Am J Med Genet A, 2006, 140 (6): 586-593.
[24] Salama A, Elshazli R. lsaid A, et al. rotein tyrosine phosphatase non—receptor type 22 (PTPN22)+1858 C>T gene polymorphism in Egyptian cases with rheumatoid arthritis [J]. Cell Immunol, 2014, 290 (1): 62-65.
[25] Zhao L, Qiu YR. Associations of Protein Tyrosine Phosphatase Nonreceptor 22 (PTPN22) Gene Polymorphisms with RA in the Han Population of Guangzhou in China [J]. J Tropical Med, 2009.9 (5): 493-495.
[26] Wang YP, Zhou Y, Fei Y. Relationship between PTPN22 gene polymorphism and rheumatoid and lupuserythematosus [J]. Chin J Public Health, 2009, 25 (12): 1535-1536.
[27] Bai SY, Zhang LM, Wang CX, et al. Study on the relationship between polymorphism of PTPN22 and rheumatoid arthritis [J]. J Taishan Med Colle, 2010, 31 (2): 100-102.
[28] Kong XT, Wang LH, Wang JJ, et al. Research progress on the correlation between PTPN22 C1858T and autoimmune diseases [J]. Chin J Neuroimmunol & Neurol, 2016, 23 (6): 442-447.
[29] Hamza RT, Awwad KS, Temsah KA, et al. R620W polymorphism of protein tyrosine phosphatase PTPN22 in Egyptian children and adolescents with systemic lupus erythematosus: relation to thyroid autoimmunity [J]. Int J Adolesc Med Health. 2013, 25 (2): 143-149.
[30] Tang L, Wang Y, Zheng S, et al. PTPN22 polymorphisms, but not R620W, were associated with the genetic susceptibility of systemic lupus erythematosus and rheumatoid arthritis in a Chinese Han population [J]. Hum Immunol. 2016, 77 (8): 692-698.
[31] Zhen RZ, Li R, Zhang SH. PTPN22 gene polymorphism and autoimmune endocrine diseases [J]. Inte J Endocrinol Metab, 2007, 27 (2): 89-91.
[32] Alkhateeb A, Marzouka NA, TashtoUShR. Variants in PTPN22 and SMOC2 genes and the risk of thyroid disease in the Jordanian Arab population [J]. Endocrine, 2013, 44 (3): 702-709.
[33] Ray D, Tomar N, Gupta N, et al. Protein tyrosine phosphatase non-receptor type 22 (PTPN22) gene R620W variant and sporadic idiopathic hypoparathyroidism in Asian Indians [J]. Int J Immuno-genet. 2006, 33 (4): 237-240.
[34] Ban Y, Tozaki T, Taniyama M, et a1. Association of the protein tyrosine phosphatase nonreceptor 22 haplotypes with autoimmune thyroid disease in the Japanese population [J]. Thyroid, 2010, 20 (8): 893-839.
[35] Xue L, Pan C, Gu Z, et al. Genetic heterogeneity of susceptibility gene in different ethnic populations: refining association study of PTPN22 for Graves'disease in a Chinese Han population [J]. PLoS One, 2013, 8 (12): e84514.
[36] Pan RW, Zhang EY, Mei WJ, et al. Study on the relationship between PTPN22-1123G>C gene polymorphism and Hashimoto's Thyroiditis in Wenzhou population [J]. Chin J Healt Labo Techn, 2012, 22 (2): 240-241.
[37] Huo YL, Chang YF, Yang JF, et al. Association between PTPN22 Gene Polymorphism and Hashimoto’s Thyroiditis in Zhangjiakou Han Population [J]. Chine J Med Guide, 2017, 19 (12): 1306-1309.
[38] Li HY, Ma JQ, Wang CC, et al. Correlation Analysis between Thyroid Function and Autoantibodies in Hashimoto Thyroiditis Patients with Different Iodine Nutritional Status [J]. Amer J Biom Life Scie 2021, 9 (1): 10-19.
[39] Wang CC, Mu ZX, Chen YX, et al. Study on Th17/Treg Cells and Cytokines in Hashimoto's Thyroiditis with Different Iodine Nutrition Status [J]. Science J Public Health, 2021, 9 (1): 12-22.
[40] Juliger S, Bongartz M, Luty AJ, et al. Functional analysis of a promoter variant of the gene encoding the interferon-gamma receptor chainI [J]. Immunogenetics, 2003, 54 (10): 675-680.
Cite This Article
  • APA Style

    Wang Cuicui, Mu Zhaoxin, Hou Zhenjiang, Chen Yunxia, Liu Jianfeng, et al. (2021). Correlation Analysis of Th17/Treg Cells and PTPN22 Gene Polymorphism in HT Patients with Different Iodine Nutritional Status. Science Journal of Public Health, 9(2), 64-71. https://doi.org/10.11648/j.sjph.20210902.15

    Copy | Download

    ACS Style

    Wang Cuicui; Mu Zhaoxin; Hou Zhenjiang; Chen Yunxia; Liu Jianfeng, et al. Correlation Analysis of Th17/Treg Cells and PTPN22 Gene Polymorphism in HT Patients with Different Iodine Nutritional Status. Sci. J. Public Health 2021, 9(2), 64-71. doi: 10.11648/j.sjph.20210902.15

    Copy | Download

    AMA Style

    Wang Cuicui, Mu Zhaoxin, Hou Zhenjiang, Chen Yunxia, Liu Jianfeng, et al. Correlation Analysis of Th17/Treg Cells and PTPN22 Gene Polymorphism in HT Patients with Different Iodine Nutritional Status. Sci J Public Health. 2021;9(2):64-71. doi: 10.11648/j.sjph.20210902.15

    Copy | Download

  • @article{10.11648/j.sjph.20210902.15,
      author = {Wang Cuicui and Mu Zhaoxin and Hou Zhenjiang and Chen Yunxia and Liu Jianfeng and Ma Jinqun and Liu Chunyan},
      title = {Correlation Analysis of Th17/Treg Cells and PTPN22 Gene Polymorphism in HT Patients with Different Iodine Nutritional Status},
      journal = {Science Journal of Public Health},
      volume = {9},
      number = {2},
      pages = {64-71},
      doi = {10.11648/j.sjph.20210902.15},
      url = {https://doi.org/10.11648/j.sjph.20210902.15},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.sjph.20210902.15},
      abstract = {Background: The incidence of Hashimoto's thyroiditis (HT) may be related to environmental, immune, and genetic factors. Different iodine nutritional status can affect thyroid function. Th17/Treg cell imbalance is involved in the pathogenesis of autoimmune thyroid diseases, and PTPN22 is an important susceptibility gene related to autoimmune diseases. To study the relationship between Th17/Treg cells and cytokines and PTPN22 gene polymorphism in HT patients with different iodine nutritional status is to determine the role of immune and genetic factors in the pathogenesis of HT. Objective: To investigate the correlation between Th17/Treg cells and factors protein tyrosine phosphatase non-receptor type 22 (PTPN22) gene-1123G>C site (rs2488457) polymorphism in peripheral blood mononuclear cells (PBMC) of Hashimoto's thyroiditis (HT) patients with different iodine nutritional status. Methods: 100 HT patients and 60 healthy subjects in Cang Zhou are selected from 2019 to 2020. Flow cytometry and real-time fluorescent quantitative PCR are used to detecting the proportion and ratio of Th17 and Treg cells in PBMC, as well as retinoic acid-related orphan receptor-γt (ROR-γt) and fork head/winged spiral transcription factor 3 (Foxp3) mRNA expression levels. Single allele-specific primer-polymerase chain reaction (SASP-PCR) technology is taken to sequence PTPN gene promoter-1123SNP leading to calculate the gene Type and allele frequency. Results: Th17 and Treg cells and factors in the PBMC of HT patients have a certain correlation with the-1123G>C locus of PTPN22 gene (rs2488457). The distribution frequency of rs2488457 genotype is consistent with Hardy Weinberg's law of genetic equilibrium. The distribution frequencies of various genotypes and alleles are significantly different between HT patients and the control group (PC site C/G, C/C genotype can increase of the risk of HT, while G/G genotype can decrease of the risk of HT. In Conclusion: The polymorphism of rs2488457 is related to susceptibility to HT. Carrying C/G and C/C genotypes may be risk factors for HT, and G/G genotypes may be protective factors for HT, but it has nothing to do with iodine nutrition status.},
     year = {2021}
    }
    

    Copy | Download

  • TY  - JOUR
    T1  - Correlation Analysis of Th17/Treg Cells and PTPN22 Gene Polymorphism in HT Patients with Different Iodine Nutritional Status
    AU  - Wang Cuicui
    AU  - Mu Zhaoxin
    AU  - Hou Zhenjiang
    AU  - Chen Yunxia
    AU  - Liu Jianfeng
    AU  - Ma Jinqun
    AU  - Liu Chunyan
    Y1  - 2021/04/26
    PY  - 2021
    N1  - https://doi.org/10.11648/j.sjph.20210902.15
    DO  - 10.11648/j.sjph.20210902.15
    T2  - Science Journal of Public Health
    JF  - Science Journal of Public Health
    JO  - Science Journal of Public Health
    SP  - 64
    EP  - 71
    PB  - Science Publishing Group
    SN  - 2328-7950
    UR  - https://doi.org/10.11648/j.sjph.20210902.15
    AB  - Background: The incidence of Hashimoto's thyroiditis (HT) may be related to environmental, immune, and genetic factors. Different iodine nutritional status can affect thyroid function. Th17/Treg cell imbalance is involved in the pathogenesis of autoimmune thyroid diseases, and PTPN22 is an important susceptibility gene related to autoimmune diseases. To study the relationship between Th17/Treg cells and cytokines and PTPN22 gene polymorphism in HT patients with different iodine nutritional status is to determine the role of immune and genetic factors in the pathogenesis of HT. Objective: To investigate the correlation between Th17/Treg cells and factors protein tyrosine phosphatase non-receptor type 22 (PTPN22) gene-1123G>C site (rs2488457) polymorphism in peripheral blood mononuclear cells (PBMC) of Hashimoto's thyroiditis (HT) patients with different iodine nutritional status. Methods: 100 HT patients and 60 healthy subjects in Cang Zhou are selected from 2019 to 2020. Flow cytometry and real-time fluorescent quantitative PCR are used to detecting the proportion and ratio of Th17 and Treg cells in PBMC, as well as retinoic acid-related orphan receptor-γt (ROR-γt) and fork head/winged spiral transcription factor 3 (Foxp3) mRNA expression levels. Single allele-specific primer-polymerase chain reaction (SASP-PCR) technology is taken to sequence PTPN gene promoter-1123SNP leading to calculate the gene Type and allele frequency. Results: Th17 and Treg cells and factors in the PBMC of HT patients have a certain correlation with the-1123G>C locus of PTPN22 gene (rs2488457). The distribution frequency of rs2488457 genotype is consistent with Hardy Weinberg's law of genetic equilibrium. The distribution frequencies of various genotypes and alleles are significantly different between HT patients and the control group (PC site C/G, C/C genotype can increase of the risk of HT, while G/G genotype can decrease of the risk of HT. In Conclusion: The polymorphism of rs2488457 is related to susceptibility to HT. Carrying C/G and C/C genotypes may be risk factors for HT, and G/G genotypes may be protective factors for HT, but it has nothing to do with iodine nutrition status.
    VL  - 9
    IS  - 2
    ER  - 

    Copy | Download

Author Information
  • Department of Medical Technology of Cangzhou Medical College, Cangzhou, China

  • Institute of Thyroid Diseases Affiliated to Cangzhou Medical College, Cangzhou Thyroid Disease Engineering Technology Research Center, Cangzhou, China

  • Institute of Thyroid Diseases Affiliated to Cangzhou Medical College, Cangzhou Thyroid Disease Engineering Technology Research Center, Cangzhou, China

  • Cangzhou People's Hospital Endocrinology, Cangzhou, China

  • Cangzhou People's Hospital Endocrinology, Cangzhou, China

  • Cangzhou People's Hospital Endocrinology, Cangzhou, China

  • Cangzhou People's Hospital Endocrinology, Cangzhou, China

  • Sections