Effect of Iodine Excess on Th1, Th2, Th17, and Treg Cell Subpopulations in the Thyroid of NOD.H-$ 2^{h4} $ Mice
Abstract Iodine is an indispensable micronutrient for thyroid hormone synthesis and metabolism. Iodine excess may trigger and exacerbate autoimmune thyroiditis (AIT). The pathogenetic mechanism of iodine excess-induced AIT is partly regarded as T helper type 1 (Th1) cell and/or T helper type 17 (Th1...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Yang, Xiao [verfasserIn] Gao, Tianshu [verfasserIn] Shi, Rui [verfasserIn] Zhou, Xiyu [verfasserIn] Qu, Jinqiao [verfasserIn] Xu, Jia [verfasserIn] Shan, Zhongyan [verfasserIn] Teng, Weiping [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2014 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Biological trace element research - [S.l.] : Springer US, 1979, 159(2014), 1-3 vom: 17. Apr., Seite 288-296 |
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| Übergeordnetes Werk: |
volume:159 ; year:2014 ; number:1-3 ; day:17 ; month:04 ; pages:288-296 |
| Links: |
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| DOI / URN: |
10.1007/s12011-014-9958-y |
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| Katalog-ID: |
SPR023629665 |
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| 100 | 1 | |a Yang, Xiao |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Effect of Iodine Excess on Th1, Th2, Th17, and Treg Cell Subpopulations in the Thyroid of NOD.H-$ 2^{h4} $ Mice |
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| 520 | |a Abstract Iodine is an indispensable micronutrient for thyroid hormone synthesis and metabolism. Iodine excess may trigger and exacerbate autoimmune thyroiditis (AIT). The pathogenetic mechanism of iodine excess-induced AIT is partly regarded as T helper type 1 (Th1) cell and/or T helper type 17 (Th17) cell dominant autoimmune disease. It is still unknown whether other cluster of differentiation 4+ T (CD4+T) cell subpopulations are involved. Therefore, we studied the profile of all the CD4+T cell subpopulations of the thyroid in iodine excess-induced nonobese diabetic-$ H2^{h4} $ (NOD.H-$ 2^{h4} $) mice to explore the potential immunologic mechanism of iodine excess-induced AIT. A total of 40 healthy 8-week-old NOD.H-$ 2^{h4} $ mice were randomly allocated into the normal group (NG, n = 20) and the test group (TG, n = 20), which were fed with double-distilled water and 0.05 % sodium iodine (NaI) for 8 weeks, respectively. Compared to the NG, in the TG, the incidence of AIT was significantly higher, the expressions of interleukin-17 (IL-17), interleukin-23 (IL-23), interleukin-6 (IL-6), and transforming growth factor-β (TGF-β) remarkably increased by immunohistochemistry, which were further verified by reverse transcription polymerase chain reaction (RT-PCR), while the protein and mRNA expressions of interleukin-4 (IL-4) and interferon-γ (INF-γ) decreased markedly. In the AIT mice, the expressions of retinoic acid-related orphan receptor gamma t (RORγt), retinoic acid-related orphan receptor alpha (RORα), and signal transducer and activator of transcription 3 (STAT3) were much higher, the expression of forkhead/winged helix transcription factor p3 (Foxp3) significantly lower by western blot, and the proportion of Th17 cells by flow cytometry method (FCM) much larger compared to those of the NG group. In conclusion, Th17 cells may promote an inflammatory reaction in the development of iodine-excess-induced AIT, which is negatively regulated by Th1, T helper type 2 (Th2), and regulatory T (Treg) cells. | ||
| 650 | 4 | |a Iodine excess |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Autoimmune thyroiditis |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a NOD.H-2 |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a mice |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Th1 |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Th2 |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Th17 |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Treg |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Gao, Tianshu |e verfasserin |4 aut | |
| 700 | 1 | |a Shi, Rui |e verfasserin |4 aut | |
| 700 | 1 | |a Zhou, Xiyu |e verfasserin |4 aut | |
| 700 | 1 | |a Qu, Jinqiao |e verfasserin |4 aut | |
| 700 | 1 | |a Xu, Jia |e verfasserin |4 aut | |
| 700 | 1 | |a Shan, Zhongyan |e verfasserin |4 aut | |
| 700 | 1 | |a Teng, Weiping |e verfasserin |4 aut | |
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10.1007/s12011-014-9958-y doi (DE-627)SPR023629665 (SPR)s12011-014-9958-y-e DE-627 ger DE-627 rakwb eng 570 ASE Yang, Xiao verfasserin aut Effect of Iodine Excess on Th1, Th2, Th17, and Treg Cell Subpopulations in the Thyroid of NOD.H-$ 2^{h4} $ Mice 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Iodine is an indispensable micronutrient for thyroid hormone synthesis and metabolism. Iodine excess may trigger and exacerbate autoimmune thyroiditis (AIT). The pathogenetic mechanism of iodine excess-induced AIT is partly regarded as T helper type 1 (Th1) cell and/or T helper type 17 (Th17) cell dominant autoimmune disease. It is still unknown whether other cluster of differentiation 4+ T (CD4+T) cell subpopulations are involved. Therefore, we studied the profile of all the CD4+T cell subpopulations of the thyroid in iodine excess-induced nonobese diabetic-$ H2^{h4} $ (NOD.H-$ 2^{h4} $) mice to explore the potential immunologic mechanism of iodine excess-induced AIT. A total of 40 healthy 8-week-old NOD.H-$ 2^{h4} $ mice were randomly allocated into the normal group (NG, n = 20) and the test group (TG, n = 20), which were fed with double-distilled water and 0.05 % sodium iodine (NaI) for 8 weeks, respectively. Compared to the NG, in the TG, the incidence of AIT was significantly higher, the expressions of interleukin-17 (IL-17), interleukin-23 (IL-23), interleukin-6 (IL-6), and transforming growth factor-β (TGF-β) remarkably increased by immunohistochemistry, which were further verified by reverse transcription polymerase chain reaction (RT-PCR), while the protein and mRNA expressions of interleukin-4 (IL-4) and interferon-γ (INF-γ) decreased markedly. In the AIT mice, the expressions of retinoic acid-related orphan receptor gamma t (RORγt), retinoic acid-related orphan receptor alpha (RORα), and signal transducer and activator of transcription 3 (STAT3) were much higher, the expression of forkhead/winged helix transcription factor p3 (Foxp3) significantly lower by western blot, and the proportion of Th17 cells by flow cytometry method (FCM) much larger compared to those of the NG group. In conclusion, Th17 cells may promote an inflammatory reaction in the development of iodine-excess-induced AIT, which is negatively regulated by Th1, T helper type 2 (Th2), and regulatory T (Treg) cells. Iodine excess (dpeaa)DE-He213 Autoimmune thyroiditis (dpeaa)DE-He213 NOD.H-2 (dpeaa)DE-He213 mice (dpeaa)DE-He213 Th1 (dpeaa)DE-He213 Th2 (dpeaa)DE-He213 Th17 (dpeaa)DE-He213 Treg (dpeaa)DE-He213 Gao, Tianshu verfasserin aut Shi, Rui verfasserin aut Zhou, Xiyu verfasserin aut Qu, Jinqiao verfasserin aut Xu, Jia verfasserin aut Shan, Zhongyan verfasserin aut Teng, Weiping verfasserin aut Enthalten in Biological trace element research [S.l.] : Springer US, 1979 159(2014), 1-3 vom: 17. Apr., Seite 288-296 (DE-627)342893726 (DE-600)2072581-4 1559-0720 nnns volume:159 year:2014 number:1-3 day:17 month:04 pages:288-296 https://dx.doi.org/10.1007/s12011-014-9958-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 159 2014 1-3 17 04 288-296 |
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10.1007/s12011-014-9958-y doi (DE-627)SPR023629665 (SPR)s12011-014-9958-y-e DE-627 ger DE-627 rakwb eng 570 ASE Yang, Xiao verfasserin aut Effect of Iodine Excess on Th1, Th2, Th17, and Treg Cell Subpopulations in the Thyroid of NOD.H-$ 2^{h4} $ Mice 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Iodine is an indispensable micronutrient for thyroid hormone synthesis and metabolism. Iodine excess may trigger and exacerbate autoimmune thyroiditis (AIT). The pathogenetic mechanism of iodine excess-induced AIT is partly regarded as T helper type 1 (Th1) cell and/or T helper type 17 (Th17) cell dominant autoimmune disease. It is still unknown whether other cluster of differentiation 4+ T (CD4+T) cell subpopulations are involved. Therefore, we studied the profile of all the CD4+T cell subpopulations of the thyroid in iodine excess-induced nonobese diabetic-$ H2^{h4} $ (NOD.H-$ 2^{h4} $) mice to explore the potential immunologic mechanism of iodine excess-induced AIT. A total of 40 healthy 8-week-old NOD.H-$ 2^{h4} $ mice were randomly allocated into the normal group (NG, n = 20) and the test group (TG, n = 20), which were fed with double-distilled water and 0.05 % sodium iodine (NaI) for 8 weeks, respectively. Compared to the NG, in the TG, the incidence of AIT was significantly higher, the expressions of interleukin-17 (IL-17), interleukin-23 (IL-23), interleukin-6 (IL-6), and transforming growth factor-β (TGF-β) remarkably increased by immunohistochemistry, which were further verified by reverse transcription polymerase chain reaction (RT-PCR), while the protein and mRNA expressions of interleukin-4 (IL-4) and interferon-γ (INF-γ) decreased markedly. In the AIT mice, the expressions of retinoic acid-related orphan receptor gamma t (RORγt), retinoic acid-related orphan receptor alpha (RORα), and signal transducer and activator of transcription 3 (STAT3) were much higher, the expression of forkhead/winged helix transcription factor p3 (Foxp3) significantly lower by western blot, and the proportion of Th17 cells by flow cytometry method (FCM) much larger compared to those of the NG group. In conclusion, Th17 cells may promote an inflammatory reaction in the development of iodine-excess-induced AIT, which is negatively regulated by Th1, T helper type 2 (Th2), and regulatory T (Treg) cells. Iodine excess (dpeaa)DE-He213 Autoimmune thyroiditis (dpeaa)DE-He213 NOD.H-2 (dpeaa)DE-He213 mice (dpeaa)DE-He213 Th1 (dpeaa)DE-He213 Th2 (dpeaa)DE-He213 Th17 (dpeaa)DE-He213 Treg (dpeaa)DE-He213 Gao, Tianshu verfasserin aut Shi, Rui verfasserin aut Zhou, Xiyu verfasserin aut Qu, Jinqiao verfasserin aut Xu, Jia verfasserin aut Shan, Zhongyan verfasserin aut Teng, Weiping verfasserin aut Enthalten in Biological trace element research [S.l.] : Springer US, 1979 159(2014), 1-3 vom: 17. Apr., Seite 288-296 (DE-627)342893726 (DE-600)2072581-4 1559-0720 nnns volume:159 year:2014 number:1-3 day:17 month:04 pages:288-296 https://dx.doi.org/10.1007/s12011-014-9958-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 159 2014 1-3 17 04 288-296 |
| allfields_unstemmed |
10.1007/s12011-014-9958-y doi (DE-627)SPR023629665 (SPR)s12011-014-9958-y-e DE-627 ger DE-627 rakwb eng 570 ASE Yang, Xiao verfasserin aut Effect of Iodine Excess on Th1, Th2, Th17, and Treg Cell Subpopulations in the Thyroid of NOD.H-$ 2^{h4} $ Mice 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Iodine is an indispensable micronutrient for thyroid hormone synthesis and metabolism. Iodine excess may trigger and exacerbate autoimmune thyroiditis (AIT). The pathogenetic mechanism of iodine excess-induced AIT is partly regarded as T helper type 1 (Th1) cell and/or T helper type 17 (Th17) cell dominant autoimmune disease. It is still unknown whether other cluster of differentiation 4+ T (CD4+T) cell subpopulations are involved. Therefore, we studied the profile of all the CD4+T cell subpopulations of the thyroid in iodine excess-induced nonobese diabetic-$ H2^{h4} $ (NOD.H-$ 2^{h4} $) mice to explore the potential immunologic mechanism of iodine excess-induced AIT. A total of 40 healthy 8-week-old NOD.H-$ 2^{h4} $ mice were randomly allocated into the normal group (NG, n = 20) and the test group (TG, n = 20), which were fed with double-distilled water and 0.05 % sodium iodine (NaI) for 8 weeks, respectively. Compared to the NG, in the TG, the incidence of AIT was significantly higher, the expressions of interleukin-17 (IL-17), interleukin-23 (IL-23), interleukin-6 (IL-6), and transforming growth factor-β (TGF-β) remarkably increased by immunohistochemistry, which were further verified by reverse transcription polymerase chain reaction (RT-PCR), while the protein and mRNA expressions of interleukin-4 (IL-4) and interferon-γ (INF-γ) decreased markedly. In the AIT mice, the expressions of retinoic acid-related orphan receptor gamma t (RORγt), retinoic acid-related orphan receptor alpha (RORα), and signal transducer and activator of transcription 3 (STAT3) were much higher, the expression of forkhead/winged helix transcription factor p3 (Foxp3) significantly lower by western blot, and the proportion of Th17 cells by flow cytometry method (FCM) much larger compared to those of the NG group. In conclusion, Th17 cells may promote an inflammatory reaction in the development of iodine-excess-induced AIT, which is negatively regulated by Th1, T helper type 2 (Th2), and regulatory T (Treg) cells. Iodine excess (dpeaa)DE-He213 Autoimmune thyroiditis (dpeaa)DE-He213 NOD.H-2 (dpeaa)DE-He213 mice (dpeaa)DE-He213 Th1 (dpeaa)DE-He213 Th2 (dpeaa)DE-He213 Th17 (dpeaa)DE-He213 Treg (dpeaa)DE-He213 Gao, Tianshu verfasserin aut Shi, Rui verfasserin aut Zhou, Xiyu verfasserin aut Qu, Jinqiao verfasserin aut Xu, Jia verfasserin aut Shan, Zhongyan verfasserin aut Teng, Weiping verfasserin aut Enthalten in Biological trace element research [S.l.] : Springer US, 1979 159(2014), 1-3 vom: 17. Apr., Seite 288-296 (DE-627)342893726 (DE-600)2072581-4 1559-0720 nnns volume:159 year:2014 number:1-3 day:17 month:04 pages:288-296 https://dx.doi.org/10.1007/s12011-014-9958-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 159 2014 1-3 17 04 288-296 |
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10.1007/s12011-014-9958-y doi (DE-627)SPR023629665 (SPR)s12011-014-9958-y-e DE-627 ger DE-627 rakwb eng 570 ASE Yang, Xiao verfasserin aut Effect of Iodine Excess on Th1, Th2, Th17, and Treg Cell Subpopulations in the Thyroid of NOD.H-$ 2^{h4} $ Mice 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Iodine is an indispensable micronutrient for thyroid hormone synthesis and metabolism. Iodine excess may trigger and exacerbate autoimmune thyroiditis (AIT). The pathogenetic mechanism of iodine excess-induced AIT is partly regarded as T helper type 1 (Th1) cell and/or T helper type 17 (Th17) cell dominant autoimmune disease. It is still unknown whether other cluster of differentiation 4+ T (CD4+T) cell subpopulations are involved. Therefore, we studied the profile of all the CD4+T cell subpopulations of the thyroid in iodine excess-induced nonobese diabetic-$ H2^{h4} $ (NOD.H-$ 2^{h4} $) mice to explore the potential immunologic mechanism of iodine excess-induced AIT. A total of 40 healthy 8-week-old NOD.H-$ 2^{h4} $ mice were randomly allocated into the normal group (NG, n = 20) and the test group (TG, n = 20), which were fed with double-distilled water and 0.05 % sodium iodine (NaI) for 8 weeks, respectively. Compared to the NG, in the TG, the incidence of AIT was significantly higher, the expressions of interleukin-17 (IL-17), interleukin-23 (IL-23), interleukin-6 (IL-6), and transforming growth factor-β (TGF-β) remarkably increased by immunohistochemistry, which were further verified by reverse transcription polymerase chain reaction (RT-PCR), while the protein and mRNA expressions of interleukin-4 (IL-4) and interferon-γ (INF-γ) decreased markedly. In the AIT mice, the expressions of retinoic acid-related orphan receptor gamma t (RORγt), retinoic acid-related orphan receptor alpha (RORα), and signal transducer and activator of transcription 3 (STAT3) were much higher, the expression of forkhead/winged helix transcription factor p3 (Foxp3) significantly lower by western blot, and the proportion of Th17 cells by flow cytometry method (FCM) much larger compared to those of the NG group. In conclusion, Th17 cells may promote an inflammatory reaction in the development of iodine-excess-induced AIT, which is negatively regulated by Th1, T helper type 2 (Th2), and regulatory T (Treg) cells. Iodine excess (dpeaa)DE-He213 Autoimmune thyroiditis (dpeaa)DE-He213 NOD.H-2 (dpeaa)DE-He213 mice (dpeaa)DE-He213 Th1 (dpeaa)DE-He213 Th2 (dpeaa)DE-He213 Th17 (dpeaa)DE-He213 Treg (dpeaa)DE-He213 Gao, Tianshu verfasserin aut Shi, Rui verfasserin aut Zhou, Xiyu verfasserin aut Qu, Jinqiao verfasserin aut Xu, Jia verfasserin aut Shan, Zhongyan verfasserin aut Teng, Weiping verfasserin aut Enthalten in Biological trace element research [S.l.] : Springer US, 1979 159(2014), 1-3 vom: 17. Apr., Seite 288-296 (DE-627)342893726 (DE-600)2072581-4 1559-0720 nnns volume:159 year:2014 number:1-3 day:17 month:04 pages:288-296 https://dx.doi.org/10.1007/s12011-014-9958-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 159 2014 1-3 17 04 288-296 |
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10.1007/s12011-014-9958-y doi (DE-627)SPR023629665 (SPR)s12011-014-9958-y-e DE-627 ger DE-627 rakwb eng 570 ASE Yang, Xiao verfasserin aut Effect of Iodine Excess on Th1, Th2, Th17, and Treg Cell Subpopulations in the Thyroid of NOD.H-$ 2^{h4} $ Mice 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Iodine is an indispensable micronutrient for thyroid hormone synthesis and metabolism. Iodine excess may trigger and exacerbate autoimmune thyroiditis (AIT). The pathogenetic mechanism of iodine excess-induced AIT is partly regarded as T helper type 1 (Th1) cell and/or T helper type 17 (Th17) cell dominant autoimmune disease. It is still unknown whether other cluster of differentiation 4+ T (CD4+T) cell subpopulations are involved. Therefore, we studied the profile of all the CD4+T cell subpopulations of the thyroid in iodine excess-induced nonobese diabetic-$ H2^{h4} $ (NOD.H-$ 2^{h4} $) mice to explore the potential immunologic mechanism of iodine excess-induced AIT. A total of 40 healthy 8-week-old NOD.H-$ 2^{h4} $ mice were randomly allocated into the normal group (NG, n = 20) and the test group (TG, n = 20), which were fed with double-distilled water and 0.05 % sodium iodine (NaI) for 8 weeks, respectively. Compared to the NG, in the TG, the incidence of AIT was significantly higher, the expressions of interleukin-17 (IL-17), interleukin-23 (IL-23), interleukin-6 (IL-6), and transforming growth factor-β (TGF-β) remarkably increased by immunohistochemistry, which were further verified by reverse transcription polymerase chain reaction (RT-PCR), while the protein and mRNA expressions of interleukin-4 (IL-4) and interferon-γ (INF-γ) decreased markedly. In the AIT mice, the expressions of retinoic acid-related orphan receptor gamma t (RORγt), retinoic acid-related orphan receptor alpha (RORα), and signal transducer and activator of transcription 3 (STAT3) were much higher, the expression of forkhead/winged helix transcription factor p3 (Foxp3) significantly lower by western blot, and the proportion of Th17 cells by flow cytometry method (FCM) much larger compared to those of the NG group. In conclusion, Th17 cells may promote an inflammatory reaction in the development of iodine-excess-induced AIT, which is negatively regulated by Th1, T helper type 2 (Th2), and regulatory T (Treg) cells. Iodine excess (dpeaa)DE-He213 Autoimmune thyroiditis (dpeaa)DE-He213 NOD.H-2 (dpeaa)DE-He213 mice (dpeaa)DE-He213 Th1 (dpeaa)DE-He213 Th2 (dpeaa)DE-He213 Th17 (dpeaa)DE-He213 Treg (dpeaa)DE-He213 Gao, Tianshu verfasserin aut Shi, Rui verfasserin aut Zhou, Xiyu verfasserin aut Qu, Jinqiao verfasserin aut Xu, Jia verfasserin aut Shan, Zhongyan verfasserin aut Teng, Weiping verfasserin aut Enthalten in Biological trace element research [S.l.] : Springer US, 1979 159(2014), 1-3 vom: 17. Apr., Seite 288-296 (DE-627)342893726 (DE-600)2072581-4 1559-0720 nnns volume:159 year:2014 number:1-3 day:17 month:04 pages:288-296 https://dx.doi.org/10.1007/s12011-014-9958-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 159 2014 1-3 17 04 288-296 |
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Enthalten in Biological trace element research 159(2014), 1-3 vom: 17. Apr., Seite 288-296 volume:159 year:2014 number:1-3 day:17 month:04 pages:288-296 |
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Iodine excess Autoimmune thyroiditis NOD.H-2 mice Th1 Th2 Th17 Treg |
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Yang, Xiao @@aut@@ Gao, Tianshu @@aut@@ Shi, Rui @@aut@@ Zhou, Xiyu @@aut@@ Qu, Jinqiao @@aut@@ Xu, Jia @@aut@@ Shan, Zhongyan @@aut@@ Teng, Weiping @@aut@@ |
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Iodine excess may trigger and exacerbate autoimmune thyroiditis (AIT). The pathogenetic mechanism of iodine excess-induced AIT is partly regarded as T helper type 1 (Th1) cell and/or T helper type 17 (Th17) cell dominant autoimmune disease. It is still unknown whether other cluster of differentiation 4+ T (CD4+T) cell subpopulations are involved. Therefore, we studied the profile of all the CD4+T cell subpopulations of the thyroid in iodine excess-induced nonobese diabetic-$ H2^{h4} $ (NOD.H-$ 2^{h4} $) mice to explore the potential immunologic mechanism of iodine excess-induced AIT. A total of 40 healthy 8-week-old NOD.H-$ 2^{h4} $ mice were randomly allocated into the normal group (NG, n = 20) and the test group (TG, n = 20), which were fed with double-distilled water and 0.05 % sodium iodine (NaI) for 8 weeks, respectively. Compared to the NG, in the TG, the incidence of AIT was significantly higher, the expressions of interleukin-17 (IL-17), interleukin-23 (IL-23), interleukin-6 (IL-6), and transforming growth factor-β (TGF-β) remarkably increased by immunohistochemistry, which were further verified by reverse transcription polymerase chain reaction (RT-PCR), while the protein and mRNA expressions of interleukin-4 (IL-4) and interferon-γ (INF-γ) decreased markedly. In the AIT mice, the expressions of retinoic acid-related orphan receptor gamma t (RORγt), retinoic acid-related orphan receptor alpha (RORα), and signal transducer and activator of transcription 3 (STAT3) were much higher, the expression of forkhead/winged helix transcription factor p3 (Foxp3) significantly lower by western blot, and the proportion of Th17 cells by flow cytometry method (FCM) much larger compared to those of the NG group. 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|
| author |
Yang, Xiao |
| spellingShingle |
Yang, Xiao ddc 570 misc Iodine excess misc Autoimmune thyroiditis misc NOD.H-2 misc mice misc Th1 misc Th2 misc Th17 misc Treg Effect of Iodine Excess on Th1, Th2, Th17, and Treg Cell Subpopulations in the Thyroid of NOD.H-$ 2^{h4} $ Mice |
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Yang, Xiao |
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electronic Article |
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570 - Life sciences; biology |
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springer |
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1559-0720 |
| topic_title |
570 ASE Effect of Iodine Excess on Th1, Th2, Th17, and Treg Cell Subpopulations in the Thyroid of NOD.H-$ 2^{h4} $ Mice Iodine excess (dpeaa)DE-He213 Autoimmune thyroiditis (dpeaa)DE-He213 NOD.H-2 (dpeaa)DE-He213 mice (dpeaa)DE-He213 Th1 (dpeaa)DE-He213 Th2 (dpeaa)DE-He213 Th17 (dpeaa)DE-He213 Treg (dpeaa)DE-He213 |
| topic |
ddc 570 misc Iodine excess misc Autoimmune thyroiditis misc NOD.H-2 misc mice misc Th1 misc Th2 misc Th17 misc Treg |
| topic_unstemmed |
ddc 570 misc Iodine excess misc Autoimmune thyroiditis misc NOD.H-2 misc mice misc Th1 misc Th2 misc Th17 misc Treg |
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ddc 570 misc Iodine excess misc Autoimmune thyroiditis misc NOD.H-2 misc mice misc Th1 misc Th2 misc Th17 misc Treg |
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Elektronische Aufsätze Aufsätze Elektronische Ressource |
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Biological trace element research |
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570 - Life sciences; biology |
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Biological trace element research |
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(DE-627)342893726 (DE-600)2072581-4 |
| title |
Effect of Iodine Excess on Th1, Th2, Th17, and Treg Cell Subpopulations in the Thyroid of NOD.H-$ 2^{h4} $ Mice |
| ctrlnum |
(DE-627)SPR023629665 (SPR)s12011-014-9958-y-e |
| title_full |
Effect of Iodine Excess on Th1, Th2, Th17, and Treg Cell Subpopulations in the Thyroid of NOD.H-$ 2^{h4} $ Mice |
| author_sort |
Yang, Xiao |
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Biological trace element research |
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Biological trace element research |
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eng |
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500 - Science |
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2014 |
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txt |
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288 |
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Yang, Xiao Gao, Tianshu Shi, Rui Zhou, Xiyu Qu, Jinqiao Xu, Jia Shan, Zhongyan Teng, Weiping |
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159 |
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570 ASE |
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Elektronische Aufsätze |
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Yang, Xiao |
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10.1007/s12011-014-9958-y |
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570 |
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verfasserin |
| title_sort |
effect of iodine excess on th1, th2, th17, and treg cell subpopulations in the thyroid of nod.h-$ 2^{h4} $ mice |
| title_auth |
Effect of Iodine Excess on Th1, Th2, Th17, and Treg Cell Subpopulations in the Thyroid of NOD.H-$ 2^{h4} $ Mice |
| abstract |
Abstract Iodine is an indispensable micronutrient for thyroid hormone synthesis and metabolism. Iodine excess may trigger and exacerbate autoimmune thyroiditis (AIT). The pathogenetic mechanism of iodine excess-induced AIT is partly regarded as T helper type 1 (Th1) cell and/or T helper type 17 (Th17) cell dominant autoimmune disease. It is still unknown whether other cluster of differentiation 4+ T (CD4+T) cell subpopulations are involved. Therefore, we studied the profile of all the CD4+T cell subpopulations of the thyroid in iodine excess-induced nonobese diabetic-$ H2^{h4} $ (NOD.H-$ 2^{h4} $) mice to explore the potential immunologic mechanism of iodine excess-induced AIT. A total of 40 healthy 8-week-old NOD.H-$ 2^{h4} $ mice were randomly allocated into the normal group (NG, n = 20) and the test group (TG, n = 20), which were fed with double-distilled water and 0.05 % sodium iodine (NaI) for 8 weeks, respectively. Compared to the NG, in the TG, the incidence of AIT was significantly higher, the expressions of interleukin-17 (IL-17), interleukin-23 (IL-23), interleukin-6 (IL-6), and transforming growth factor-β (TGF-β) remarkably increased by immunohistochemistry, which were further verified by reverse transcription polymerase chain reaction (RT-PCR), while the protein and mRNA expressions of interleukin-4 (IL-4) and interferon-γ (INF-γ) decreased markedly. In the AIT mice, the expressions of retinoic acid-related orphan receptor gamma t (RORγt), retinoic acid-related orphan receptor alpha (RORα), and signal transducer and activator of transcription 3 (STAT3) were much higher, the expression of forkhead/winged helix transcription factor p3 (Foxp3) significantly lower by western blot, and the proportion of Th17 cells by flow cytometry method (FCM) much larger compared to those of the NG group. In conclusion, Th17 cells may promote an inflammatory reaction in the development of iodine-excess-induced AIT, which is negatively regulated by Th1, T helper type 2 (Th2), and regulatory T (Treg) cells. |
| abstractGer |
Abstract Iodine is an indispensable micronutrient for thyroid hormone synthesis and metabolism. Iodine excess may trigger and exacerbate autoimmune thyroiditis (AIT). The pathogenetic mechanism of iodine excess-induced AIT is partly regarded as T helper type 1 (Th1) cell and/or T helper type 17 (Th17) cell dominant autoimmune disease. It is still unknown whether other cluster of differentiation 4+ T (CD4+T) cell subpopulations are involved. Therefore, we studied the profile of all the CD4+T cell subpopulations of the thyroid in iodine excess-induced nonobese diabetic-$ H2^{h4} $ (NOD.H-$ 2^{h4} $) mice to explore the potential immunologic mechanism of iodine excess-induced AIT. A total of 40 healthy 8-week-old NOD.H-$ 2^{h4} $ mice were randomly allocated into the normal group (NG, n = 20) and the test group (TG, n = 20), which were fed with double-distilled water and 0.05 % sodium iodine (NaI) for 8 weeks, respectively. Compared to the NG, in the TG, the incidence of AIT was significantly higher, the expressions of interleukin-17 (IL-17), interleukin-23 (IL-23), interleukin-6 (IL-6), and transforming growth factor-β (TGF-β) remarkably increased by immunohistochemistry, which were further verified by reverse transcription polymerase chain reaction (RT-PCR), while the protein and mRNA expressions of interleukin-4 (IL-4) and interferon-γ (INF-γ) decreased markedly. In the AIT mice, the expressions of retinoic acid-related orphan receptor gamma t (RORγt), retinoic acid-related orphan receptor alpha (RORα), and signal transducer and activator of transcription 3 (STAT3) were much higher, the expression of forkhead/winged helix transcription factor p3 (Foxp3) significantly lower by western blot, and the proportion of Th17 cells by flow cytometry method (FCM) much larger compared to those of the NG group. In conclusion, Th17 cells may promote an inflammatory reaction in the development of iodine-excess-induced AIT, which is negatively regulated by Th1, T helper type 2 (Th2), and regulatory T (Treg) cells. |
| abstract_unstemmed |
Abstract Iodine is an indispensable micronutrient for thyroid hormone synthesis and metabolism. Iodine excess may trigger and exacerbate autoimmune thyroiditis (AIT). The pathogenetic mechanism of iodine excess-induced AIT is partly regarded as T helper type 1 (Th1) cell and/or T helper type 17 (Th17) cell dominant autoimmune disease. It is still unknown whether other cluster of differentiation 4+ T (CD4+T) cell subpopulations are involved. Therefore, we studied the profile of all the CD4+T cell subpopulations of the thyroid in iodine excess-induced nonobese diabetic-$ H2^{h4} $ (NOD.H-$ 2^{h4} $) mice to explore the potential immunologic mechanism of iodine excess-induced AIT. A total of 40 healthy 8-week-old NOD.H-$ 2^{h4} $ mice were randomly allocated into the normal group (NG, n = 20) and the test group (TG, n = 20), which were fed with double-distilled water and 0.05 % sodium iodine (NaI) for 8 weeks, respectively. Compared to the NG, in the TG, the incidence of AIT was significantly higher, the expressions of interleukin-17 (IL-17), interleukin-23 (IL-23), interleukin-6 (IL-6), and transforming growth factor-β (TGF-β) remarkably increased by immunohistochemistry, which were further verified by reverse transcription polymerase chain reaction (RT-PCR), while the protein and mRNA expressions of interleukin-4 (IL-4) and interferon-γ (INF-γ) decreased markedly. In the AIT mice, the expressions of retinoic acid-related orphan receptor gamma t (RORγt), retinoic acid-related orphan receptor alpha (RORα), and signal transducer and activator of transcription 3 (STAT3) were much higher, the expression of forkhead/winged helix transcription factor p3 (Foxp3) significantly lower by western blot, and the proportion of Th17 cells by flow cytometry method (FCM) much larger compared to those of the NG group. In conclusion, Th17 cells may promote an inflammatory reaction in the development of iodine-excess-induced AIT, which is negatively regulated by Th1, T helper type 2 (Th2), and regulatory T (Treg) cells. |
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Effect of Iodine Excess on Th1, Th2, Th17, and Treg Cell Subpopulations in the Thyroid of NOD.H-$ 2^{h4} $ Mice |
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https://dx.doi.org/10.1007/s12011-014-9958-y |
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Gao, Tianshu Shi, Rui Zhou, Xiyu Qu, Jinqiao Xu, Jia Shan, Zhongyan Teng, Weiping |
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Gao, Tianshu Shi, Rui Zhou, Xiyu Qu, Jinqiao Xu, Jia Shan, Zhongyan Teng, Weiping |
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10.1007/s12011-014-9958-y |
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2024-07-03T20:13:26.869Z |
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Iodine excess may trigger and exacerbate autoimmune thyroiditis (AIT). The pathogenetic mechanism of iodine excess-induced AIT is partly regarded as T helper type 1 (Th1) cell and/or T helper type 17 (Th17) cell dominant autoimmune disease. It is still unknown whether other cluster of differentiation 4+ T (CD4+T) cell subpopulations are involved. Therefore, we studied the profile of all the CD4+T cell subpopulations of the thyroid in iodine excess-induced nonobese diabetic-$ H2^{h4} $ (NOD.H-$ 2^{h4} $) mice to explore the potential immunologic mechanism of iodine excess-induced AIT. A total of 40 healthy 8-week-old NOD.H-$ 2^{h4} $ mice were randomly allocated into the normal group (NG, n = 20) and the test group (TG, n = 20), which were fed with double-distilled water and 0.05 % sodium iodine (NaI) for 8 weeks, respectively. 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| score |
7.400383 |