T、B淋巴细胞在自身免疫性甲状腺疾病中的作用机制研究进展

Abstract
Figure/Table
References (47)
Related Citation (15)

Download: PDF (609 KB) HTML (1 KB)
Export: BibTeX | EndNote (RIS)

Abstract The incidence rate of autoimmune thyroid diseases (AITD) is on the rise. The interaction of complex environmental factors, genetic factors and endocrine hormone may be the causes of the disease. The pathogenesis of AITD is mainly the activation of T lymphocytes and B lymphocytes, which produce autoantibodies targeted at thyroid tissues, so as to cause different degrees of thyroid injury and produce functional changes. In T lymphocytes, helper T lymphocytes are closely related to AITD. It has many subtypes, such as Th1, Th2, Th17, Treg, and so on. Th1/Th2 cell imbalance and Th17 cell activation are involved in the occurrence of AITD, while Treg cells can play an important role in immune suppression function; B lymphocyte activation is the core pathological process of the occurrence of Graves′ disease, while Breg cells can inhibit the autoimmune response and regulate the effect of T lymphocytes, which is a potential therapeutic target of AITD. This paper reviews the mechanism of T and B lymphocytes involved in AITD, which provides some ideas for finding effective therapeutic approaches.

Key words： Autoimmune thyroid disease T lymphocyte B lymphocyte Mechanism

	Service

	E-mail this article
	Add to my bookshelf
	Add to citation manager
	E-mail Alert
	RSS
	Articles by authors
	LI Yang ZUO Xinhe HUA Chuan ZHAO Yong

Cite this article:

LI Yang ZUO Xinhe HUA Chuan ZHAO Yong. Research progress on the mechanism of T and B lymphocytes involved in autoimmune thyroid disease[J]. 中国医药导报, 2019, 16(23): 49-52.

URL:

http://www.yiyaodaobao.com.cn/EN/ OR http://www.yiyaodaobao.com.cn/EN/Y2019/V16/I23/49

[1] Pyzik A，Grywalska E，Matyjaszek-Matuszek B，et al. Immune disorders in Hashimoto′s thyroiditis：what do we know so far? [J]. J Immunol Res，2015，2015：979167.
[2] Carlé A，Pedersen IB，Knudsen N，et al. Epidemiology of subtypes of hyperthyroidism in Denmark：a population-based study [J]. Eur J Endocrinol，2011，164（5）：801-809.
[3] Volpé R，Iitaka M. Evidence for an antigen-specific defect in suppressor T-lymphocytes in autoimmune thyroid disease [J]. Exp Clin Endocrinol，1991，97（2/3）：133-138.
[4] Tanda ML，Piantanida E，Lai A，et al. Thyroid autoimmunity and environment [J]. Horm Metab Res，2009，41（6）：436-442.
[5] Rydzewska M，Jaromin M，Pasierowska IE，et al. Role of the T and B lymphocytes in pathogenesis of autoimmune thyroid diseases [J]. Thyroid Res，2018，11：2.
[6] Yang Q，Jeremiah Bell J，Bhandoola A. T-cell lineage determination [J]. Immunol Rev，2010，238（1）：12-22.
[7] Romagnani S. Regulation of the T cell response [J]. Clin Exp Allergy，2006，36（11）：1357-1366.
[8] J?覿ger A，Kuchroo VK. Effector and regulatory T-cell subsets in autoimmunity and tissue inflammation [J]. Scand J Immunol，2010，72（3）：173-184.
[9] Mosmann TR，Coffman RL. TH1 and TH2 cells：different patterns of lymphokine secretion lead to different functional properties [J]. Annu Rev Immunol，1989，7：145-173.
[10] Ochs HD，Oukka M，Torgerson TR. TH17 cells and regulatory T cells in primary immunodeficiency diseases [J]. J Allergy Clin Immunol，2009，123（5）：977-983，quiz 984-985.
[11] Ohkura N，Kitagaua Y，Sakaguchi S. Development and maintenance of regulary T cells [J]. Immunity，2013，38（3）：414-423.
[12] Van Parijs L，Abbas AK. Homeostasis and self-tolerance in the immune system：turning lymphocytes off [J]. Science，1998，280（5361）：243-248.
[13] Ben-Skowronek I，Szewczyk L，Kulik-Rechberger B，et al. The differences in T and B cell subsets in thyroid of children with Graves′ disease and Hashimoto's thyroiditis [J]. World J Pediatr，2013，9（3）：245-250.
[14] Kraiem Z，Baron E，Kahana L，et al. Changes in stimulating and blocking TSH receptor antibodies in a patient undergoing three cycles of transition from hypo to hyper-thyroidism and back to hypothyroidism [J]. Clin Endocrinol（Oxf），1992，36（2）：211-214.
[15] Chardès T，Chapal N，Bresson D，et al. The human anti-thyroid peroxidase autoantibody repertoire in Graves' and Hashimoto′s autoimmune thyroid diseases [J]. Immunogenetics，2002，54（3）：141-157.
[16] Michalek K，Morshed SA，Latif R，et al. TSH receptor autoantibodies [J]. Autoimmun Rev，2009，9（2）：113-116.
[17] Le?觟vey A，Nagy E，Balazs G，et al. Lymphocytes resided in the thyroid are the main source of TSH-receptor antibodies in Basedow′s-Graves′ disease? [J]. Exp Clin Endocrinol，1992，99（3）：147-150.
[18] Rapoport B，Mclachlan SM. Graves′ hyperthyroidism is antibody-mediated but is predominantly a Th1-type cytokine disease [J]. J Clin Endocrinol Metab，2014，99（11）：4060-4061.
[19] Eshaghkhani Y，Sanati MH，Nakhjavani M，et al. Disturbed Th1 and Th2 balance in patients with Graves′ disease [J].Minerva Endocrinol，2016，41（1）：28-36.
[20] Amatya N，Garg AV，Gaffen SL. IL-17 Signaling：The Yin and the Yang [J]. Trends Immunol，2017，38（5）：310-322.
[21] Wilson NJ，Boniface K，Chan JR，et al. Development，cytokine profile and function of human interleukin 17-producing helper T cells [J]. Nat Immunol，2007，8（9）：950-957.
[22] González-Amaro R，Marazuela M. T regulatory（Treg）and T helper 17（Th17）lymphocytes in thyroid autoimmunity [J]. Endocrine，2016，52（1）：30-38.
[23] Song RH，Yu ZY，Qin Q，et al. Different levels of circulating Th22 cell and its related molecules in Graves' disease and Hashimoto′s thyroiditis [J]. Int J Clin Exp Pathol，2014，7（7）：4024-4031.
[24] Liu Y，Tang X，Tian J，et al. Th17/Treg cells imbalance and GITRL profile in patients with Hashimoto's thyroiditis [J]. Int J Mol Sci，2014，15（12）：21674-21686.
[25] Cortés JR，Sánchez-Díaz R，Bovolenta ER，et al. Maintenance of immune tolerance by Foxp3+ regulatory T cells requires CD69 expression [J]. J Autoimmun，2014，55：51-62.
[26] Allan SE，Passerini L，Bacchetta R，et al. The role of 2 FOXP3 isoforms in the generation of human CD4+ Tregs [J]. J Clin Invest，2005，115（11）：3276-3284.
[27] Inoue N，Watanabe M，Morita M，et al. Association of functional polymorphisms related to the transcriptional level of FOXP3 with prognosis of autoimmune thyroid diseases [J]. Clin Exp Immunol，2010，162（3）：402-406.
[28] Mao C，Wang S，Xiao Y，et al. Impairment of regulatory capacity of CD4+CD25+ regulatory T cells mediated by dendritic cell polarization and hyperthyroidism in Graves′ disease [J]. J Immunol，2011，186（8）：4734-4743.
[29] Kanamori M，Nakatsukasa H，Okada M，et al. Induced Regulatory T Cells：Their Development，Stability，and Applications [J]. Trends Immunol，2016，37（11）：803-811.
[30] Cerosaletti K，Schneider A，Schwedhelm K，et al. Multiple autoimmune-associated variants confer decreased IL-2R signaling in CD4+ CD25（hi）T cells of type 1 diabetic and multiple sclerosis patients [J]. PLoS One，2013， 8（12）：e83811.
[31] Maloy KJ，Powrie F. Regulatory T cells in the control of immune pathology [J]. Nat Immunol，2001，2（9）：816-822.
[32] Levings MK，Sangregorio R，Roncarolo MG. Human cd25（+）cd4（+）t regulatory cells suppress naive and memory T cell proliferation and can be expanded in vitro without loss of function [J]. J Exp Med，2001，193（11）：1295-1302.
[33] Vandenborre K，Van Gool SW，Kasran A，et al. Interaction of CTLA-4（CD152）with CD80 or CD86 inhibits human T-cell activation [J]. Immunology，1999，98（3）：413-421.
[34] Sakaguchi S，Wing K，Onishi Y，et al. Regulatory T cells：how do they suppress immune responses? [J]. Int Immunol，2009，21（10）：1105-1111.
[35] Kondo M. Lymphoid and myeloid lineage commitment in multipotent hematopoietic progenitors [J]. Immunol Rev，2010，238（1）：37-46.
[36] Kambayashi T，Laufer TM. Atypical MHC class Ⅱ-expressing antigen-presenting cells：can anything replace a dendritic cell? [J]. Nat Rev Immunol，2014，14（11）：719-730.
[37] Kuklina EM，Smirnova EN，Nekrasova IV，et al. Role of B cells in presentation of autoantigens to CD4（+）T cells in patients with autoimmune thyroiditis [J]. Dokl Biol Sci，2015，464：263-266.
[38] Rosser EC，Mauri C. Regulatory B cells：origin，phenotype，and function [J]. Immunity，2015，42（4）：607-612.
[39] Morshed SA，Davies TF. Graves′ Disease Mechanisms：The Role of Stimulating，Blocking，and Cleavage Region TSH Receptor Antibodies [J]. Horm Metab Res，2015，47（10）：727-734.
[40] Gilbert JA，Kalled SL，Moorhead J，et al. Treatment of autoimmune hyperthyroidism in a murine model of Graves′ disease with tumor necrosis factor-family ligand inhibitors suggests a key role for B cell activating factor in disease pathology [J]. Endocrinology，2006，147（10）：4561-4568.
[41] Hong SH，Braley-Mullen H. Follicular B cells in thyroids of mice with spontaneous autoimmune thyroiditis contribute to disease pathogenesis and are targets of anti-CD20 antibody therapy [J]. J Immunol，2014，192（3）：897-905.
[42] Salvi M. Immunotherapy for Graves′ ophthalmopathy [J]. Curr Opin Endocrinol Diabetes Obes，2014，21（5）：409-414.
[43] Kristensen B，Hegedüs L，Lundy SK，et al. Characterization of Regulatory B Cells in Graves′ Disease and Hashimoto′s Thyroiditis [J]. PLoS One，2015，10（5）：e0127949.
[44] Maravillas-Montero JL，Acevedo-Ochoa E. Human B Regulatory Cells：The New Players in Autoimmune Disease [J]. Rev Invest Clin，2017，69（5）：243-246.
[45] Miyagaki T，Fujimoto M，Sato S. Regulatory B cells in human inflammatory and autoimmune diseases：from mouse models to clinical research [J]. Int Immunol，2015，27（10）：495-504.
[46] Kristensen B. Regulatory B and T cell responses in patients with autoimmune thyroid disease and healthy controls [J]. Dan Med J，2016，63（2）.
[47] Qin J，Zhou J，Fan C，et al. Increased Circulating Th17 but Decreased CD4（+）Foxp3（+）Treg and CD19（+）CD1d（hi）CD5（+）Breg Subsets in New-Onset Graves' Disease [J]. Biomed Res Int，2017，2017：8431838.