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Cytokines and autoimmune thyroid disease research_89

By Pedro Smith,2014-10-30 14:44
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Cytokines and autoimmune thyroid disease research_89

Cytokines and autoimmune thyroid disease research

     Abstract cytokines (Cytokines) role of the thyroid cells in thyroid-stimulating hormone (TSH) together, the thyroid cells induced by major histocompatibility complex (MHC) - ? antigen

    abnormal expression, into antigen-presenting cells, leading to

    auto-immune pathological damage, the formation of autoimmune thyroid disease (AITD).

     Key words cytokines; thyroid cells; thyroid disease

     Cytokines by immune cells or immune cells synthesized and

    secreted after activation with the regulation and mediated immune response, inflammation of the a group of small molecular weight polypeptides or glycoproteins [1]. From the hematopoietic system, immune system or inflammatory response in activated cells, its cells monocytes, macrophages, lymphocytes, fibroblasts, keratinocytes, endothelial cells, stellate cells, bone marrow cells and glomerular membrane cells were secreting cytokines. Include interleukin (IL), tumor necrosis factor (TNF), interferon (IFN) and so on. These factors participate in an important component of the immune system, through its endocrine, autocrine and paracrine way, regulating thyroid cell differentiation, growth and secretory function, and to participate in autoimmune thyroid disease

    (AITD) in the occurrence and development process. This article on Cytokines and AITD nearly 10 years of research are reviewed.

     1 cytokine secretion of thyroid function

     In immunology, cytokines can be divided into four

    categories: (1) has antiviral activity of cytokines, mainly IFN; (2) has immunomodulatory activity of cytokines, with IL-

    2, IL-4, IL -5, IL-7, IL-9, IL-10, IL-12, transforming growth

    factor (TGF-β); (3) with the inflammatory cytokine-mediated

    activity, including TNF, IL-1, IL - 6, etc.; (4) has the

    activity of cells of hematopoietic growth factors, including IL-3, colony-stimulating factor (CSF), erythropoietin (EPO) [2].

     Thyroid cells can produce IL-6, TNF-α, IL-1, IFN-r and

    other major cytokines.

     1.1 Interleukin-6IL-6 is a multifunctional cytokine, may be mediated by immune and inflammatory response. Was using in situ hybridization or RT-PCR techniques, from the molecular

    level to prove, thyroid tissues and cells containing IL-6mRNA

    [3,4]. In addition, in cultured human and FRTL-5 thyroid cell

    line, etc. are still to express IL-6 protein molecules [3,5].

    Moreover, thyroid disease devastating the level of serum IL-6

    significantly increased [6]. Description of thyroid cells have the ability to produce IL-6. IL-6 may also be monocyte -

    macrophages, activated T cells, vascular endothelial cells and fibroblasts, bone marrow stromal cells and other cell secretion. Thyroid cells to produce IL-6 regulation by many

    factors, including IL-1 and thyroid-stimulating hormone (TSH)

    The role of the most obvious, they can co-stimulate IL-6

    synthesis and secretion. IL-1 can also promote the IL-6m RNA

    expression. Available data show that tumor necrosis factor (TNF)-α, γ-interferon (IFN-γ), fetal serum, growth factor

    and prostaglandin e 2 and so on can also increase the thyroid cells to produce IL-6 [7].

     1.2 tumor necrosis factor-TNF, there are two molecular

    forms, namely, TNF-α, TNF-β. TNF apart from thyroid may also be activated extracellular single-core - macrophages, which

    can cause hemorrhagic necrosis of tumor tissue, also known as Cachectin. TNF-α can induce a variety of cytokines (IL-1, IL-

    6, IL-8, TNF-γ) gene transcription and expression, etc., so that synthesis and release. TNF-β produced by activated

    lymphocytes. A combination of both in the same membrane receptor, and has very similar biological functions. TNF has immunomodulatory role in promoting IL-2R and the major

    histocompatibility complex class I antigen (MHC-I) expression.

    But also the role of TNF and TNFR neutral sphingomyelinase,

    hydrolysis of sphingomyelin (SM), generating ceramide (CH), CH, as the first two messenger-activated protein kinase

    (CAPK), mediated by apoptosis. In addition, some scholars believe that TNF-dependent conversion of arachidonic acid

    (prostaglandins) process to produce free radicals and peroxides, as the first two messengers into the nucleus, resulting in damage to cell DNA chain, and lipid peroxidation, dissolved enzyme enzyme activation and membrane permeability-

    increasing protein overflow, resulting in cell lysis [8].

     1.3 IFN-γ, inter alia thyroid cells, IFN-γ by T cells,

    macrophages and NK cells to produce, by its very nature as a glycoprotein. IFN has anti-virus, anti-tumor, immunomodulatory

    and other biological functions. IFN immune regulation include: the promotion of macrophage phagocytosis, activated NK (natural killer cells) to increase their antigen expression, enhanced target cells sensitized lymphocyte cytotoxicity.

     Thyroid cells produced IL-1, IL-6, TNF-α, IFN-γ of

    these hormone-like substances, which on the one hand to

    maintain the body's steady-state, and are also involved in a

    variety of the pathogenesis of autoimmune diseases, thyroid gland micro-environmental damage, thyroid dysfunction [7].

     2 cytokines on the thyroid function

     Cytokines are an important class of biological regulators of thyroid, in thyroid function in regulating growth and differentiation play a pivotal role. Them by influencing the antigen-presenting, information transmission, and gene transcription, LgE synthesis and inactivation, the expression of adhesion molecules, multi-faceted regulating immune injury

    in thyroid tissue (positive regulatory role), while others suppress the immune injury in thyroid tissue ( negative regulatory role).

     The primary function of thyroid cells, synthesis of

    thyroglobulin, peroxidase and thyroid hormone secretion. IL-1,

    IL-6, IFN-γ, TNF-α and so can reversibly inhibit thyroid cell synthesis of thyroid globulin (Ig), peroxidase (TPO), reduction of three thyroid hormone triiodothyronine (T3) and

    four-triiodothyronine (T4) release. Weetman, etc. (1994) Hamilfom et al (1991) to explore the molecular effects of cytokines on thyroid function, suggesting that IL-1, IL-6,

IFN-γ, TNF-α and so can inhibit thyroid globulin and

    peroxidase mRNA expression. Kraiem (1990) data indicate that IL-1, IL-6, IFN-γ, TNF-α and so can inhibit thyroid-

    stimulating hormone (TSH) stimulation of thyroid cells. Yanmazakj (1996) also mentioned that IL-1, TNF-α can inhibit

    thyroid-stimulating hormone-releasing hormone (TRH) release,

    IL-1 on thyroid cells, inhibit iodide uptake.