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 . 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) .
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 . 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 .
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 .
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 .
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.