چاپ صفحه |  صفحه نخست سامانه |  چکیده مقاله |  نویسندگان |  دانلود مقاله | دانشگاه علوم پزشکی تبریز |
| نویسنده ثبت کننده مقاله | سیاوش دستمالچی |
| مرحله جاری مقاله | تایید نهایی |
| دانشکده/مرکز مربوطه | مرکز تحقیقات بیوتکنولوژی(زیست فناوری) |
| کد مقاله | 61727 |
| عنوان فارسی مقاله | فاکتور نکروز دهنده تومور آلفا و راهکارهای مهار آن: مقاله مروری |
| عنوان لاتین مقاله | Tumor necrosis factor-alpha and its inhibition strategies: Review article |
| ناشر | 3 |
| آیا مقاله از طرح تحقیقاتی و یا منتورشیپ استخراج شده است؟ | بلی |
| عنوان نشریه (خارج از لیست فوق) | مجله دانشکده پزشکی، دانشگاه علوم پزشکی تهران، |
| نوع مقاله | Review Article |
| نحوه ایندکس شدن مقاله | ایندکس شده سطح سه – Scopus |
| آدرس لینک مقاله/ همایش در شبکه اینترنت | http://tumj.tums.ac.ir/browse.php?a_id=8092&sid=1&slc_lang=en |
| Tumor necrosis factor-alpha (TNF-α) is a pro-inflammatory cytokine produced by a variety of cells, including hematopoietic and non-hematopoietic cells, malignant cells, macrophages, B lymphocytes, T lymphocytes, natural killer cells, neutrophils, astrocytes, endothelial cells, and smooth muscle cells. TNF-α is a homo-trimeric molecular whose individual subunits are composed of antiparallel beta-sheets, forming a regular triangular prism shape. TNF-α binds to three receptor molecules through its receptor-binding sites, which are at the base of its pyramid structure. Biological responses to TNF-α are mediated through two different receptors: TNFR1 and TNFR2. These receptors are transmembrane glycoproteins with extracellular domains containing multiple cysteine-rich repeats that are structurally and functionally homologous, and the intracellular domains that are discrete and transduce their signals through both overlapping and distinct pathways. However, though TNF-α was initially discovered as an anti-tumor agent, it has been revealed that TNF-α and other ligands of this family are involved in some diseases like cancer, neurological, pulmonary, cardiovascular and autoimmune diseases and metabolic disorders. In general, TNF-α activates the control systems involved in cell proliferation, differentiation, inflammation and cell death, and the regulation of immune system. Although a normal level of TNF-α is very important for the regulation of immune responses, the persistence of the immune response as a result of inappropriate and excessive production of TNF-α can cause some inflammatory or autoimmune diseases. Accordingly, either neutralization TNF-α or blockade of its receptors using TNF-α inhibitors can be an effective therapeutic strategy to prevent or treat such inflammatory diseases. Several methods have been used to inhibit TNF-α, including the production of chimeric or fully human antibodies, soluble TNF-α receptors, or anti-TNF-α small molecules. The two previous agents are mostly capable of inhibiting the binding of TNF-α to its associated receptors, while anti-TNF-α small molecules, in addition to the above, inhibit the biosynthesis of TNF-α by blocking TNF-α mRNA biosynthesis, through the inhibition of its post-translational processing, or by blocking TNF-α receptors. Therefore, in this review article, we discuss the structure and characteristics of TNF-α and its related receptors: TNF-α signaling, TNF-α-mediated inflammatory diseases as well as TNF-α inhibition strategies. |
| نویسنده | نفر چندم مقاله |
|---|---|
| سیاوش دستمالچی | سوم |
| نام فایل | تاریخ درج فایل | اندازه فایل | دانلود |
|---|---|---|---|
| Tehran Univ Med J-v75n3p159-en.pdf | 1396/08/16 | 589807 | دانلود |
