TUMOR NECROSIS FACTOR-ALPHA AND ITS INHIBITION STRATEGIES: REVIEW ARTICLE

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FARAJZADEH DAVOUD; KARIMI GHARIGH SEDIGHEH; DASTMALCHI SIAVOUSH

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Journal: Tehran University Medical Journal Year:2017 | Volume:75 | Issue:3 Page(s): 159-171

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Title

TUMOR NECROSIS FACTOR-ALPHA AND ITS INHIBITION STRATEGIES: REVIEW ARTICLE

Author(s)

FARAJZADEH DAVOUD | KARIMI GHARIGH SEDIGHEH | DASTMALCHI SIAVOUSH | Issue Writer Certificate

Keywords

INFLAMMATIONQ1

INHIBITION AGENTSQ1

REVIEWQ2

TUMOR NECROSIS FACTOR-ALPHAQ2

Abstract

Tumor necrosis factor-alpha (TNF-a) 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-a 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-a are mediated through two different receptors: TNFR1 and TNFR2.These receptors are trans membrane 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-a 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-aactivates the control systems involved in cell proliferation, differentiation, INFLAMMATION and cell death, and the regulation of immune system. Although a normal level of TNF-a 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-a or blockade of its receptors using TNF-a inhibitors can be an effective therapeutic strategy to prevent or treat such inflammatory diseases. Several methods have been used to inhibit TNF-a, including the production of chimeric or fully human antibodies, soluble TNF-a receptors, or anti-TNF-a small molecules. The two previous agents are mostly capable of inhibiting the binding of TNF-a to its associated receptors, while anti-TNF-a small molecules, in addition to the above, inhibit the biosynthesis of TNF-a by blocking TNF-a mRNA biosynthesis, through the inhibition of its post-translational processing, or by blocking TNF-a receptors. Therefore, in this REVIEW article, we discuss the structure and characteristics of TNF-a and its related receptors: TNF-a signaling, TNF-a-mediated inflammatory diseases as well as TNF-a inhibition strategies.

Cites

REVIEW OF NKG2D FUNCTION AND ITS RELATED LIGANDS: REVIEW ARTICLE

References

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APA: Copy

FARAJZADEH, DAVOUD, KARIMI GHARIGH, SEDIGHEH, & DASTMALCHI, SIAVOUSH. (2017). TUMOR NECROSIS FACTOR-ALPHA AND ITS INHIBITION STRATEGIES: REVIEW ARTICLE. TEHRAN UNIVERSITY MEDICAL JOURNAL (TUMJ), 75(3), 159-171. SID. https://sid.ir/paper/39037/en

Vancouver: Copy

FARAJZADEH DAVOUD, KARIMI GHARIGH SEDIGHEH, DASTMALCHI SIAVOUSH. TUMOR NECROSIS FACTOR-ALPHA AND ITS INHIBITION STRATEGIES: REVIEW ARTICLE. TEHRAN UNIVERSITY MEDICAL JOURNAL (TUMJ)[Internet]. 2017;75(3):159-171. Available from: https://sid.ir/paper/39037/en

IEEE: Copy

DAVOUD FARAJZADEH, SEDIGHEH KARIMI GHARIGH, and SIAVOUSH DASTMALCHI, “TUMOR NECROSIS FACTOR-ALPHA AND ITS INHIBITION STRATEGIES: REVIEW ARTICLE,” TEHRAN UNIVERSITY MEDICAL JOURNAL (TUMJ), vol. 75, no. 3, pp. 159–171, 2017, [Online]. Available: https://sid.ir/paper/39037/en

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