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Necrosis Factors Proteins

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Necrosis Factors Proteins

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Necrosis Factors Proteins Background

Necrosis

The death of local tissues and cells in vivo is called necrosis. The metabolism of necrotic tissue cells ceases and the function is lost. The morphological changes of necrosis can be caused by the degradation of the hydrolase in the injured cells, or by the action of the hydrolase released by the walking white blood cells. There are many causes of necrosis. All factors that can cause damage (hypoxia, physical factors, chemical factors, biological factors, and immune response, etc.), as long as their effects reach a certain intensity or last a certain time, the metabolism of damaged tissues and cells is completely Stopping can cause local tissue and cell death.

Necrosis Factors

The death of local tissues and cells in vivo is called necrosis. The metabolism of necrotic tissue cells ceases and the function is lost. The morphological changes of necrosis can be caused by the degradation of the hydrolase in the injured cells, or by the action of the hydrolase released by the walking white blood cells. There are many causes of necrosis. All factors that can cause damage (hypoxia, physical factors, chemical factors, biological factors, and immune response, etc.), as long as their effects reach a certain intensity or last a certain time, the metabolism of damaged tissues and cells is completely Stopping can cause local tissue and cell death. In 1975, Carswell et al. Found that after injection of LPS into mice inoculated with BCG, the serum contained a factor that can kill certain tumor cells or cause tumor necrosis in the body, called tumor necrosis factor (TNF).

Necrosis Factors Proteins Figure 1. Crystal structure of TNFa.

Definition

In 1985, Shalaby named TNF produced by macrophages as TNF-α and lymphotoxin (LT) produced by T lymphocytes as TNF-β. TNF-α is also called malignant hormone.

(1) TNF-α is a monocyte factor, mainly produced by monocytes and macrophages, and LPS is a strong stimulant. IFN-γ, M-CSF, and GM-CSF can stimulate the production of TNF-α by monocytes/macrophages, while PGE can inhibit it. The former mononuclear cell line U937 and the former myeloid cell line HL-60 can produce higher levels of TNF-α under PMA stimulation. T lymphocytes, T-cell hybridomas, and T-lymphoid cell lines, such as NK cells, can also secrete TNF-α under PMA stimulation. SAC, PMA, and anti-IgM can stimulate normal B cells to produce TNF-α. In addition, neutrophils, LAK, stellate cells, endothelial cells, and smooth muscle cells can also produce TNF-α.

(2) TNF-β is a lymphokine, both antigen and mitogen can stimulate T lymphocytes to secrete TNF-β. PMA stimulates RPMI1788B lymphoblasts to secrete high levels of TNF-β.

TNF Gene

The human and mouse TNF-β genes are located on chromosomes 6 and 17 respectively. The HuTNF-β molecule is composed of 205 amino acid residues and a signal peptide containing 34 amino acid residues. The mature HuTNF-β molecule is 171 amino acid residues and has a molecular weight of 25 kDa. The rHuTNF-β molecule is composed of 202 amino acid residues, including a signal peptide of 33 amino acid residues, and the mature molecule has 169 amino acid residues, which has 79% homology with HuTNF-β. HuTNF-β and HuTNF-α DNA have a homology sequence of 56% and a homology of 36% at the amino acid level.

Pharmacology

TNF promotes the inflammatory response, which in turn causes many clinical problems associated with autoimmune diseases, such as rheumatoid arthritis, ankylosing spondylitis, inflammatory bowel disease, psoriasis, suppurative sweat glanditis, and refractory asthma. These diseases can sometimes be treated by using TNF inhibitors. This inhibitory effect can be achieved by infliximab (Remicade), adalimumab (Humira), cetuzumab PEGylation (Cimzia) or bait circulating receptor fusion proteins such as etanercept (Enbrel) binds TNFα to achieve higher affinity than TNFR.

Reference:

  1. Beutler B, et al.; Identity of tumour necrosis factor and the macrophage-secreted factor cachectin. Nature. 1985, 316 (6028): 552–4.

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