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Tumor necrosis factor definition 1:
It is mainly produced by activated monocytes/macrophages, which can kill and inhibit tumor cells, promote neutrophil phagocytosis, resist infection, cause fever, induce acute phase protein synthesis of hepatocytes, and promote differentiation of myeloid leukemia cells into macrophages. Promotes cell proliferation and differentiation, is an important inflammatory factor, and is involved in the pathological damage of certain autoimmune diseases.
Definition 2:
A cytokine that is naturally produced by macrophage responses to bacterial infections or other immune sources. Synergistic with interferon kills tumor cells.
Definition 3:
Produced primarily by activated monocytes/macrophages, it kills and inhibits cytokines in tumor cells. Promotes neutrophil phagocytosis, anti-infection, causes fever, induces acute phase protein synthesis of hepatocytes, promotes differentiation of myeloid leukemia cells into macrophages, promotes cell proliferation and differentiation, is an important inflammatory mediator, and participates in certain autoimmunity Pathological damage to the disease.
Tumor necrosis is a small molecule protein secreted by macrophages. TNF-α is mainly secreted by mononuclear-macrophages; TNF-β is mainly secreted by activated T lymphocytes, which have similar pyrogenicity. The small dose is unimodal heat, and the large dose is bimodal fever; TNF can stimulate the production of IL-1 both in vitro and in vivo. Not heat resistant, inactivated at 70 ° C for 30 min
Introduction:
In 1975, Carswell et al found that mice injected with BCG injected with LPS contained a factor that could kill certain tumor cells or cause blood necrosis in tumor tissues in vivo, called tumor necrosis factor (TNF). In 1985, Shalaby named the TNF produced by macrophages as TNF-α, and the lymphotoxin (LT) produced by T lymphocytes was named TNF-β. TNF-α is also known as nausea.
TNF production:
(1)
TNF-α is a mononuclear factor produced mainly by monocytes and macrophages, and LPS is a strong stimulator. IFN-γ, M-CSF and GM-CSF have a stimulating effect on monocyte/macrophage production of TNF-α, while PGE has an inhibitory effect. The pre-monocytic cell line U937 and the promyelocytic cell line HL-60 produced higher levels of TNF-α under PMA stimulation. T lymphocytes, T cell hybridomas, and T lymphoid cell lines can also secrete TNF-α under the stimulation of PMA by NK cells or the like. SAC, PMA, and anti-IgM 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, and both antigen and mitogen can stimulate T lymphocytes to secrete TNF-β. PMA stimulates RPMI1788B lymphoblasts to secrete high levels of TNF-β.
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