Genetic engineers developed a way to add the gene encoding TNF to a kind of white blood cell that is effective at locating cancer cells but not effective at harming them.
The difference between acute and chronic toxicity is that acute toxicity is caused by a single chemical exposure that might be fatal; the adverse effect is high and symptoms may be reversible. While chronic toxicity is caused by multiple chemical exposures; the adverse effect is low and symptoms typically not reversible.
Kupffer cells, also known as Browicz-Kupffer cells, are specialized macrophages located in the liver that form part of the reticuloendothelial system (aka: mononuclear phagocyte system). The cells were first observed by Karl Wilhelm von Kupffer in 1876. The scientist called them "sternzellen" (star cells or stellate cells) but thought, falsely, that they were an integral part of the endothelium of the liver blood vessels and that they originated from it. In 1898, after several years of research, Tadeusz Browicz, a Polish scientist, identified them, correctly, as macrophages.  Their development begins in the bone marrow with the genesis of promonocytes and monoblasts into monocytes, and then on to peripheral blood monocytes, completing their differentiation into Kupffer cells. The red blood cell is broken down by phagocytic action, and the hemoglobin molecule is split. The globin chains are reutilized, while the iron-containing portion or heme is further broken down into iron, which is reutilized and bilirubin, which is conjugated with glucuronic acid within hepatocytes and secreted into the bile. Helmy et al. identified a receptor present in Kupffer cells, the complement receptor of the immunoglobulin family (CRIg). Mice without CRIg could not clear complement system-coated pathogens. CRIg is conserved in mice and humans and is a critical component of the innate immune system. Kupffer cells activation are responsible for early ethanol-induced liver injury, common in chronic alcoholics. Chronic alcoholism and liver injury deal with a two hit system. The second hit is characterized by an activation of the Toll-like receptor 4 (TLR) and CD14, receptors on the Kupffer cell that internalize endotoxin (LPS). This activates the transcription of pro-inflammatory cytokines (TNF alpha) and production of superoxides (a pro-oxidant). TNFalpha will then enter the stellate cell in the liver, leading to collagen synthesis and fibrosis. Fibrosis will eventually cause cirrhosis, or loss of function of the liver
TNF blockers are used to inhibit inflammation in people who suffer from TNF or tumor necrosis factor. Vascular calcification does not appear in the side effects that may occur from taking a TNF blocker.
G. Kollias has written: 'TNF pathophysiology' -- subject(s): Pathophysiology, Immunology, Genetic Transcription, Tumor necrosis factor, Physiology, Tumor Necrosis Factors
Tumor Necrosis Factor or TNF, is a cytokine which is involved in the inflammatory process. Cytokines are chemical substances which deliver messages between cells in the body.
IL-1 IL-12 IL-6 and TNF -a
TNF,gamma interferon, IL-1,IL-3
There must be a whistle on original TNF bag
Embrel is an anti-TNF (Tumor Necrosis Factor Blocker).
PGC-1 alpha and beta can be overexpressed in skeletal muscle. This overexpression leads to anti-inflammatory effects. Both alpha and beta reduce TNF alpha levels. TNF alpha is a pro-inflammatory substance. When you challange muscle with inflammatory insults: Injecting LPS (lipopolysacharide, or TNF alpha, or induce muscle inflammation by downhill running) then overexpression of PGC-1 alpha and beta protect against inflammation
For difficult to treat (refractory) sarcoidosis and sarcoidosis involving the nervous system (neurosarcoidosis), recent research using biologic medications that inhibit tumor necrosis factor (TNF-blockers) has been beneficial. The TNF-blockers used were adalimumab (Humira) and infliximab.