Tumor necrosis factor is an important inflammatory mediator, as shown by blocking inflammatory shock using antibody to tumor necrosis factor, a therapy used today for the treatment of many human autoimmune diseases.
Passive immunization against cachectin/tumor necrosis factor protects mice from lethal effect of endotoxin.
Report that established the idea that adenosine released from injured cells may negatively regulate inflammation by acting on the adenosine A2 receptor, a G protein-coupled receptor.
The antiinflammatory mechanism of methotrexate. Increased adenosine release at inflamed sites diminishes leukocyte accumulation in an in vivo model of inflammation.
