Serum sickness proteins to form immune complexes. These complexes precipitate, enter the walls of blood vessels, and activate the complement cascade, initiating an inflammatory response and consuming much of the available complement component 3 (C3). The result is a leukocytoclastic vasculitis. This results in hypocomplementemia, a low C3 level in serum. They can also cause more reactions resulting in typical symptoms of serum sickness. Serum sickness can be developed as a result of exposure to antibodies derived from animals. These sera or antitoxins are generally administered to prevent or treat an infection or envenomation. Some of the drugs associated with serum sickness
Envelope glycoprotein GP120 the neuronal cells, and it is also known to activate STAT1 and induce interleukins IL-6 and IL-8 secretion in neuronal cells. Envelope glycoprotein GP120 Envelope glycoprotein GP120 (or gp120) is a glycoprotein exposed on the surface of the HIV envelope. It was discovered by Professors Tun-Hou Lee and Myron "Max" Essex of the Harvard School of Public Health in 1988. The 120 in its name comes from its molecular weight of 120 kDa. Gp120 is essential for virus entry into cells as it plays a vital role in attachment to specific cell surface receptors. These receptors are DC-SIGN, Heparan Sulfate