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This form of microglial cell is commonly found at specific locations throughout the entire brain and spinal cord in the absence of foreign material or dying cells. This "resting" form of microglia is composed of long branching processes and a small cellular body.
The blood–brain barrier is a structure composed of endothelial cells and astrocytes that forms a barrier between the brain and circulating blood. Physiologically, this enables the brain to be protected from potentially toxic molecules and cells in the blood.
Foreign body giant cells are involved in the foreign body reaction, phagocytosis, and subsequent degradation of biomaterials which may lead to failure of the implanted material. [4] When produced, the FBGC's place themselves along the surface of the implantation, and will remain there for as long as the foreign material remains in the body. [1]
This marks the beginning of an autoimmune attack which destroys myelin in active lesions. [50] When the attack is resolved, a characteristic glial scar is formed by astrocytes. Current models can be divided into two categories: inside-out and outside-in. In the former, it is hypothesized that a problem in CNS cells produces an immune response ...
Entering the systemic immune system, these antigens are recognized as foreign and an immune response is mounted against them. The result is the sensitization of immune cells against a self-protein, causing an autoimmune attack on both the damaged eye and the non-damaged eye. [9]
Foreign body granuloma formation consists of protein adsorption, macrophages, multinucleated foreign body giant cells (macrophage fusion), fibroblasts, and angiogenesis. It has also been proposed that the mechanical property of the interface between an implant and its surrounding tissues is critical for the host response.
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Membrane attack complex (Terminal complement complex C5b-9) A membrane attack complex attached to a pathogenic cell The membrane attack complex (MAC) or terminal complement complex (TCC) is a complex of proteins typically formed on the surface of pathogen cell membranes as a result of the activation of the host's complement system, and as such is an effector of the immune system.