Connection between Platelets and Immunity
Platelets play a central role in both innate and adaptive immunity.
Platelets are a unique type of mammalian blood cell. They are anucleate molecules which play an integral role in host hemostasis, innate and immune defence and repair. Platelets are present in blood circulation but they are unable to move themselves so they passively move with the blood circulation. At sites of infection or injury in a host organism, platelets will be deployed rapidly where they will display their role in defence and signaling.
Innate Immunity
Innate immunity refers to non specific defence mechanisms that come into play immediately or within hours of antigens appearance in the body. These mechanisms include physical barriers such as skin, chemicals in the blood and immune system cells that attack foreign cells in the body. Th innate immune response is activated by chemical properties of the antigen (The Biology Project, University of Arizona, 2000).
Adaptive Immunity
Adaptive immunity refers to antigen specific immune response. The adaptive immune response is more complex than the innate. The antige first must be processed and recognised. Once an antigen has been recognised, the adaptive immune system creates an army of immune cells specifically designed to attack that antigen. Adaptive immunity also includes "memory" that makes future responses against a specific antigen more efficient (The Biology Project, University of Arizona, 2000).
Hemostasis
Hemostasis is a process which causes bleeding to stop and retention of blood within a damaged blood vessel. Hemostasis is crucial to animals in the case of a damaged blood vessel. It is the first stage of wound heeling.
Activation of Platelets
There are two types of platelet activation, primary and secondary, both which lead to platelet aggregation.
Primary platelet activation occurs when the specialised surface receptors of platelets bind to the negative charges of an injured endothelial area (expose collagen).
Secondary platelet activation refers to activation of the platelets by their actin and microtubule system as well as by their secretion of coagulation factors. The potency of platelet agonist varies depending on activation response (J. Thromb. Haemost., 2003).
The Process of Activation
Platelets are not usually attracted to endothelial surfaces. As endothelial surfaces act to inhibit platelet activation by producing:
1. Nitric oxide
2. Endothelial ADPase, which clears away the platelet activator, ADP.
3. PGI2
Primary Activation
Under physiological conditions, collagen is not exposed to the bloodstream. However, when an injury of a blood vessel occurs, collagen and Von Willebrand Factor (vWF), from the subendthelium is exposed to the bloodstream. vWF is a glycomeric protein produced by endothelial cells, which acts as a cell adhesion ligand enabling endthelial cells to adhere to collagen in the basement membrane. When the platelets come in contact with collagen or vWF they are activated (M. Hermann et al, 1997).