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.

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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. The 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).

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figure 2. immune system and acquired immunity

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).

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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).

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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 (S. Severin et al, 2013).

The Process of Activation

Platelets are not usually attracted to endothelial surfaces. As endothelial surfaces act to inhibit platelet activation by producing:

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).

Examples of platelet activating factors:

Secondary Activation

Following primary activation, the microtubule system which is located below the plasma membrane and the actin cytoskeleton system of the platelets activate the reaction (S. Severin et al, 2013). This increases aggregation.

A thrombus or blood clot is the final product in the blood coagulation set of hemostasis. This happens when filopodia are produced which provide the framework for platelets to attach to each other and also collagen fibres. Endothelial production of prostacyclines and nitrogen monoxide ceases. Their role is to prevent the factors production of factors responsible for aggregation. Accordingly, the thrombocytes can now produce their own stimulating factors. TXA2, serotonin, adenosine Diphosphate that will stimulate other thrombocytes increasing the aggregation as well as the secretion of coagulation factors (Szent István Egyetem, 2011).

Aggregation at Sites of Bacterial Invasion

Previous studies (P. B. Maguire, D. J. Fitzgerald) would indicate that platelets also: