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| == Connection between Platelets and Immunity == | |
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| Itt írjon a(z) PlateletImmunity-ról/ről Hemostasis |
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| Platelets' foremost role is hemostasis. It not only helps the animal from blood loss but it also prevents microorganisms from entering the animal which may cause disease. The role of Platelets in homeostasis would suggest evolution from more primitive multifunctional innate defensive cells as although highly differentiated they have inflammatory and antimicrobial systems and link clotting and immune cascades (A.S Weyrich et al). Hemostasis is crucial to animals, when a blood vessel of theirs becomes damaged or injured. It is the first stage of wound healing. Platelets are present in the blood circulation at a volume of 2-8 x 1011/l, depending on the species. They are unable to move themselves so they passively move with the blood circulation (page 131). After an injury to a blood vessel occurs, vascular constriction is the organisms initial reaction. Platelets are not usually attracted to endothelial surfaces. When an injury of a blood vessel happens, platelets combine with their specialized surface receptors to the negative charges of the endothelial regions. This is primary aggregation (page 200-201). Also, Von Willebrand factor, which is a multimeric glycoprotein released by the endothelial cells plays a key role in the adhesion of platelets to the subendothelium.(M. Hermmann et al). This allows platelet aggregation to increase. Secondary activation follows. The microtubule system which is located beneath the plasma membrane and the actin cytoskeleton system of the platelets activate the reaction (S. Severin et al). This causes white thrombosis to arise. This happens when by filopodia are produced which provides the framework for platelets to attach to each other and also collagen fibres. Endothelial production of prostacyclines and nitrogen monoxyde ceases. Their role is to prevent the production of factors responsible for aggregation. Accordingly, the thrombocytes can now produce their own stimulating factors. These include TXA2, serotonin, adenosine-diphosphates that will stimulate other thrombocytes increasing the aggregation as well as the secretion of coagulation factors (page 201 and 202). This shows how platelets are pivitol in hemostasis. Without them, a relatively innocuous injury to a blood vessel may be fatal. They help heal wounds and by doing this help to prevent harmful microorganisms which could be disease causing from entering the animal. If these disease causing microorganisms were to off got into the body the animal would have to endure processes such as the production of antibodies to fight the infection. These processes are energy consuming and put the animal under stress. Therefore platelet's role in hemostasis can be looked upon as a temporary mechanical barrier between the organism and the outer environment, reducing the threat of disease when an animal is wounded. |
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'' 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: |
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| 1. Nitric oxide | |
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| 2. Endothelial ADPase, which clears away the platelet activator, ADP. | |
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| 3. PGI,,2,, | |
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| '''''Primary Activation''''' | |
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A.S Weyrich et al The evolving role of platelets in inflammation J.Thromb. Haemost., 1 (2003), pp. 1897-1905) http://www.jstor.org/discover/10.2307/30107584?searchUri=%2Faction%2FdoBasicSearch%3FQuery%3Dvon%2Bwillebrand%26Search%3DSearch%26gw%3Djtx%26prq%3Dplatelets%2Bvon%2Bwillebrand%26hp%3D25%26acc%3Doff%26aori%3Doff%26wc%3Don%26fc%3Doff&Search=yes&searchText=von&searchText=willebrand&uid=3738216&uid=2129&uid=2134&uid=2&uid=70&uid=4&sid=21102878826017 http://onlinelibrary.wiley.com/doi/10.1111/jth.12053/pdf |
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). |
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).