 | Term | Definition |
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innate immune system |
Our defense when our first line of defense is invaded, this is activated and usually eliminates the invaders. aka nonspecific interior defense |
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adaptive immune system |
incase of an attack on our body, and our innate immune system is overwhelmed, this line of defense is activated. this out our last line of defense. takes days or weeks to activate unless we have previously been exposed to the invader. |
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plasma |
the proteins that make up the noncellular fraction of the blood |
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complement |
a set of microbe-attacking proteins in blood, lymph, and extracellular fluids. the activation of these make up the first response of the innate immune system to invading microorganisms. |
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phagocytes |
the first effective attack on the invaders |
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phagoctosis |
the method that a class of leukocytes use to destroy pathogens. |
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alternative pathway |
the activation of a complement in the innate response, when no antibodies are present. Hydrolysis occurs and proteins are introduced that lead to the splitting of C3 into C3a and c3b....this all takes place before the antibody is produced |
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C3b |
a fragment of a complement component that plays a critical role in the immune response. it catalyzes the splitting of more molecules of C3, to form molecules of itself....but only if invading microbes are present. they form spontaneously and and quickly destroyed. when microbially cells are present, it is stabalized by binding to their surfaces. it interacts with other complement proteins to form C3 convertase, which is a powerful enzyme that rapidly forms many more molecules of itself. |
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terminal complement pathway |
a immune response of C3b, when C3 enters this pathway, it leads to the formation of the membrane-attack complex |
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membrane attack complex |
the killing of microbial invaders by making holes in their membranes, cytolysis |
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opsonin |
a critical role of C3b as a molecule that can facilitate phagocytosis |
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C5a |
a product of C3b that attracts phagocytes. |
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neutrophils |
they circulate in the blood, but enter any infected tissue, They are the most abundant WBC we have. they live for about two days and only live for a few hours after entering the infected tissue. they are non-specific eaters. |
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macrophage |
the long-lived, mature form of a monocyte that has left the bloodstream and taken up residence in tissue, |
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recognition |
the first and critical step of phagocytosis. it is the ability of phagocytes to direct their killing power exclusively toward invading microorganisms, not other host cells, |
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cell-surface receptors |
the proteins that are found on the outer surface. these proteins can bind to molecules on the surface of microbial cells that are not present on host cells. |
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phagosome |
a membrane bound vacule within the phagocyte that traps the bacterial cell. It is formed by the psuedopods. |
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phagolysosome |
a phagosome and a lysosome found in a macrophage. the lysosome can include chemicals like lysozyme, lactic acid, nitric oxide, and other oxidants...which are able to kill the bacteria. |
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expulsion |
after the bacterium is digested, the phagolysosome fuses with the cell membrane and expels indigestible debris |
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cytokines |
as bacteria are degraded, these cellular components are released by the macrophage. they signal other components of the immune sustem to respond to invaders, organizing a coordinated defense. can result in local or systemic effect |
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inflammation |
cytokines are able to coordinate and expand the antipathogen activities of the innate immune system. this is one state which is the fluid accumulates within the affected tissues (causes swelling, redness, and pain) |
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erythema |
inflammation causes the capillaries to dilate, blood has an increased permeability (swelling is caused by WBC and serum proteins entering the affected tissue), and causes this. the visibly red color and the warming of the tissue. |
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chemotactic |
describes phagocytes ability to attraction to the site of the battle against the infection because of a concentration gradient. |
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inflammatory mediators |
some of the cytokines that cause inflammation. |
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pus |
a yellow fluid mixture of dead microorganisms, leukocytes, microorganisms, and tissue cells |
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interferons |
a small protein that interferes with viral replication. there are many different kinds: alphas, betas, gammas. they are host specific, viral non-specific, but they are induced by only some viruses (not all viruses produce these). |
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fibroblast |
a type of cell tissue that produces Beta interferons |
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specific immune regulators |
while the most powerful antiviral interferons belong to alpha and beta groups, the gamma group contains these.... |
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antiviral proteins |
enzymes (created and released interferons by other cells that have been infected by a virus) that interfere with viral protein synthesis and thereby stop the spread of infection. |
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natural killer cells |
cells that fight viral and other intracellular infections by killing infected host cells, thereby stopping multiplication of the pathogen. their killing potential is stimulated 20-100 fold after being exposed to certain cytokines (IL-2 and IFN); as they attack the infected cells, these cells also produce cytokines that stimulate macrophages. |
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classical pathway |
cascade that involves an antibody |
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cascade |
the breaking and binding of complements to each other |
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serum proteins |
complement proteins. when they are activated they will break apart and combine with otehrs to create new proteins..... protease cascade |
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eosinophils |
WBC that is found in these 2 situations: some allergies and during parasitic infections |
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monocytes |
WBC that are found in the blood, can phagocytize, but have no granules. they are not just found in the blood, they are able to enter the tissue, change shape, and become macrophages |
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opsonins |
a coating on bacteria to help engulf it |
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complement proteins |
nonspecific defense that have receptors that help them bind to the pathogen |
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antibody |
a specific defense that covers the pathogen to help phagocytize the bacteria |
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respiratory burst |
the activation of phsagocytosis by neutrophils. neutrophils start making superoxide |
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nonspecific interior defense |
inflammation, phagocytosis, complement, and interferon |
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leukocytes |
neutrophils, monocytes, basophils, eosinophils, lymphocytes, platelets |
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lymphocyte |
30% of WBC, function is for specific immunity |
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monocyte |
8% of WBC, function is for phagocytosis/specific immunity |
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neutrophils |
60% of WBC, function is for phagocytosis...it is a major component of our second line of defense. they are the first to arrive at an infection to eat debris and microbes |
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eosinophils |
2% of WBC, function is for phagocytosis/specific immunity |
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basophils |
0.5% of WBC, function is for phagocytosis/hypersensitivity |
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inflammation |
hallmarks include: swelling (edema), redness(erythema), heat, pain |
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Polymorpho nuclear leukocytes |
a cell with a nucleus that has many lobes. aka a neutrophil, this cell cleans invading bacteria (a phagocyte) |
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mononuclear leukocyte |
a cell with a normal nucleus |
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granulocytes |
found in PMNL (neutrophils, eosinophils, basophils). thegranules may contain lysozyme, protease, DNAase, RNAase, lipase...all of which can break down macromolecules |
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agranulocytes |
MNL-monocyes |
