nonspecific defenses, first responders, born with this, recognizes pathogens by predetermined patterns; Toll-Like Receptors (TLR), no memory, first and second line of defense
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adaptive immunity
develop as you grow, second to respond, clears infections, learns and remembers each pathogen encountered, memory to previously encountered pathogens, acts faster, third line of defense
largest physical barrier; keratin: skin, nails, hair; epithelial cells tightly packed, tough layer that few pathogens can penetrate
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first line of defense: mucous membrane
prevent entry and attachment of bacteria, layer of epithelial cells, secrete mucous; gastrointestinal, genitourinary, respiratory tracts; invasins help bacteria get through the mucous membrane
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invasins
helps bacteria get through the mucous membrane
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first line of defense: ciliary escalator
found in different parts of the respiratory tract, cilia and mucous help trap microbes, sneezing and coughing releases microbes, smoking damages cilia which increases respiratory infections
signal phagocyte is attracted to, chemical attraction of the phagocyte to the microbe, chemotactic factors can attract phagocytes
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phagocytosis: adherence
TLR on the phagocyte bind to the PAMP on the microbe
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phagocytosis: phagosome
formation of the microbe and phagocytic vesicle
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phagocytosis: phagolysosome
fusion of the phagosome with a lysosome
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lysosome
organelle containing digestive enzymes
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evade phagocytosis examples
protein A, M protein, capsule, leukocidins, mycolic acid
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inflammation
second line of defense, can occur during an immune response, signs and symptoms: redness, warmth, swelling, pain;
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three stages of inflammation
1. vasodilation and increased permeability of blood vessels 2. phagocyte migration and phagocytosis 3. tissue repair
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2. phagocyte migration and phagocytosis
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3. tissue repair
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histamine
causes increased permeability of blood vessels
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so that certain molecules like WBC can be released to the site of infection
why does vasodilation and increased permeability of blood vessels occur during inflammation
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fever
increase in internal body temperature to levels that are above normal; inhibit microbial growth of some microbes; help stimulate immune reactions; activated by endotoxins
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fever caused by
infection from bacteria, their toxins, or viruses
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endotoxins
what are fevers activated by
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second line of defense
what line of defense are fevers part of
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antimicrobial substances
complement (C') in the blood; made by leukocytes to kill microbes: interferons
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complement system
innate, 30 proteins made by the liver which circulate in the blood and are only functional when activated, activation is a cascade of ordered interactions between these proteins, 3 outcomes of complement activation
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activated protein fragments
C3b, C3a
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inactive protein fragments
C3, C2, C1
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three outcomes of complement activation
opsonization, inflammation, cytolysis
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classical pathway
antigen-antibody complex with C1; C1 activates C2 and C4; C2 split into C2b and C2a; C4 split into C4b and C4a; C2aC4b combine and activate C3; C3 split into C3a and C3b
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inflammation
C3a function in all pathways
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cytolysis and opsonization
C3b function in all pathways
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alternative pathway
lipid-carbohydrate complex on the surface of the microbe as it binds to C3 through the complement proteins: factor B, factor D, factor P; C3 splits into C3a and C3b
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lectin pathway
mannose-binding lectin binds to the mannose on the surface of the microbe which activates C2 and C4; C2 split into C2b and C2a; C4 split into C4b and C4a; C2aC4b complex activates C3; C3 splits into C3a and C3b
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complement activation outcome: cytolysis
C3 splits into C3a and C3b; C3b activated and splits into C5; C5 splits into C5a and C5b; C5b combines with C6, C7, C8, C9 to form the membrane attack complex (MAC) on the membrane of the pathogen
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membrane attack complex (MAC)
results in cytolysis which causes lysis and death of the pathogen, a pore, attacks plasma membrane
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gram-negative bacteria
which bacteria are susceptible of the membrane attack complex
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complement activation outcome: opsonization
C3 splits into C3a and C3b; C3b acts as an opsonin and binds to the pathogen to coat the pathogen and enhance phagocytosis
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opsonin
protein that can coat the pathogen and enhance phagocytosis making it easier for the phagocyte to adhere to the microbe through its C3 receptors
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opsonin examples
C3b and antibodies
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complement activation outcome: inflammation
C3 splits into C3a and C3b; C3a binds to the C3a receptors on a mast cell, C3b splits into C5; C5 splits into C5a and C5b; C5a binds to the C5a receptors on the mast cell causing the mast cell to release histamine from granules (degranulation)
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chemotactic factors
attract phagocytes to site of inflammation
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chemotactic factors examples
C5a and C3a
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interferon-gamma
activates neutrophils and macrophages to kill microbes by causing an increase in phagocytosis
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interferon-alpha and interferon-beta
produced by cells in response to viral infections and cause neighboring cells to produce antiviral proteins (AVPs) that inhibit viral replication, help fight off viral infections, signaling molecules, produced by infected cells
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antiviral proteins
AVPs
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antiviral action of alpha and beta interferons
virus induces infected host cell to produce alpha and beta interferons; interferons released from infected cell and make contact with uninfected neighboring host cell; interferons induce uninfected neighboring cell to synthesize antiviral proteins; AVPs in uninfected neighboring cell will degrade viral mRNA and inhibit protein synthesis
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acquired immunity
what is adaptive immunity also known as
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stem cells
can differentiate into B cells and T cells, will migrate to different lymphoid organs where they can perform their specific function
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thymus
T cells mature here
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red bone marrow
B cells mature here
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adaptive immunity types
humoral immunity and cellular immunity
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humoral immunity
B cells and antibodies, B cells have a B cell receptor (BCR) on the surface of the cell, antibodies outside cell circulating for a pathogen
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cellular immunity
T cells have a T cell receptor (TCR), T Helper cell, cytotoxic T cell (CTL), focusing on destroying intracellular pathogens
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antigen
protein or polysaccharide recognized by the immune system, components of invading microbes or foreign substances