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72 Cards in this Set
- Front
- Back
What is immunity?
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All mechanisms by which the body protects against foreign agents
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Two “arms” of immune response
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Innate immunity(non-specific)
-born with -fast acting -barriers, cells, and serum proteins Acquired (adaptive) immunity(specific) -improves with exposure -primarily mediated by lymphocytes (T and B cells) |
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Examples of Innate defenses
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-Barriers (e.g. skin, mucous membranes)
-Chemical mediators -Interferon (fight viral infection) -Complement (C.L.I.O) -Phagocytosis -Toll-like receptors -Inflammation -NK cells (recognize tumor or viral cells – “altered-self cells” |
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Barriers
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Two major surfaces by which most microbes/Ag enter body:
-Skin -Mucous membranes |
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Epidermis
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Live and Dead cells with keratin
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Epidermis is renewed every _____ days
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15-30
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When Epidermis is damaged it secretes _______ and _____
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IL-8 / Tumor Necrosis Factor(TNF) (inflammatory)
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Dermis is ________ and contains (3) _________
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Vascularized
Hair follicles, Sweat glands, & Sebaceous glands (oil can coat microbes) |
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Langerhans cells (DC) in skin
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move Ags to LN
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Normal flora in skin
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Can inhibit pathogenic microbes
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Restriction enzymes
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enzymes in skin that restrict growth of viruses
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Bacteriocins
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inhibit bacteria in skin (ex. colicins)
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Innate defenses of skin
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Epidermis
Dermis Langerhans cells (DC) Normal flora |
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Mucous membranes
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Respiratory, Digestive, Genitourinary Tracts
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sIgA (secretory immunoglobulin) is an ________ componant of mucus membrane immune function
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adaptive
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Mucin
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coats (traps) microbes
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Mucociliary escalator
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– movement of mucous up to be expelled (cough/sneeze) or swallowed
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examples of 2 pathologies associated with mucociliary escalator
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Cystic fibrosis patients – abnormal cilia and mucous
Smoking – temporary paralysis of cilia |
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Lysozyme functions by
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cleavage of bacterial cell wall (b1,4 linkage of peptidoglycan)
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immune defences in mucus membranes
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secretory immunoglobulin [sIgA](adaptive)
& Mucin and Lysozyme |
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Respiratory tract contains ________ which is important in immune function
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Surfactants
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Surfactants
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-Pathogen-binding proteins
-Important in alveolar function |
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Surfactants are members of ________ family
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Collectin
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Surfactants bind _______ and ________
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pathogen and phagocytes
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Surfactants binds pathogen and phagocytes using
Globular lectin-like “head” to bind _____ and a Collagen-like “tail” to interact with ______ |
microbe/Macrophage
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an example of surfactant is __________ which can activate complement proteins
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Mannan-binding lectin (MBL)
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Chemical mediators of innate defenses
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Stomach acid/digestive enzymes
Lysozyme Interferon Complement cascade |
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Lysozymes are involved in
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destruction of microbes
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Interferon has _______ activity
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antiviral
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Complement cascade has _______ activity and consists of (3)
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antimicrobial/Cell lysis, opsonization, inflammation
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the low _____ of stomach acid helps to kill microbes
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pH
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Reduced acid production increase risk for ______ infections
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Salmonella
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Some microbes can overcome the low pH of the stomach. For example, ___________ creates microenvironments where pH is not as low
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Helicobacter pylori
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Interferon has _________ properties
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Anti-viral
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Interferon causes cells to become resistant to viral infection by inducing changes in _________ and inhibiting _________
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cell surface receptors/viral replication
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Interferon inhibits viral replication by (2) ________
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inducing CHANGES in host cell molecules needed for viral replication and
stimulating of APOPTOSIS of infected cells |
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types of interferon
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alpha, beta, and gamma
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a and b IFN have ________ than g IFN
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more potent antiviral properties
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a and b IFN are involved in activation of ______ activity and
increased activity (class I presentation) |
NK cell /TAP
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g IFN is involved in
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immune system activation
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g IFN is produced by
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Th1 cells
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TAP
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series of enzymes that chop up proteins for presentation w/ class I, role inCD8+ cells
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What are the three activities of alpha and beta IFN
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1) induce resistance to viral replication in all cells by destroying viral mRNA
2)Increase MCH class I expression and Ag presentation in all cells by increased recognition of CTL or cytotoxic T lymphocytes. 3)Activate NK cells to kill virus-infected cells |
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CTL
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cytotoxic T lymphocytes.
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phagocytosis involves ________ by _________
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Recognition, ingestion, and digestion/Monocyte/macrophage, neutrophil
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Resident (tissue) macrophages (Mf)
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First cells to encounter microbe
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Resident (tissue) macrophages (Mf) are activated by
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-molecules on microbes binding to toll-like receptors (TLRs)
-Antibodies (Abs) coating microbe |
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e.g., of Resident (tissue) macrophages (Mf)
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alveolar Mf (lung), Kupffer cells (liver), osteoclasts (bone), microglial cells (brain), histiocytes (CT), mesangial cells (kidney)
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Neutrophils vs. Monocytes/Mf?
Rapid increase during the acute phase response |
Neutrophils
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Found in healthy tissues
Macrophage or Neutrophil? |
Macrophages
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Short lived (die after phagocytosis)
Macrophage or Neutrophil? |
Neutrophils
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Rapidly form pus
Macrophage or Neutrophil? |
Neutrophils
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Long lived (survive phagocytosis)
Macrophage or Neutrophil? |
Macrophages
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Only found in inflamed tissues
Macrophage or Neutrophil? |
Neutrophils
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Slowly form granuoloma (with T cell help
Macrophage or Neutrophil? |
Macrophages
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Slight increase in blood during inflammation
Macrophage or Neutrophil? |
Macrophages
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How do macrophage/neutrophils recognize of microbes
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1) Changes in adhesion molecules
Extravasation (neutrophils go through the endothelial cells to get to microbe) 2) Acute phase proteins- Opsonize microbe 3) Microbe specific receptors CR4 and CD14 – neutrophil binding to LPS Toll-like receptors |
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Mf recognition of microbes
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Most receptors on Mf bind microbe molecules NOT
found on human cells |
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Toll-like receptors
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-transmembrane signalling protein on Mf or neut used in innate defenses for recognition of microbes
-Many different forms (~10) -Can bind to many substances (LPS, DNA, RNA, yeast cell wall components) |
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Upon stimulation of TLRs
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get inflammatory response
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Neutrophil localization to site of infection
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Neutrophil “rolling”
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Chemokine
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(a/k/a IL-8)
small molecule involved in inflammation |
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Neutrophil recognition of microbes
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CR = complement receptors
FcR = binds to Fc region of Ab |
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Cytokines (e.g., IL-1B; TNF-a) are
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regulatory produce a variety of responses including fever, inflammation etc.
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Acute phase response
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some cytokines produced by macrophages (IL-6, TNF-alpha, IL-1) float away from site of inflammation/damage to the liver and cause hepatocytes to produce C-reactive protein (CRP) and MBL (mannan-binding lectin). These molecules bind to sugars on microbe to allow for opsonization & complement activation
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Septic shock
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Occurs when TLR and other receptors on Mf & neuts recognize microbe and over produce inflammatory cytokines (e.g., TNF-alpha) resulting in a systemic inflammatory reaction.
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Destruction of ingested microbe results in
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Respiratory burst (increased oxygen consumption) within phagocytic cell and production of reactive oxygen and nitrogen intermediates designed to kill the microbe
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Purpose of inflammation-
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vasodialation draw more WBCs to area
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Granuloma
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chronic inflammation
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NK cells
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-Considered to be a lymphocyte but NOT antigen specific.
-Kill virally-infected cells and tumor cells (altered self cells-changes in surface proteins) -once bind to cell they release lytic mediators |
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How does NK cell know to kill altered self cell
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altered self cell will be lacking some sort of surface marker
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Temporal relationship between innate and adaptive immunity
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Temporal relationship between innate and adaptive immunity
Some damage occurs in the body for example the epithelial cells. (t=0) Phagocytic cells (neutrophils, monocytes) get called to the area. They release cytokines.(t=2hr) Cytokines stimulate inflammation.(t=4hr) Cytokines can activate compliment (cell lysis, inflammation, opsinization). Cytokines call in NK cells. (t=12hr ) The story may stop here. If microbe not destroyed, then B or T cells called to the area (t=1D). The B cells then produce effector antibodies and the T cells produce effector cytokines. |