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38 Cards in this Set
- Front
- Back
2.1
immune exclusion |
innate immunity presenting pathogens from growing on skin and mucosal barriers
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2.2
mucins |
help clump bacteria
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2.3
lactoferrin |
iron binding glycoprotein
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2.4
cationic proteins |
sweat and secretions
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2.5
lysosomes contain |
- lysozymes
- lactoferrin - histatins (histidine-rich proteins) - cationic proteins |
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2.6
desquamation |
shedding skin carries away bacterias
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2.7
defensins |
soluble antimicrobial factors
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2.8
functions of normal microbiota |
- compete for: nutrients, receptors
- produce antagonists - maintainence low, constant expression of MHC 11 (keep immune system primed to encounter pathogens) - cross protective antibodiesq |
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2.9
PAMPs pathogen associated molecular patterns |
foreign triggers for innate immunity and can signal immune cell cytokine secretion
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2.10
PAMPs for bacteria |
- peptidoglycan
- nucleic acid (unmethylated CpG DNA) - Flagellin - Pillin - Lipopolysaccharide (Lipid A) - Lipoteichoic Acid - Glycolipids |
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2.11
PAMPs: fungi |
- mannose
- zymosan |
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2.12
PAMPs: viruses |
- double stranded RNA
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2.13
phagocytic cells |
- trash collectors of the immune system
- take up pathogens - macrophages - monocyte inflammation: - polymorphonuclear leukocyte (PMN) - neutrophil |
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2.14
cells releasing inflammatory mediators |
- mast cells
- eosinophils |
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2.15
antigen-presenting cells (APC) |
- take it up, break it up, display
- dendritic cells lie below the epithelium in the dermis and are alerted to invading foreign particles - macrophages |
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2.16
histamines in acute inflammation |
- break capillaries to leak, releasing phagocytes and clotting factors into cound
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2.17
MAC membrane attack complexes |
- poke holes in membranes of pathogens
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2.18
Mannose-binding lectin (PRR) |
on bacteria surfaces, pattern recognition receptor
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2.19
C-reactive protein (PRR) |
binds phosphocholine on bacteria
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2.20
Complement components |
- facilitate uptake using C36 opsonin
- make potent chemokines for reinforcement using C3a, C4a and C5a |
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2.21
Opsonin |
coat the surface of the bacteria, make it more readily phagocytosed
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2.22
interferons (IFN) alpha and beta |
- produced when virally infected host product double stranded RNA
- induced other uninfected and nucleated cells to be virally resistant - give negative feedback to infected cells |
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2.23
viruses, MHC I and NKs |
viruses down regulate MHC I => NKs look for cells w/ too few MHC I complexes
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2.24
MHC II |
present breakdown products of pathogens taken up extracellularly
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2.25
MHC I |
- monitors cytosolic bioreplication
- present pieces of whatever is being made on the surface of the cell to alert immune system - keeps immune system 'on' at basal levels |
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2.26
endocytic receptors |
- PRR on the surface of phagocytes
- like a handle on the cell - recognize lots of capsule elements found on pathogens |
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2.27
chemotasis |
phagocyte drawn to the infection site
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2.28
phagolysosome |
lysosome fuses w/ phagosome
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2.29
respiratory burst |
- takes up O2 in the phagolysosome
- to generate O2 intermediates (H2O2) - No produced |
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2.30
IL-8 |
- chemotactic
- recruits granulocytes and T cells to infection |
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2.31
IL-12 |
- activate NK cells
induce differentiation of CD4 T cells -> TH1 cells |
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2.32
acute phase response |
fevers and increased production of cytokines
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2.33
NK, gamma delta-T cell, CD5 beta cell |
- innate immune responders
- primitive forms of lymphocytes |
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2.34
CD5 beta cells |
- B1 cells
- protects internal body cavities - produce IgM |
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2.35
Chediak-Higashi Syndrome |
- failure to fuse lysosome and phagosomes to form phagolysosomes
- immune cells will take up pathogens, but can't destroy them |
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2.36
IL-1 and TNF-alpha |
- vascular endothelium to make them more leaky
- allowing other inflammatory and immune molecules access to the infection - intracellular killing deficiency |
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2.37
chronic granulomatous disease |
- failure to form killing agents in lysosomes
- no respiratory burst - intracellular killing deficiency - defect in the NADPH oxidase system -> failure to produce a superoxide radical - deficiency of G6P dehydrogenase -> failure of respiratory burst - deficiency of myeloperoxidase -> failure to produce halide oxidizing agents |
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2.38
leukocyte adhesion deficiency |
- lack of cell adhesion molecules - WBC can't bind endothelium to be pulled out of blood
- infection in tissue, but don't see any inflammatory cells - all still in blood vessels. |