Fichas
Innate immunity
Fichas del conjunto (79)
- 1Name the 3 types of barriers in innate immunity + 1 examples for eachPhysical - skin. Chemical - antimicrobial peptides, enzymes in tears and stomach acid, . Mechanical - Cilia, fluid flow, expulsion from the rectum
- 2Name 2 things the innate immunity does not have in terms of recognizing pathogensNo specificity. No memory.
- 3What type of molecules does the innate immune response use to spot pathogensPRRs - Pattern recognition receptors, which recognize PAMPS
- 4What does PAMPS stand for and what can they consist ofPathogen associated molecular patterns. Can consist of - sugars, proteins, lipid bearing molecules, or a mix of these
- 5Name 2 examples of enzymes found in blood and tears, and what they can doLysozymes. Secretory phospholipase A. They disrupt cell walls by cleaving sugars in peptidoglycan.
- 6Where are antimicrobial peptides in the innate immune system stored, and what can they do. Name 2.Neutrophils. They an inhibit DNA/RNA synthesis, and disrupt the membrane. Histatins & Defensins
- 7What are collectins, what distinct feature do they have, and how do they workPRRs. They have collagen tails. They bind to sugar chains of bacteria.
- 8What are the 4 main functions of the complement systemThe lysis of cells & pathogens. Opsonisation. Triggering inflammation. Clearing immune complexes.
- 9How does complement help induce inflammationFragments of complement arrange themselves in a gradient near the infected site, with large fragments nearest the infection and smallest fragments farthest away. This gradient attracts neutrophils, which follow the gradient to the site of infection.
- 10What is opsonization (and what can opsins be)Coating the bacteria with opsins, so as to make them easier to target. Opsins can be antibodies, complement or collections.
- 11In the blood, complement components circulate as _Inactive proforms
- 12Name the 3 different complement pathwaysClassical. Lectin. Alternative
- 13What is the classical pathway dependent on that the lectin and alternative pathways ware notActivation via binding to Antibodies
- 14Describe activation in the classical complement pathway1. IgM or IgG activate complement via antigen binding (forming an immune complex). 2. This induces conformational change in the Fc portion of IgM, exposing the binding site for C1. 3. Each C1 macromolecular complex (c1qr2s2) must bind to at least 2 Fc sites for a stable interaction
- 15What is the difference between IgG & IgM in the activation of the classical complement pathway1. IgM is planar, so needs antigen binding in order to bind C1, whereas IgG molecules near each other can bind and activate C1 without a conformational change needed. 2. IgM has 5 Fc portions so is better at activation C1.
- 16Describe the first 3 steps in amplification during the classical complement pathway1. C1q binds antigen-bound antibody. 2. C1r activates auto catalytically and activates 2nd C1r. 3. Both C1rs together activate C1s.
- 17Describe the steps 4 - 6 in amplification during the classical complement pathway4. C1s cleaves C4 & C2. 5. C4 binds near C1, C2 binds C4 = C3 convertase. 6. C3 convertase hydrolyses hundreds of C3 fragments = amplification.
- 18Describe steps 7 - 9 in amplification during the classical complement pathway7. C4 + C2 + C3 = C5 convertase. 8.C5 is cleaved & binds C6. 9. Leading to initiation of the membrane attack complex.,
- 19What are lectinsProteins that recognise & bind to specific carbohydrate targets
- 20How is the lectin pathway activatedBy the binding of MBL (mannose binding-lectin, a collectin) to mannose residues on glycoproteins/carbohydrates on the surface of microorganisms (eg. HIV-1, Salmonella, Fungi)
- 21What happens after MBL Is bound, during the lectin pathwayMBL-associated proteases MASP-1 & MASP-2 bind to MBL, and this active complex cleaves C2 +C4
- 22Describe what happens in the alternative complement pathway1. C3 spontaneously hydrolyses into C3a & C3b via C3 convertase. 2. C3b binds to a cell membrane + factor B. 3. This complex is cleaved by factor D into C3bBb, which hydrolyses more C3 = amplification.
- 23What is the half life of C3bBbBetween 5 - 30 mins
- 24Describe what MAC doesForms a pore in he membrane. Allows diffusion of ions & small particles out of the cell. Allows water into the cell, causing it to burst.
- 25How does the C1 inhibitor workIt binds C1r2s2 and causes dissociation from C1q. It prevents C1 activating C4 + C2.
- 26Name some membrane bound complement inhibitors and what they do (collectively)C4bBp, C1, DAF, factor H. They prevent C3 activation.
- 27Which complement inhibitors prevent insertion of C5b67 MAC into the membraneS protein & Homologous restriction factor (HRF)
- 28What do patients with a complement deficiency usually experenceRecurrent infections
- 29Which complement deficiency leaves patients prone to meningitisC8
- 30Which complement deficiency leads to Hereditary Angioedema, and how can this be treatedC1 inhibitor deficiency. Can be treated with injections of C1 inhibitor.
- 31Which 2 immune cells are phagocytic cellsNeutrophils & Macrophages
- 32Phagocytosis definitionThe capture and degradation of foreign particles by neutrophils and macrophages
- 33Describe the process of phagocytosis1. Microbes bind to phagocyte receptors. 2. Microbe is internalized via endocytosis = phagosome. 3. Phagosome fuses with lysosome = phagolysosome. 4. Activation of the phagocyte
- 34What are the 2 ways in which a phagocyte can kill pathogens1. Microbes are killed y lysosomal enzymes in he phagosome. 2. Killing of phagocytosed microbes by ROS & NO.
- 35Name the 5 phagocytic receptorsComplement. Fc. Toll-like. Mannose. Scavenger.
- 36Name examples of chemokines that attract phagocytes to the site of infection, and what they induce expression of.IL6, IL1, TNF. They induce expression of selectins & integrin ligands.
- 37List the 4 steps in phagocyte recruitment1. Rolling. Activation. Arrest/adhesion. 4. Transendothelial migration into the tissue.
- 38List the 5 PRRsToll-like. Rig1 - like. NOD-like. AIM2-like. C-type lectin.
- 39What is this, and what does TIR stand forToll like receptor. Toll interleukin 1 receptor - important for activation
- 40On TLRs what is the site of pathogen bindingLeucine rich repeats in the extracellular domain
- 41What can TLR2 recognise that TLR4 cannotGram positive bacteria (as well as gram negative)
- 42Which TLRs are extracellular (Cell surface)1, 2, 4, 5, 6, 10
- 43Where are TLR 3, 7, 8, & 9 foundWithin the endosome
- 44What does the TLR-2/TLR-6 complex recogniseDiacyl lipopeptides
- 45What does the TLR-2/TLR-1 complex recogniseTriacyl lipopeptides
- 46What does TLR5 recogniseFlagellin
- 47What does TLR4 recognise, and what is it famous for triggeringLPS. Septic shock.
- 48What does TLR3 recognisedsRNA
- 49What does TLR7 recognisessRNA
- 50What does TLR9 recogniseCpG DNA
- 51What does TLR8 recognisessRNA
- 52What endogenous molecules can cell surface TLR recogniseHSP70, Fibrinogen, Fibronectin & HMG as well as DNA/RNA
- 53TLRs only function as heterodimers: True or FalseFalse they can also be homodimers
- 54What does the binding and dimerization of TLRs doBrings their TIR domains close together, inducing signalling
- 55What does TLR signaling induceChemokines, pro inflammatory cytokines, MHC & costimulatory molecules, iNOS & antimicrobial peptides
- 56What are the 2 pathways involved in TLR signalingMyD88 dependent + MyD88 independent aka trif pathway
- 57MyD88 pathway in TLRMyD88/Mal -> IRAK1/4 ->(A) IKK complex -> IkB + NFkB or (B) MAPK -> AP1
- 58MyD88 independent pathway in TLRTrif/TRAM -> IKKe/TBK1/TRAGF3 -> IRF3/7
- 59Which TLR only needs TrifTLR3
- 60Which TLR is activated in HIVTLR8
- 61Which TLR is activated in TB2 & 4
- 62Which TLR is activated in SLE7 & 9
- 63Which TLR is activated in Alzheimers2 & 4
- 64NOD-like receptors: What are they and what are the 2 groups1. Nucleotide-binding leucine rich. 2. Cytoplasmic PRRs. 3. Main groups are NLRCs ( C stands for caspase recruitment domain aka CARD) & NLRP (P stands for pyrin domain).
- 65What is the difference between NOD1 & NOD2NOD1 binds iE-DAP on peptidoglycan (mainly gran negative bacteria). NOD2 binds muramyl dipeptide (both gram pos and neg)
- 66Which NOD mutation is associated with Crohns diseaseNOD2
- 67Binding of bacterial ligands to NOD proteins induces recruitment of _ , which activates _ leading to _RPK2, TAK1, NFkB activation
- 68What NLR mutation causes hereditary periodic fever syndromesNLRP3
- 69What does NLRP3 interact withdouble stranded RNA; single stranded DNA; Muramyl dipeptide, and some viral PAMPS.
- 70What does NLRP3 activate, and howThe inflammasome. By activating caspase 1.
- 71What is the inflammasome and what (generally) is it activated byHigh molecular weight complexes that activate inflammatory caspases and cytokine IL-1b. Activated by cellular infection or cell stress.
- 72What do RIG-1-like receptors detectCytoplasmic RNA, a replication intermediate for RNA viruses
- 73Describe RLR signalling1. Cytoplasmic replication of virus produces uncapped RNA with a 5'-triphosphate. 2. Viral RNA binding to RIG-1 induced RIG-1 to associate with the adaptor MAvs, causing dimerization. 3. MAVs induces production of inflammatory cytokines and interferons via activation of NFkB & IRFs
- 74What are AIM2 - like receptors, what 2 domains do they have (+function)PYHIN proteins. HIN domain - dsDNA & ssDNA binding. Pyrin domain - activates inflammasome.
- 75Name 2 AIM2 - like receptors &their functionAIM2 - recognizes dsDNA. IFI16 - recognizes viral DNA in the cytoplasm AND nucleus.
- 76Acute Phase Response: What is it, what is it induced by, where is it produced, what can it activate/inducePoorly defined set of proteins that circulate in the blood. 2. Induced by cytokines such as TNF, IL-6 and IL-1 during infection and inflammation.
3. Mainly produced by the liver. 4. Can activate the complement pathway & induce opsonisation/phagocytosis - 77What is a characteristic & measurable attribute of acute phase responseCRP & ESR (erythrocyte sedimentation rate)
- 78Which complement component does CRP activateC1q
- 79What does CRP bindBinds polysaccharide and phosphorylcholine on bacterial surface or necrotic cells
Información
- Descripción
- Undergraduate Immunology Fichas sobre Innate immunity, creado por Joanna Elliott el 17/04/2015.
- Creado por
- Joanna Elliott
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