week 5 notes 390
week 5 notes 390 bio 390
U of L
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This 3 page Class Notes was uploaded by Mary-elizabeth Notetaker on Friday September 23, 2016. The Class Notes belongs to bio 390 at University of Louisville taught by Shira Rabin in Fall 2016. Since its upload, it has received 3 views. For similar materials see Intro to Immunology. in Biology at University of Louisville.
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Date Created: 09/23/16
Week 5 Tuesday, September 20, 2016 1:01 PM Anatomical barriers to infection ○ Level 1: Skin- most important..many microbes on it, but don’t let them inside(unless wounded) □ 3rd degree burns- most ppl die bc no longer have skin barrier so get many infections Mucus- get microbes out of body (out nose or into stomach acid to kill them) Tears- salty so keeps microbe lvls down. Enzymes in tears kill microbes Peristalsis- in intestines, moves microbes through ○ Secretions from body, general proteins to kill unwanted things Lysozyme- tears, skin.. Degrades cell wall of bacteria Lactoferrin- tears, skin.. holds iron & prevents from being taken up by microbes(so cant grow as fast) Other proteins: □ defensins, cathelicidins- from skin, degrade cell walls □ Psoriasin- peptide from skin cells, somewhat specific even tho innate(anomaly) Put pepetide with staf/ecoli… staf grows on plate but not ecoli bc peptide kills it □ Calprotectin- kills staf but not ecoli Phagocytosis- eating foreign cells ○ Steps: Bacterium becomes attached to membrane evaginations called pseudopodia Bacterium ingested- forms phagosome Phagosome(microbe inside vesicle) fuses w lysosome(have hydrolytic enzymes to break things down) Bacterium killed and digested by lysosomalenzymes Digestion products are released from cells ○ ROS(reactive oxygen species)- create hydroxyl radicals and hydrogen peroxide inside lysosomes To eliminate them to use oxygen, expose microbes to them and proteins are degreaded, lipids & dna come apart(why they are in lysosome bc has ways to deal with it) ○ ID of pathogen Prevent pathogen access to deep tissues On microbes or self cells: □ PAMPs (pathogen associated molecular patterns) Part of iis but antigen part of sis □ DAMPs( damage " " ")- in self cells when has been damaged On immune cells- PRRs (pattern recognition receptors)- recognize PAMPs/DAMPs □ Toll-like receptors(TLRs) Ex) drosophilia- toll mutations("weird"):back to front axis rearranged ◊ Involved in activation of iis ◊ Tested resistance to fungus(aspergillus)- normals could resist, toll mutation ones were killed.. Realized protein affected location and immune system(haveno sis, only iis) Similar proteins in verts: TLRs ◊ Major PRR ◊ Dimer, EC leucine rich domains that bind PAMPs & DAMPs ◊ Found on macs & DCs ◊ TIR domain Many diff TLRS: Many diff TLRS: ◊ TL2: binds 2 things below(mycobac and yeast) Lipoproteins Zymosan ◊ TLR4: binds bac and binds LPS to bring it in LPS- component of cell wall of gram neg bacteria ◊ TLR5- combining flagellin makes flagella(mvmt) Flagellin ◊ TLR7/TLR8: rna w particular motifs and modifications to viruses ssRNA Location helps det what each TLR will bind ◊ Plasma memb(outside cell)- TLR4, TLR5 ◊ Endosome/lysosome(inside cell)- TLR7/8 Endosomes- phagosomes when they are in cell- have hooks to bind internal things – Face inside cell(to get dna/rna), but TIR domain in cytoplasm TIR domains recruit adaptors--> specificity ◊ Diff adaptor proteins lead to diff events Mac can tell t & b cells what it bound to when certain TLR bound ◊ Pathways: NF-kb MAPK IRF(interferon regulating factor) ◊ Intracellular TLRs--> IFN synth □ RIG1-like receptors- recognize viral dsRNAs Cytosolic PRRs.. RNA helicases Pathways: ◊ Major response: Antiviral IFN responses(IL1/IL18) mac response & notify neighbors- virus ◊ Proinflamm cytokines □ NOD-like receptors(NLRs) Cytosolic Activated by PAMPs Antiviral IFN resp(IL1/IL18) Signaling pathways then occur(mac brings in cell, lysosome, activated, release cytokines, etc) □ Signaling pathways of PRR: activate many genes Anitmicrobial peptides(defensins, cathelicidins) Type 1 IFNs (potent antiviral activity) Cytokines(inflammIL1, TNFa, IL6) Chemokines Inflamm resp-rx to any traumatic tissue event (redness, warmth, swelling, pain, loss of fxs)… iis ○ Chief fxs: Mobilization/attraction Repair- DAMPs come in bc self cells damaged..macs come in to phagocytose damages self cells Destroy/blockmicrobes .. If glass cuts you, resident sentinel cells release chemoattractantsand vasoactive factors to inc blood flow and capillary permeability, permeable capillaries allow influx of fluid(exudate) & cells, bac gets in so chemotaxis brings neutrophils/phagocytes to destory bac ○ Bigger inflamm resp--> fever Pyrogen resets hypothalamic "thermostat" □ Muscles shake to inc heat production □ Dec heat loss thru vasoconstriction Fever benefits: inhibits multiplication, impedes bac nutrition, inc metabolism & immune rxs/phagocytosis ○ Later stages Proinflamm cytokines(IL1, TNFa, IL6..bring in iis cells) Inc synth/secretion of antimicrobial proteins □ Mannose-binding lectin(MBL)- component of complement □ Complement- 30+ proteins that punch holes in cell walls Proinflamm cytokines(IL1, TNFa, IL6..bring in iis cells) Inc synth/secretion of antimicrobial proteins □ Mannose-binding lectin(MBL)- component of complement □ Complement- 30+ proteins that punch holes in cell walls Imp cells in iis: ○ NK cells- from same lymphocyte lineage as b & t cells but are iis not sis Infections(viral), cancer, damaged cells Kill self cells when activated □ Like innate versions of CD8 T cells Know to kill cell when: □ Activating receptor- binds activating ligand on cell it finds □ Inhibitory receptor(MHC)- not present on most cancerous/virally infected cells Viruses/cancer cells downregulate MHC mols (bc they put antigens on surface) □ If cell has both receptors, cell is fine □ If cell only has activating receptors that can be bound to, cell is destroyed When activated- cause apoptosis from caspase cascade □ Produce cytokines-->macrophageactivation--> TH1 response Initial activation inc pop/activity of responding NK cells--> greater response later □ Resembles memory even tho iis cell Regulation of iis response ○ Mutations in PRRs inc susceptibility to infections ○ When system remains abnormally "turned on", contributes to inflamm disorders Bac in blood, LPS on gram neg ○ Ways for microbes to evade iis response Avoid detection of PRRs: bac change flagella in way TLR5 cant bind Block signal pathways: west nile blocks NF-kb mvmt into nucleus Prevent killing or inhibition response: salmonila brought into cell and bursts out of phagosome before lysozome fuses
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