Class Note for MIC 205A at UA
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This 7 page Class Notes was uploaded by an elite notetaker on Friday February 6, 2015. The Class Notes belongs to a course at University of Arizona taught by a professor in Fall. Since its upload, it has received 17 views.
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Date Created: 02/06/15
Host Defenses to Microbes Nonspecific Defenses What is Immunity Do you have it o How do you know you have it To what antigens can you become immune How did you get it o How long does it last memory Is it always a good thing to have Elements of a Defense System Barriers Surveillance Recognition Communication Recruitment Response fast and generalized slower and more targeted specific Repair Memory sownquot Tim Mchw Hill Conwarllvb n rmmwmnpm lcr Iiimoduuiuii m display HOST DEFENSES When speailia third Fine nl defame Naturally Am clally a1un acquired m Passlve Active Pass ve inlection Malemal Veounauen Immune anlibodles mum l l The llrsl line oi neiense Is a The second line or aeiense is a surlace roiecuan composed ol cellular and chemical sysleni Ihal unalumiml and physvological cumes immediately in a play barnsis Mal keep Microbes infectious agents make ii past me an I A companmenis mans m check The mini line 0 delense includes speci c nosi delenses that mus be an L7 uniquer ior each Microbe Ihvough ihe action of specialized while blood cells ms form at immunity is us ph and aesuoy ii and niiammaimn which holds V y nng arm and has memory Physical and Chemical Barriers Skin mucus membranes Cilia mucus reflexes pH lysozyme fatty acids defensins Normal flora Genetic resistance species differences individual differences The Immune System Organs cmnginmieinlanmniicmw qulu39dlmv L a auluy Lymphall dud The Immune System Local Inc Copyright iiZ i 1quot Dendntlc cell Rellculo endothelium Lymphatics ECF extracellular tlurd a Plasma Proteins Blood plasma contains Clotting factors Complement Antibodies Molecules not related to defense Serum is missing clotting proteins The Immune System Cells Coming i l Ti 04 quot w lie l 2 r4 7 7 I 7 B I i 1 Q 1 int 41 J a i A My N J j 9E u quot 0 B U i g 1 E E 5 I Lymphocytes g 8 i 2 9Q Blood phagocytes that P rnary cells involved in g g E g n g 93 I rapidly leave the Circulation 5 ecrlic immune reactions w 5 39o g i m E 5 g m g 39 mature into macrophages to foreign matter O 5395 T D g 2 2 1a 8 E E g E S a 395 5 E 33 9 E m E 8 l a 5 E E S we 139 C c E v ca 332 war 3953 0mg i a g n i 33 2 5amp3 311 gg z I w H suchas sng cosan o 6 2 E a 3 6 f a g E o 5 g E 39 killing torergn cels ijcewllv n O aquot T z w m 0 m u w w lt V quotj I J mediated immunity l quot B cells I Macrophages Dlllerenlsale into plasma cells I Larges OhaQOClTE S quot 3 term antibodies humora l ingest and kill ioreign cells mmmm m l39 strategic pan c pa ts Ii cena n specrllc immun I eac ons V I r Mast cells Dendritic cells Specialized tissue cells a J RGIBTIVBS of macrophages that 839 ii I to basophils that r95ide throughout the lissues trigger local inflammatory V T x and PIES responsible for reaclsorzs an are responsible processrng foreign ma Ier an for many allergic symptoms presenting it to lymphocytes J The Immune System Receptors The Immune System Receptors II B cells detect extracellular antigens produce ant bodies T cells detect intracellular an gens ght viruses and intracellular pathogens Antibodies Humoral Immunity Cell Mediated Immunity Resistance to Infectious Disease Innate immunity nonspecific resistance protects us against all pathogens overthecounter defenses Adaptive immunity specific resistance is defenses against specific pathogens prescription defenses Nonspecific Host Defenses Innate Immunity Always present Immediately effective No immune memory work at the same speed each time Inflammation Triggered by tissue damage First responders are tissue macrophages Recruit cells and proteins to infection quotlt1 site I 7 Contain pathogen i 1 0quot Alert adaptive 39quotJW 5313 0 response Injury and Mediator Release Comuglit Bacteria in wound a lnjuryl Immediate Reactions Mast cells release chemical mediators Vasoconstriction Fluid and Phagocytes Enter Copyrng l 739 Inca quot I reproduction u u pig b Vascular Reactions Seepage of fluid plasma and neutrophils out of blood vessels Vasodilation Edema and Pus Formation Comuglitiil c Edema and Pus Formation Scab Neutrophils Pus Fibrous exudate quot 39 V m ror ut 1 Resolution Scar Formation gt 39 Scar Ruborinllammation i 39 iLymphocytes quot x Edema due to g collected fluid 4 i Newly healed Macrophage issue Phagocytes Phagocytes eating cells Neutrophils PMNs are present in the highest numbers in blood Macrophages big eaters in the tissues encounter the pathogen first Secrete cytokines gt inflammation systemic responses Pathogen Recognition Molecules on Phagocytes Membrane receptors bind commonly shared bacterial molecules LPS endotoxin Gram Lipoteichoic acid Gram Patterns of sugars PAMPs Nucleic acids Phagocytosis Phagocyte must bind pathogen to begin phagocytosis Microbes with capsules are difficult to bind Phagocytosis is easier if the pathogen is coated with antibodies or complement opsonins Macrophage Chemokines Cause capillary leakiness Attract PMNs Increase adhesion molecule expression on capillary endothelium and PMN surfaces Leukocyte Diapedesis 4 Chemofactic gfa 7 b Low High Signaling the Adaptive Immune System Fluid containing pathogen antigen drains from infection site into nearby lymph nodes Lymph nodes contain specific B and T lymphocytes that can make an adaptive response and produce memory cells CownulilelwMneuw lillconwamv m Mummmummimmpmmmmu a Phagocytosis quot7 vg quot Ge 39 I a o Gr 00 39 Phagosome Lysosome Primary granule Secondary granule Antimicrobial chemicals Pathogen Destruction Pathogen is killed by enzyme digestion toxic oxygen molecules and defensins Some pathogens resist killing and live in phagosome or escape to cytosol Mycobacterium tuberculosis Listeria monocytogenes Macrophage Cytokines Signal hypothalamus to increase body temperature fever Signal liver to produce acute phase proteins opsonins that aid phagocyte binding of pathogen Signal bone marrow to release more PMNs Complement Pathways CLASSICAL PATHWAY l MBLECTIN PATHWAY l ALTEBNA39IWE PATHWAV Lectin binding to Antigenantibody complexes Pathogen surfaces pathogen surfaces Li J J J f9 e 9 J7 Recruitment of Opsonization Killing inflammatory cells of pathogens of pathogens Fig 27 2001 Garland Science Complement Amplification by enzyme activity Highly regulated so our cells don t yse Membrane lesions Membrane lesions end on rings side on tubes Interferon or and 5 Function cumulem mewmuemwm he quotWe in wwmmmepu Assembly Viral o muses Degrades virus nucleic acid nucleic acid Blocks WUS Vm replication Virus infection Attachment of IFN lo speclai receplor l 7 quot 39qu Synthesis 0 oleN activation of genes lnlecled Nearby cell cell AntiViral Interferons IFNoc and IFNB made by virus infected cells Not virusspecific Bind neighboring host cells and induce synthesis of antiviral proteins to block virus replication Immune Interferon IFNy is made by T lymphocytes Activates macrophages and neutrophils to kill bacteria Natural Killer Cells All nucleated cells in body have membrane MHC tissue typing antigens In virusinfected cells MHC is reduced in amount or contains virus peptides NK cells recognize this altered MHC and kill virusinfected cells also tumor cells cmmmm Mchw Hm Cnmnms ms Pwmnssmn ruqmmd 1m mpmdunmnavdmp ay HOST DEFENSES The sewn Mn ul autumn a canmarm chemical System that cnmas meadm si mm play a mmousanems make u pas me menmmm emjuwmcmag WWW mamasmmmwma 316yggiggggggmggir mamlmunenlnmenumcmes iped c hos ewnses lmrmuslha devainped mus orsch mm Waugh me Hanan alspec ahzed mg blood can ma lnrm or unmunly i usuaHylnng 27m m m mummy
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