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31 Cards in this Set
- Front
- Back
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why is immunity to infectious orrganisms important
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major cause of death & disease in world
immune response necessary for survival increased presence of Ab resistant bacteria increased cowding, travel allows exposre to evolvin viruses |
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immunity to viruses occurs by
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recognition of infection: innate immune response
recognition of viral antigens adaptive immune response (4-6 days after) immunologic protection & memory anti-host pathological effects of vigorous immune repsonse to virus |
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how does body (immune system) know that it is being infected
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recognition of viral infection (all cells) RIG 1 R's recognize viral ds RNA toll like R's 3.7,8, 9 recognize dsRNA, viral ssRNA, CpG DNA
- foreign activates RIG R's & induce IFN release by infected cells & attach to uninfected cells & produce kinase R activation of innate immune response - IFN regulatory factor & NfkB: INF a/B & infalmmatory cytokines: TNFa, IL 6, IL 12 |
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how does interferon induce a cell to an antiviral state
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translation of protein kinase R
- blocks eukaryoic initiation factor 2a - activates bcl2 & caspase initiating apoptosis 2'5' oligoadenylate synthetase: activation of Rnase L degrades vRNA Mx protein blocks trx activation |
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type I ntereron also activates
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DC's
macs NK cells T & B cells innate & adaptive immunity activated |
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DC's & macs funcions
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phagocytosis
Ag presentation release of cytokines killiing of virus infected cells |
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IFNa/b actions
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protects neighboring uninfected cells
intracellular defences 1. PKR (protein kinase): apop & blocks viral protein syn 2. 2'5' oligoadenylate synthetase; RNase L (latent endonuclease) : degrades viral mRNA 3. Mx protein: blocks viral trx |
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NK cells
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activated by innate cytokines: Interferon a, IL 12
cytotoxic to virus infected cells produce interferon-g to activate adaptive immune response - adaptive virus specific effector immune response releases lytic granules that kill some virus infected cells |
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Wat does adaptive response recognize as foreign
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viral antigens on ec infectious virus
- membrane & capsid Ag's on infected cells; viral structural proteins inserted in host cell membrane primary adoptive response to virus infection is T cell mediated; leading to resolution of infection - Ab response is slightly later & contributes to recovery from infection CD4+ & CD8+ cells |
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CD4+ cells in adoptive immune response
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Th1 cells: activate macs, induce T & NK cell activation & proliferation; promotes B cell production of Ig
Th2 cells: provide help for b cells to activate, differentiate, & produce Ab - also activates eosinophils |
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CD8+ cells in adoptive response
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cytotoxic to infected host cells
produce INF- g & TNF : inhibit virus replication principle surveillance system operating aainst virus infected cells by direct killing through released effector molecules & triggering of "death signnal" (fas ligand) to induce apoptosis - perforin, granzymes, granulysin, fas ligand |
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Ab response to virus infecion
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CD4+ t cells helpviral Ag specific B cells in LN's proliferation
- IL 3,4,5,6 clonal expansion divide & differentiation (IgM) somatic hypermutation & selection (selects high affinity IgG) plasma cells migrate to bone marrow ec virus: block binding of virus to host cells, prevent infecion enhance phagocytosis & mediates opsonizationof virus particles (activates complement) IgM & IgG (serum) IgA (ep & mucosal : lungs & gut) virus infected cells: Ab binding to viral A's on infected cells - activation of complement system = lysis of infected cell & induction of Ab dependent cell cytotoxicity (ADCC) |
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protective immunity & immunologic memory
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preformedAb & T cells
memory T & b cells rapidly expand & differentiate into effector cells -1-2 days instead of 4-5 |
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why do we need immunologic memory
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for immunosuppressed ppl (like pregos) would have memory & be protected
also protect old, b/c thymus degrades - protection depends on past experiences & t and b cells |
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anti-host effects of virus to impair immune response
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1. immune evasion
- antigenic variation - antigen shift & drift (swine flu H1N1) - molecular mimicry 2. avoidance of recognition - latency infection of immune "privileged" host sites - impair immune recognition by reducing MHC expression on infected cells 3.impair host response - inhibition of humoral immunity & infalmmatory response - immunosuppression of host - infection of host immune cells |
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pathological consequences of immune responses induced by viral infection
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1. excessive cytokine production
acute respiratory distress syndrome : ARDS cytokine storm H5N1 ebola virus pathoogy induced by virus induced cytokine damage to epithelial cells - increases leakage and makes BP low 2. Antiviral Ab's can form immune complexes: IC disease: glomerulonephritis 3. virus specific Tcells can cause host tissue damage & induce autoimmunity - hep B: t cells killing hepatocytes - Coxsacki B virus: t cell against b cells - enterovirus: T cells against cardiomyocytes |
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host immune responses to ebola and cell damage due to direc infection of monocytes & macs cuase
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release of cytokines associatd with infalmmation & fever
infection of endothelial cells also cause cytopathic effect & damage to endothelial barrier that, together with cytokine effects, leads to loss of vascular integrity cytokine dysregulation & virus infection may synergize at endothelial surface, promoting hemorrhage & vasomoto collapse |
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immunity to bacteria & fungi
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induce inflammatory responses
produce cytotoxic endotoxins (LPS) or exotoxns diphtheria toxin) recognition is bacteria bearing PAMPs and recognized by host pattern recognition molecules ( toll like R) of innate immune system |
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innate immune response to bacteria & fungi
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chemotaxis: C3a & C5a recruit phagocytic cells to bacteria following complement activation via alternate pathway
phaocytes (macs & neutrophils) engulf & destroy bacteria |
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adaptive effecto response to bacterial infection
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CD4+ t cells: produce cytokines
cytotoxic CD8+ t cells: ic organism killed by killing infectedcell - very important in response to M. Tuberculosis secrete IFN-g to activate macs Ab dependent anti bacterial defenses |
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CD4 cells produce what cytokines in adaptive ffector response to bacterial infection
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INF-g & TNF to activate macs & induce infalmmation
IL4,5,6 to induce Ab formation Th17 cells produce IL-17 & IL 22 : important for resistence tto ex bacteria |
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AB dependent anti bacterial defenses in adaptive effector response
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neutralize toxins
blocks binding of microbes to cellular R's increased opsonization & phagocytosis activates & efficient targeting of complement |
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Bacterial defenses against host responsse to infecion
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encapsulation, evade complement activation
kill phagocytes before ingestion R to phagocytosis, phagosome-lysosome fusion & lysosomal killing Intracellular microbes that can survive in phagocytic or other host cells |
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immunopathological rxns induced by bacteria
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excessive cytokine release: endotoxin septicemic shock
- LPS from gram neg bacteria superantigen induction of masive cytokine release - toxic shock syndrome of staphlococcal toxin (potato salad) - induces state where t cells can't kill infection T cell stimulation by superantigens: recognition of V-B alone; high freq of antigen specific cells (<10%) |
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immunity to fungi; 4 major categories
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superficial mycoses include: jock rot, athletes foot
subcutaneous mycoses include: malessezia furfur respiratory mycoses includes: aspergillosis, histoplasmosis, blastomycosis candida albicans is yeast infection - primarily an innate response, neutrophils & macs essential for killing fungi - T cell response is protective including CD4+ Th1 (DTH) & Th17 cells |
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immunity to protozoa & worms : general
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complicated life style
complex relationship with host & immune system poor immune response to chronic infections immune evasion by antigenic variation no in vitro culture system |
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innate immune response against protozoa & water
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PRR's on phagocytic cells recognize PAMPs on parasite
TLRs 2, 9 , 11 classical PRR's: collectins, lectins, scavenger R Complement R's CrR3 activate phagocytic cells, kill or damage parasites - macs important for smaller parasites - neutrophils clean up damage - eosinophils responsible for helminths; IL 5 required, associated with IgE - mast cells control GI helminths |
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adoptive immune response against parasites & worms
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not as effective
T cells fundamental to control infection & confer protection cytokines produces b cells produce: IgM, IgG : activate complement, neutralize attachment, enhance phagocytosis, ADCC IGE biinds mast cells & basophils sensitizing them to parasite Ag's |
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cytokines produced in adoptive immune response to parasites & worms
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TH1
- INF-g - TNFa - IL2 TH2 - IL 3, 4, 5, 6, 9, 10, 13 |
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protozoe & worms escape mechanisms
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reesist destruction by complement
intracellular parasites resistant to O2 metabolites & lysosomal enzymes hyper antigen variation hide from immune response interefere with immune response |
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processes involved in expulsion of nematodes from gut
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specific t dependent processes
- plasma cells secrete Ab; lead to metabolic damage in intestinal epithelial and damages worm non specific inflammatory processes: TNF, IL 1 - stimulate goblet cell proliferation - increased mucus secretion - allows for expulsion of damaged wormin intestinal luman |
