lecture 7 exam 2 Flashcards by Morgan Thomas

major physiologic functions will

protect the host against microbial infections

bacteria, viruses, parasites, yeast

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major physiology immune response to pathogens are

mediated by the combined effector mechanisms of innate and adaptive immunity
responds in distinct and specialized ways to different types of microbes
microbe survival and pathogenicity in a host are influenced by ability of microbe to evade or resist the effector mechanisms of immunity -> some pathogens require intervention to eradicate them
tissue injury and disease may be caused by the host response to microbe

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responses to bacterial infection

innate

adaptive: Bcell/NK cell
adaptive: Tcell

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innate immunity response to bacterial infectoin

complement system: alternate & lectin
natural antibodies
phagocytes: nitric oxide, myeloperoxidase, lysozyme, defensins
acute phase proteins: lactoferrin

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adaptive Bcell/NK cell immunity response to bacterial infection

complement system: classical
antigen specific antibodies
ADCC: by NK and eosinophils

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adaptive Tcell immunity response to bacterial infection

CD4+ Th1 IFNgamma secretion: activates macrophage!
CD8+ CTLs: killing cell infected w intracellular bacteria
CD4+ Th17 activation: IL17 secretion will recruit neutrophils, antimicrobial peptides

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antibody responses to extracellular bacteria

neutralization
osponization and Fc receptor mediated phagocytosis (BCR)
phagocytosis of C3b coated bacteria (complement)
inflammation (complement)
lysis of microbe (complement

ex: salmonella, staphylococcus aureus, Ecoli

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T cell response to extracellular bacteria

CD4+ helper cell releases:

IL17, TNF -> inflammation
IFNgamma -> macrophage activation = phagocytosis and bacteria killing
various cytokines -> antibody response

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synergistic antibacterial immune mechanisms

innate immunity: defensins, lysozymes, complement
antibody mediated immunity: antibodies
cell mediated immunity: T cells, activated macrophages

all these work together to kill bacteria

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immunity to intracellular bacteria

initially the innate immune system has neutrophils (IL17) and macrophages (TNFgamma) and NK cells come to site and control infection through cytokines -> macrophages release IL12 to activate NK and NK release IFN gamma

as infection time goes on the TCells and macrophages work in adaptive immunity - T cells bind macrophage/APC w CD40L and release IFNgamme to activate macrophages for eradication of infection!

ex: brucella abortus, mycobacterium, ehrlichia canis

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immunity to intracellular microbe

CTLs!
phagocytosed bacteria in vesicles and cytoplasm -> bind CD4+ Tcell which releases IFNgamma to activate macrophage to kill bacteria in phagolysosome and then CD8+ CTL will bind MHC1 + ag complex and kill the infected cell

ex: bacteria, virus, protozoa

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CTL lysis of infected cell

intracellular bacteria, virus, protozoa w MHC1/Th1 CD8+
infected cells degrade intracellular pathogen into peptides
peptides are loaded into MHC1 and presented to CTLs which release their perforins and granzymes
CTL induce apoptosis and/or lysis of target bad cell through creating pore for granzymes to enter (CD95)

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mechanisms of immune evasion by bacteria

immune pressure is what drives immune evasion
antigenic variation
inhibition of complement activation
resistance to phagocytosis
scavenging of ROS intermediates
resistance to complement/alternative pathway activation

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neisseria gonorrhoeae, E Coli, salmonella evade immune system by

antigenic variation

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many bacteria evade immune systems by

Inhibition of complement activation

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pneumococcus evade immune systems by

resistance to phagocytosis

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catalase + staphylococci evade immune systems by

scavenging of ROS intermediates

neisseria meningitides evade immune systems by

resistance to complement activation via sialic acid expression whihc inhibits C3 and C5 convertases

streptococcus evade immune systems by

resistnace to complement activation via M protein block C3 binding to organisms and C3b binding to complement receptors

mechanisms of immune evasion by bacteria

toxin production (LPS - cell destruction and shock)
disruption of phagosome membrane, escape into cytoplasm (listeria monocytogenes - hemolysin protein)
inactivation of ROS and NOS (mycobacterium leprae via phenolic glycolipid)
inhibition of phagolysosome formation (mycobacterium tuberculosis, legionella pneumophilia)
decrease MHC2 expression
super antigen production (S aureus toxin)
polysaccharide capsule (shield/shedding)

immune response against viruses

innate immunity

adaptive immunity

innate immunity response against virus

IFNalpha/beta (TYPE1 interferons - upregulate adenylate synthetase in macrophages)
NK cells
complement systems
natural antibodies
activated macrophages (IFNgamma)

adaptive immunity response against virus

virus specific antibodies & CTLs
neutralizaiton
opsonization
complement (classical)
ADCC NK cells

biological actions of IFNalpha/beta in innate immune response to virus

IFNa/b induces the expression of: adenylate synthetase in macrophages -> activates RNase L -> degrades viral RNA! inhibiting viral replication

NK cells adaptive immune response to virus

when inhibitory receptor engaged: NK cell NOT activated -> no cell killing when inhibitory receptor no longer engaged: NK cell ACTIVATED -> kill target bad cell! appear early in infections kill some viral infected cells and tumor cells secrete IFNgamma which activates macrophage!

adaptive immunity details for immune response against viruses

Bcell -> antibodies protect against infection ADCC (low aff FcgammaR3) on NK responds to IgG on antibody coated target cell and kills - granzymes, FasL, perforins CD8+ CTL binds infected cell and kills - eradication of established infeciton latency: integration into host genome - oncogenes lytic virus

antigenic variation evasion by virus

genetic recombination of differnet viruses among different organisms makes it harder to defend against influenza, HIV, rhinovirus

inhibition of antigen processing and presenting evasion by virus

MHC down regulation - escapes surveillance/presentation epitope mutation - antigenic variation/immune escape, reduced/failure of MHC loading blockade of TAP transporter - herpes removal of calss 1 from ER - cytomegalovirus

production of cytokine receptor homologs evasion by virus

vaccinia, poxviruses (IL1, IFNgamma), cytomegalovirus (chemokines)

prodcution of immunosuppressive cytokine evasion by virus

epstein barr (IL10)

infection of immunocompetent cells

HIV

Feline immunodeficiency virus evasion by virus

infects CD4+ T cells: -slow destruction of adaptive immunity -eventually allows other severe infections to develop and eventually lead to death diagnosis: presence of antiFIV antibodies via western blot, ELISA, IFA clinical symptoms: chronic inflammtion, infections, wgt loss and fever prevention: vaccination - no longer efficient

immune response against fungi

innate adaptive ex: tinea (ringworm)

ringworm details

common fungal skin infection in animals and humans failure of immune clearance leads to persistnet inflammation treatment w antifungal

innate immunity response to fungi

activated macrophages & neutrophils: utilize PRR-PAMPS: phagocytosis! PRR-PAMP interaction: inflammation, neutrophil recruitment (IL17) complement system: lectin and alternate pathway

adaptive immunity response to fungi

cell mediated clearance: CD4+ Th1 and Th17 activate macrophages and neutrophils injurious effect of immune response: granuloma and fivrosis (histoplasma capsulatum)

immune evasion by fungi

some fungal cells are too large to be phagocytosed express complement and ROS inhibitors - complex glycan coat/carbohydrates espcape from phagosome/alter phagolysosome: avoids destruction cryptococcus neoformans: inhibits TNF & IL12 production and stimulates IL10 production -> inflammation

immune response to helminths

cell mediated clearance | eosinophil degranulation releases

cell mediated clearance immune response to helminths

``` activated CD4+ th2 cells induce: -mucosal eosinophil and mast cells -IgE production helminths are vulnerable to: -ADCC involving eosinophils, neutrophils & macrophages ```

eosinophil degranulation releases immune response to helminths

``` major basic protein (MBP) eosinophil cationic protein (ECP) eosinophil peroxidase (EP) eosinophil neurotoxin (EN) phospholipase D lysophospholipase all these are toxic to helminths! ```