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IMMUNOLOGY VDMP817 > lecture 7 exam 2 > Flashcards

lecture 7 exam 2 Flashcards

1
Q

major physiologic functions will

A

protect the host against microbial infections

bacteria, viruses, parasites, yeast

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2
Q

major physiology immune response to pathogens are

A

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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3
Q

responses to bacterial infection

A

innate

adaptive: Bcell/NK cell
adaptive: Tcell

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4
Q

innate immunity response to bacterial infectoin

A

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

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5
Q

adaptive Bcell/NK cell immunity response to bacterial infection

A

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

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6
Q

adaptive Tcell immunity response to bacterial infection

A

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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7
Q

antibody responses to extracellular bacteria

A

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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8
Q

T cell response to extracellular bacteria

A

CD4+ helper cell releases:

  • IL17, TNF -> inflammation
  • IFNgamma -> macrophage activation = phagocytosis and bacteria killing
  • various cytokines -> antibody response
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9
Q

synergistic antibacterial immune mechanisms

A

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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10
Q

immunity to intracellular bacteria

A

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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11
Q

immunity to intracellular microbe

A

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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12
Q

CTL lysis of infected cell

A

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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13
Q

mechanisms of immune evasion by bacteria

A

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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14
Q

neisseria gonorrhoeae, E Coli, salmonella evade immune system by

A

antigenic variation

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15
Q

many bacteria evade immune systems by

A

Inhibition of complement activation

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16
Q

pneumococcus evade immune systems by

A

resistance to phagocytosis

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17
Q

catalase + staphylococci evade immune systems by

A

scavenging of ROS intermediates

18
Q

neisseria meningitides evade immune systems by

A

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

19
Q

streptococcus evade immune systems by

A

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

20
Q

mechanisms of immune evasion by bacteria

A

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)

21
Q

immune response against viruses

A

innate immunity

adaptive immunity

22
Q

innate immunity response against virus

A 
IFNalpha/beta (TYPE1 interferons - upregulate adenylate synthetase in macrophages)
NK cells
complement systems
natural antibodies
activated macrophages (IFNgamma)
23
Q

adaptive immunity response against virus

A 
virus specific antibodies & CTLs
neutralizaiton
opsonization
complement (classical)
ADCC NK cells
24
Q

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

A

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

25
Q

NK cells adaptive immune response to virus

A

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!

26
Q

adaptive immunity details for immune response against viruses

A

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

27
Q

antigenic variation evasion by virus

A

genetic recombination of differnet viruses among different organisms makes it harder to defend against

influenza, HIV, rhinovirus

28
Q

inhibition of antigen processing and presenting evasion by virus

A

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

29
Q

production of cytokine receptor homologs evasion by virus

A

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

30
Q

prodcution of immunosuppressive cytokine evasion by virus

A

epstein barr (IL10)

31
Q

infection of immunocompetent cells

A

HIV

32
Q

Feline immunodeficiency virus evasion by virus

A

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

33
Q

immune response against fungi

A

innate
adaptive

ex: tinea (ringworm)

34
Q

ringworm details

A

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

35
Q

innate immunity response to fungi

A

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

36
Q

adaptive immunity response to fungi

A

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

37
Q

immune evasion by fungi

A

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

38
Q

immune response to helminths

A

cell mediated clearance

eosinophil degranulation releases

39
Q

cell mediated clearance immune response to helminths

A 
activated CD4+ th2 cells induce:
-mucosal eosinophil and mast cells
-IgE production
helminths are vulnerable to:
-ADCC involving eosinophils, neutrophils & macrophages
40
Q

eosinophil degranulation releases immune response to helminths

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

IMMUNOLOGY VDMP817 (22 decks)

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