Immunity to Microbes Flashcards

1
Q

take home points

A
  • only those organisms who successfully evade the immune response are successful pathogens
  • primary adaptive immune response to bacteria is an antibody response. local is IgA and serum is IgG
  • in most cases the microorganism is actually destroyed in a phagocytic cell
  • only infected host cells are killed by CD8 cells
  • specific immunity acts to enhance the uptake of microorganisms by phagocytic cells or to enhance the activity of phagocytic cells
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2
Q

innate immunity

A

-numerous non-specific barriers to infection exist that limit the entry of, or in the aid of rapid clearance of microoganisms:
skin
pH barriers
flushing
lysozyme
phagocytes (with general receptors for bacteria-TLR)
-complement via alternate pathway (classical needs Ig)

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3
Q

virulence factors

A
  • ability to survive the acid environment of the stomach as demonstrated by Salmonella typhosa
  • production of spreading factors
  • production of toxins that inhibit or kill immune cells
  • the presence of an antiphagocytic capsule such as S pneumonia
  • proteins like staph aureus protein A which binds and blocks the opsonizing action of IgG
  • other antiphagocytic factors like M protein
  • some bacteria are not flushed from the resp tract or the digestive tract due to their ability to attach to the epithelium
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4
Q

primary immune defense against bacteria

A

-antibody

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5
Q

antibody

A
  • prevent attachment to epithelium, mediated by secreted IgA
  • trigger complement leading to increased opsonization or lysis
  • bind to antiphagocytic M proteins or capsules, preventing the antiphagocytic activity and acting as an opsonin
  • opsonized bacteria are not only taken up better but are also killed faster than are non-opsonized bacteria
  • neutralize toxins
  • neutralize spreading factors such as tissue damaging enzymes
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6
Q

facultative intracellular parasites

A
  • ability to survive within the phagosome
  • survive digestive enzymes of the phagolysosome or preventing the fusion of lysosomes with phagosomes
  • examples are M TB and listeria monocytogenes
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7
Q

activated macrophages

A
  • kill microorganisms much more efficiently
  • result of specific T cell response
  • TH1 helper repsonse
  • sometimes need CD8 cells to kill infected macrophage to release the stowed bacteria for activated macrophages to eat it
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8
Q

immunity to listeria

A
  • developed strain that will kill mice at high dose
  • low dose will induce immunity
  • these mice will be immune to the high dose of listeria
  • phagocytosed by macrophages but not killed
  • antibody increases the rate of phagocytosis but not the killing
  • macrophages from the site of infection are able to kill-they are activated macrophages
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9
Q

listeria cont

A
  • activated macrophages can kill many intracellular parasites (non-specific killing)
  • long term immunity is specific
  • immunity can be transferred from one animal to another will cells not serum
  • CELL MEDIATED
  • the cells that transfer specific immunity are CD4+ T cells
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10
Q

cell mediated immunity

A
  • specific immunity is a function of T cells
  • non specific killing is a function of activated macrophages
  • only live bacteria induced CMI, both live and dead produced antibody
  • mechanism of antigen presentation is important in what response occurs
  • TH1- cell TH2- antibody increases
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11
Q

two types of helper T cells

A
  • TH1 stimulate CMI
  • TH2 stimulate antibody production
  • the way the dendritic cells present can influence response
  • TH1 cells go to infected site to activate macrophages
  • TH2 cells go the lymphoid tissues to activate B cells
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12
Q

TH1

A
  • IL2, IFN gamma
  • macrophage activation
  • production of opsonizing antibodies
  • GM-CSF
  • TNF alpha
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13
Q

TH2

A
  • IL 4,5, 10, 13

- general activation of B cells to make antobodies

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14
Q

IFN gamma and CD40 ligand

A
  • kills intravesicular bacteria

- activates macrophages

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15
Q

Fas Ligand/LT

A

-kills chronically infected macrophages, releasing bacteria to be destroyed by healthy macrophages

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16
Q

IL2

A

-induces T cell proliferation

17
Q

IL3 and GM CSF

A

-induces macrophage differentiation in the bone marrow

18
Q

TNF a and LT

A

-activated endothelium to induce macrophage adhesion and exit from BV at site of infection

19
Q

CXCL2

A

-causes macrophages to accumulate at site of infection

20
Q

immune mechanisms involved in the clearance of parasites

A
  1. T cell response is important in clearance and control
  2. cytotoxic T cells are involved in limited manner-rarely kill parasites but may kill cells infected with the parasites
  3. T cells activate macrophages that kill many different parasites
  4. T cell dependent granulomata formation-interaction b/n activated macrophages that accumulate and release fibroblast growth factors-parasite walled off
  5. T cells produce factors that causes the infiltration and increased production of eosinophils-can kill worms
  6. T cells and B cells produce specific antibodies to parasite antigens
  7. parasites have escape mechanisms
21
Q

IgG and IgM

A
  • able to kill some blood borne parasites-plasmodium

- complement mediated

22
Q

antibodies and parasites

A
  • neutralize some parasites by blocking receptor specific uptake into cells
  • act as opsonin enhancing Fc and C3b mediated phagocytosis
  • IgE-helminths-mast cells kill worms
  • cellular toxicity from antibody can kill some organisms-macrophages, neutrophils, eosinophils and mast cells
23
Q

inaccessibility

A
  • parasites can hide inside the hosts cells
  • exist only in gut
  • form cysts
24
Q

avoidance of recognition

A
  • vary cell surface antigen expression

- pick up host antigen

25
Q

immunosuppresion

A

-t spiralis and leishmania can suppress host

26
Q

immunity to viruses

A
  • T cell mediated immunity important
  • antibody prevents infection
  • CTLs kill infected targets
  • NK cells stimulated by T cells
  • activated macrophages can kill infected cells
27
Q

antibody and virus

A
  • neutralizes virus
  • binding of antibody to a portion of virus required for absorption, penetration, uncoating or replication
  • steric hindrance
  • localized IgA important to resp, GU, GU tracts
  • in resp IgA is prime of antiviral
  • may also lyse virions
  • alone or with complement can increase rate of clearance by increasing rate of uptake by phagocytes
  • can prevent but not likely to kill
28
Q

CTLs and virus

A
  • not always virus strain specific
  • can immune against several strains of A with just one shot
  • uses MHC class I
29
Q

interferons

A
  • alert other cells to protect themselves
  • IFN a and b induce resistance to viral replication in all cells
  • increase MHC class I expression and antigen presentation in all cells
  • activate NK cells to kill virus infected cells