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Pathology > Immunity > Flashcards

Immunity Flashcards

1
Q

Balance of power

A

host (humans) has a generation time of 20 years
Pathogen has a generation time of minutes to days

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2
Q

host defence mechanisms (3)

A

immune system
physical and chemical barriers (skin, mucosal surface, gastric acid)
behaviour adaptation

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3
Q

Microbiome (symbiotic microorganisms) (3)

A
  1. occupy microenvironmental niches (if they weren’t there pathogens would move in)
  2. mutually beneficial and prevent disease
  3. healthy flora can grow out of control and become pathogenic
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4
Q

Three major arms of the immune response

A

innate immunity
adaptive immunity
effector mechanisms

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5
Q

what is innate immunity

A

always present allows time for adaptive immunity to kick in

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6
Q

things that innate immunity do

A
  1. recognize microbes and damaged cells
  2. activate mechanism
  3. eliminate unwanted substances
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7
Q

what does innate immunity not do

A
  1. does not have memory
  2. does not have specificity
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8
Q

components of innate immunity

A
  1. epithelial barriers
  2. phagocytes
  3. dendritic cells
  4. natural killer cells
  5. plasma proteins (complement)
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9
Q

function of epithelial barriers in the innate response

A
  1. provide mechanical barriers entry of microbes
  2. produce antimicrobial molecules (defensives and lymphocytes)
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10
Q

function of phagocytes in the innate immune response

A

sense ingest and destroy invading agents (inflammation) eat them

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11
Q

function of dendritic cells in the innate response

A

capture antigens and present to the T lymphocytes
production of cytokines
eyes that initiate army

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12
Q

function of natural killer cells in the innate response

A

first line defence in infects virus and tumour cells
do not require exposure/ activation by microorganism

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13
Q

What are natural killer cells

A

specialized lymphocytes
have abundant granules

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14
Q

Perforin NK cells

A

Poke holes in the the membrane of a microbe

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15
Q

granzyme NK cells

A

send protease enzymes in a microbe to kill it

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16
Q

function of mast cells in the innate response

A
  1. release histamine in vessels and smooth muscle that allows fluids to move between them
  2. release cytokines
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17
Q

reactions in innate immune system

A
  1. inflammation
  2. antiviral defence (antiviral state)
  3. danger signals (cytokines) to alert more aggressive immune cells
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18
Q

what is the antiviral defence of innate immunity

A

inhibit viral infection
acts on infects and uninflected cells
expression of antiviral genes to degrade viral RNA/ DNA

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19
Q

type 1 interferons

A

INFalpha and INFbeta mediates antiviral defence by
1. increase cytotoxicity and proliferation of nK cells
2. activation of T cells
3. increase antigen presentation in myeloid dendritic cells
4. stimulation of Ig production in B cells

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20
Q

what does adaptive immunity do

A

protection from infection through B and T lymphocytes following exposure to specific antigens
smarter and longer lasting then innate

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21
Q

humeral immunity

A

associated with circulatory system, antibodies = immunoglobulins

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22
Q

cellular immunity

A

part of adaptive immunity, action of T cells

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23
Q

why do B and T cells circulate In the blood and lymphatic system

A

to promote surveillance

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24
Q

why are lymphocytes anatomically segregated

A

so that they do not activate each other when not needed

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25
Q

naive lymphocytes

A

have not encountered antigen for which they are specific

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26
Q

what are effector cells

A

T lymphocyte that has been activated by dendritic cells to kill microbes

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27
Q

what are memory cells

A

live in tightened state of awareness, react rapidly and strongly to combat microbes in case it returns

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28
Q

B lymphocytes

A

kill microbes through phagocytosis
complementary activation

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29
Q

helper T lymphocytes

A

activation of macrophages
inflammation response
activation of T and B cells

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30
Q

cytotoxic T cells

A

kill infected cells

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31
Q

regulatory T cells

A

shut down the immune response

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32
Q

what is lymphocyte diversity

A

specific lymphocytes exists before exposure to antigen, when antigen enters in selects for replication of that lymphocyte

33
Q

what causes antigen receptor diversity and how does it work

A

somatic recombination of genes that encode receptors. lymphocyte maturation gene segments recombine in random sets making different receptors

34
Q

types of regions on antigen receptors

A
  1. variable region (antigen binding) susceptible to recombination
  2. constant region
35
Q

T lymphocytes

A

60-70% of circulating lymphocytes
Helper, cytotoxic and regulatory

36
Q

MHC restriction

A

T cell antigen specific TCR only recognizes antigens presented by major histocompatibility complex (MHC)

37
Q

purpose of MHC

A

ensures that T cells see only cell-associated antigens

38
Q

B lymphocytes

A

10-20% of circulating lymphocytes. only cells in the body capable of producing antibody

39
Q

how do B cells recognize antigens

A

B-cell antigen receptor complex – includes
membrane bound antibodies present on all mature native B cells

40
Q

which B cells produce antibodies and when

A

plasma cells after stimulation by helper T cell or antigen

41
Q

Effector mechanisms

A

complement systems
Antibodies

42
Q

components of the compliment system

A

more than 30 components
- activating molecules
- regulatory factors
- complement receptors
- membrane proteins which inhibit lysis of host cells

43
Q

where are components of the complement system produced

A

most produced in the liver as zymogens
- present in inactive forms in the plasma → activation required → proteolytic
enzymes → degrade other complement proteins → enzymatic cascade capable of
amplification

44
Q

critical step in complement activation

A

proteolysis of C3

45
Q

three pathways of Cleavage of C3

A

alternative
classical
lectin

46
Q

alternative pathway of Cleavage of C3

A

Triggered by microbial surface molecules absence of antibody

47
Q

classical pathway of Cleavage of C3

A

Triggered by fixation of C1 to antibody combined with antigen

48
Q

lectin pathway of Cleavage of C3

A

Triggered by binding of lectin to
carbohydrates on microbes → direct
activation of C1

49
Q

C3 convertase what it is and what it does

A

from all three pathways of C3 Cleavage
splits C3 into two functionally distinct
fragments, C3a and C3b.

50
Q

functions of the complement system

A

Ca recruit leukocytes for inflammation
Cb enhance phagocytes
MAC lysis microbes

51
Q

function of antibodies

A

neutralize pathogens
actiavte complement opsonize pathogents to enhance phagocytosis

52
Q

Staphylococcus aureus

A

gram-positive extracellular bacterium. part of our commensal flora

53
Q

Herpes Simplex Virus

A

→ a complex DNA virus, which successfully
disrupts intracellular mechanisms of viral control

54
Q

HIV

A

a small RNA virus, which turns the immune system on itself
and subvert the immune response over a period of years to decades

55
Q

three critical elements of
the innate immune response S. aureus subverts

A

(1) recruitment and actions of inflammatory cells
(2) complement activation
(3) antimicrobial mechanisms

56
Q

how does S. aureus subverts recruitment and actions of inflammatory cells (4)

A

1) staphylococcal protein - blocks P-selectin interaction
2) binds to ICAM-1 & interferes with extravasation of neutrophils
3) proteins bind chemokine receptors and block their activation
4) S.A. secreted enzyme cleaves and inactivates chemokine receptors

57
Q

Why does MAC not work of S. aureus

A

S. aureus it gram positive which is NOT compatible with S. aureus

58
Q

how does S. aureus inhibit phagocytosis (2)

A

1) protein A prevent recognition by neutrophil
2) clumping factor A complicates recognition

59
Q

how does protein A work

A

wall anchored protein binds incorrectly to IgG

60
Q

how does clumping factor A work

A

binds to fibrinogen, coats surface of bacterium

61
Q

Aureolysin in inhibition of complement sequence S. aureus

A

cleaves and inactivated C3 to prevent tagging of S. aureus

62
Q

Staphylokinase in inhibition of complement sequence S. aureus

A

cleaves surface-bound
C3b by converts host
plasminogen attached to bacterial wall
to plasmin

63
Q

Staphylococcus complement inhibitor

A

stabilizes bound C3
convertases and renders them less active to prevent cleavage

64
Q

how does S. aureus avoid NETS

A

Secreted staphylococcal nuclease enzymatically destroys
neutrophil NETs

65
Q

Neutrophil extracellular traps (NETs)

A

processed chromatin bound to granular and selected cytoplasmic proteins spiderman

66
Q

Aureolysin and Staphylokinase post phagocytosis of S. aureus

A

inactivate antimicrobial peptides (defensin)

67
Q

what inihibts ROS after S. aureus nis eaten

A
  • two superoxide dismutase enzymes
68
Q

what does modifications to the cell wall post phagocytosis of S. aureus accomplish

A

reduces activity of lysosomal enzymes

69
Q

what is Staphylococcal Toxins and Superantigens and what does it look like

A

secretion of cytolytic toxins (hemolysins) → damage of host cell membranes → the development of abscesses by direct killing of neutrophils

70
Q

what is Toxic shock syndrome

A

one of the most serious, life-threatening infections with S.
aureus → exaggerated host immune response → multisystemic

71
Q

how does toxic shock syndrome develop

A

superantigens → stimulate T cells non-specifically without normal antigenic recognition → proliferation of T-cells and a massive release of cytokines → systemic cytokine storm → extravasation of
plasma and protein → decreased blood volume, low blood pressure (shock).

72
Q

how does toxic shock syndrome kill

A

Activation of the coagulation cascade (lack of blood flow) multiorgan failure

73
Q

whats is HSV

A

Herpes simplex virus large DNA genome

74
Q

stages of HSV

A
  1. Site of entry
  2. acute: virus replicate at the site of entry
  3. latent spreads to sensory neurons innervating these sites
  4. reactivation: from neurons back to skin/mucous membrane
75
Q

TLR cascade

A

activation of TLR through incoming viral nucleic acids
NFKB
Cytokines INFs, then both
activation of immune system –> macrophages NK dendritic cells
Viral destruction DNases Proteases

76
Q

how does HSV prevent host response

A

Viral proteins that
1) degrade host mRNA (dampen INF)
2) block NFKB
3) block caspases for apoptosis

77
Q

what is HIV reverse transcriptase

A

convert RNA genome in
chromosomally integrated proviral DNA

78
Q

HIV – retrovirus

A

simple and small virus: 5 proteins + RNA

79
Q
A

Pathology (14 decks)

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