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Immunology > Innate Immunity > Flashcards

Innate Immunity Flashcards

1
Q

How does immediate innate immunity respond to infection?

A

Recognizes infection through pre-formed, non-specific and broadly specific effects

These remove infectious agents

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2
Q

How does early induced innate immunity respond to infection?

A

Recruits effector cells

Recognize infection by PAMPs then activating effector cells and inflammation

These remove infectious agents

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3
Q

How does adaptive immunity respond to infection?

A

Transport antigen to lymphoid organs

Recognition by naive B and T cells

Clonal expansion and differentiation of effector cells

Removal of infectious agents

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4
Q

Name 2 physical barriers to infection

A

Intact skin = when cut or burnt microbes can infect more easily

Mucus and cilia

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5
Q

What order are layers of the skin found?

A

Epidermis > dermis > hypodermis

From top to bottom layer

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6
Q

Role of mucus

A

Physical barrier to infection

Prevents pathogen colonization

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7
Q

What synthesizes and secretes mucus?

A

Goblet cells

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8
Q

What happens in cystic fibrosis?

A

Defective gene causes production of unusually thick and sticky mucus

Frequent lung infection because more difficult to get rid of pathogens so they colonize

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9
Q

Name chemical barriers to infection

A

Anti-microbial enzymes

Microbe-binding molecules

Acidic pH

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10
Q

Examples of anti-microbial enzymes

A

Phospholipase A2

Antimicrobial peptides

Lysozymes

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11
Q

Lysozyme mechanism of action?

A

Cleaves peptidoglycan bonds in bacterial cell walls

Cell wall is needed for bacteria to survive

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12
Q

Phospholipase A2 mechanism of action?

A

Enzyme able to insert into bacterial membrane and break it

The outside components can enter the cell = causing cell to burst

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13
Q

Name a microbe-binding molecule and its mechanism of action

A

Pulmonary surfactant = produced by alveolar type II cells

Binds to pathogen but is NON-specific

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14
Q

Antimicrobial peptides’ mechanism of action against virus?

A

Hindering virus attachment and virus-cell membrane fusion

Disrupting virus envelope

Inhibition of virus replication by interacting with viral polymerase

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15
Q

Name 3 anti-microbial peptides

A

Defensins

Cathlicidins

Histatins

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16
Q

What are the two defensin classes?

A

Alpha

Beta

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17
Q

Defensin mechanism of action?

A

One end positively charged other negatively

Bacterial cell membrane = negative so positive end of defensin is attracted and inserts itself

Then negative ends are hydrophobic so cluster together pulling membrane apart

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18
Q

Defensin functions in the body

A

Maintian a healthy gut= balancing gut microbiota

Modulate inflammation

Attract immune cells to site of infection

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19
Q

Cathelicidins action against microbes?

A

Damage microbial membrane

Inhibit bacterial DNA and protein synthesis

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20
Q

What are Histatins?

A

Anti-microbial peptides

Small and cationic

Hisitidine-rich peptides in human saliva

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21
Q

What microbe do histains fight against?

A

Anti-fungal activity

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22
Q

What feature does the microbiome demonstrate?

A

Competitive exclusion = microbiome occupies our body surface so that the pathogen find it hard to colonize

Compete for resources and space

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23
Q

What does clostridium difficile infection do to the body?

A

Diarrhea

Colitis = an inflammation of the colon)

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24
Q

What compounds does the microbiome produce?

A

Compounds toxic to pathogenic bacteria

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25
Q

What does the microbiome help mature?

A

Need microbiome when mucosal structure and immunity is not fully developed or established

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26
Q

Where are paneth cells found and what is their function?

A

Highly specialized secretory epithelial cells

Located in the small intestinal crypts of Lieberkühn.

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27
Q

What do paneth cells do?

A

Highly specialized secretory epithelial cells = secrete antimicrobial peptides

Located in the small intestinal crypts of Lieberkühn.

28
Q

Where are M cells found?

A

Found overlying GALT lymphoid follicles, such as Peyer’s patches in the ileum

29
Q

What do M cells do?

A

Microfold cells sample antigens

Clathrin-coated endocytic vesicles for larger antigens

Or via fluid phase pinocytosis for smaller antigens

30
Q

What is the structure of an M cell?

A

Short microvilli or none

Allows antigens to come in close proximity to apical surface

Basolateral invagination allows for positioning of APCs and lymphocytes = close to lumen

31
Q

M cells and antigen interaction?

A

M cells acquire antigens through apical surface

Antigens pass through M cells via vesicular transport to basolateral membrane

They are released from basolateral membrane

APCs uptake antigens and process them for presentation to T cells and other lymphocytes

32
Q

What do absorptive endothelial progenitor cells do?

A

Secrete cytokines

33
Q

What is the role of tight junctions?

A

Blocks movement of bacteria and PAMPs into lamina propria

34
Q

What are germ-line encoded?

A

Pattern Recognition Receptors?

35
Q

What does germ-line encoded mean?

A

Means that the information for PRRs is inherited = they have an innate ability to recognize certain patterns in pathogens

36
Q

What is required for adaptive immunity activation?

A

Activation of innate immunity

37
Q

Name 5 PRRs

A

Toll-like receptors
NOD-like receptors
RIG-I-like receptors
Mannose receptors
Phagocytic receptors

38
Q

How many TLRs are there in humans vs mice?

A

10 in humans and 12 in mice

39
Q

What is the ligand of TLR-3?

A

dsRNA

40
Q

What is the ligand of TLR-4?

A

Lipopolysaccharide

41
Q

What is lipopolysaaccharide?

A

Cell-wall component of gram-negative bacteria = sensed by TLR4

42
Q

What is the ligand of TLR-5?

A

Flagellin

43
Q

What is the ligand of TLR-7 and TLR-8?

A

ssRNA

44
Q

What is the ligand of TLR-9?

A

CpG-ODN

45
Q

What is CpG-ODN?

A

C linked to D oligodeoxynucleotides = single strand

46
Q

Where are TLRs found?

A

Both on the cell membrane and in the endosome

47
Q

What is the structure of TLRs?

A

Leucine rich repeat motif
Cysteine rich flanking motif
TIR domain

48
Q

What part of the TLR sites in the cytoplasm?

A

TIR domain = tail

49
Q

What is the TLR4 signalling pathway to activate gene expression of IL-6, TNFalpha etc?

A

When LPS is bound the receptor will dimerize
TIR domains are brought together = activating the domain
TIR domains recruits MyD88 = no enzyme activity
IRAK1/4 binds MyD88 at Death domain
IRAK1/4 go to activate MAPK and NFkB

50
Q

What is the TLR4 signalling pathway to activate IFN-beta gene expression

A

When LPS is bound, the receptors will dimerize
TIR domains are brought together = activatingthe domain
TIR domains recruits TRIF
TRIF activates both kinases = IKK and TBK1
Which then activate IRF3 and NFkB

51
Q

What two domains does MyD88 have?

A

TIR and Death domains

TIR binds to TLR4s TIR domain

52
Q

Where are NOD-like receptors expressed?

A

Cytoplasm because they detect intracellular bacteria

53
Q

What form are NOD proteins found in?

A

Inactive form

54
Q

What is the structure of NOD-like receptors?

A

LRR
NOD
CARD

55
Q

What are the differences between NOD1 & NOD2?

A

NOD1 has 1 CARD domain but NOD2 has 2
NOD

NOD1 activation triggered by iE-DAP in gram-negative bacteria

NOD2 activation triggered by MDP in both gram-positive and -negative bacteria.

56
Q

What does NLR activation ultimately lead to?

A

Nuclear Factor kappa B (NFkB) activation by removing the inhibitor (IkB)

57
Q

What happens when bacterial ligand binds to NOD protein?

A

Either iE-DAP or MDP binds
RIPK2 recruited and binds the CARD domain
TAK is phosphorylated by RIPK2
TAK is activated and then phosphorylates IKK
IKK phosphorylates IkB leading to its ubiquitination and subsequent degradation by the proteasome
NFkB is free to act as a transcription factor

58
Q

Where are NOD2 strongly expressed?

A

In Paneth cells found in the small intestine

59
Q

What does NOD2 induce?

A

Alpha-defensin expression

60
Q

What mutation can cause Crohn’s disease?

A

Loss of function mutation in NOD2 = less anti-microbial production

More bacterial growth causing chronic gut inflammation

61
Q

What mutation can cause Blau syndrome?

A

Gain of function mutation in NOD2 = activates signalling in absences of infection

Spontaneous inflammation in joints, eyes and skin

62
Q

Where are RIG-I-like receptors found and why?

A

Expressed in cytoplasm because important to detect viral infection

63
Q

What are the two types of RIG-I-like receptors?

A

RIG-I and MDA-5

64
Q

What do the two RLRs recognize?

A
  1. RIG-I = unmodified 5’-tiphosphate end of ssRNA
  2. MDA – 5 = recognize dsRNA
65
Q

What is the structure of RIG-I-like Receptors?

A

Repressor Domain
Helicase
CARD

Immunology (8 decks)

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