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BDS2 PMI > PMI02-2003 > Flashcards

PMI02-2003 Flashcards

1
Q

What organisms have innate immunity?

A

Plants

Vertebrates and invertebrates

Fungi

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2
Q

What innate barriers are in place to prevent adherence?

A

Normal flora (commensals)

Local chemical factors

Phagocytes (esp in lungs)

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3
Q

What innate responses are triggered when the epithelium is breached?

A

Wound healing

AMPs

Phagocytes

Complement

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4
Q

What innate cells/substances are involved when there is local infection of tissues?

A

Complement

Cytokines and chemokines

Phagocytes

NK cells, macrophages

Dendritic cells

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5
Q

Where is mucosal epithelia found?

A

Lining externally exposed body cavities

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6
Q

What do most mucosal epithelia secrete and what is the importance of this?

A

Mucus

Harder for microbes to adhere and it helps to remove microbes/debris

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7
Q

What cells produce alpha-defensins?

A

Neutrophils

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8
Q

What cells produce beta-defensins?

A

Epithelial cells

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9
Q

Give examples of antibacterial peptides.

A

Defensins

S100As

Cathepsins

Cryptidins

Phospholipase A

Lactoferrin

Histatin

Lysozyme

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10
Q

What is lactoferrin?

A

Scavenger protein for iron

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11
Q

How large are antibacterial peptides and which cells usually produce them?

A

20-60 amino acids long

Secreted by epithelial cells naturally

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12
Q

What is the complement cascade?

A

Collection of proteins in serum and tissue fluid which detect microbes and generate responses

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13
Q

What are the three methods of activation of the complement cascade?

A

Classical pathway

Mannose-binding lectin pathway

Alternative pathway

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14
Q

Describe the classical pathway of complement activation.

A
  1. Non-specific or specific antibodies bind to antigen on pathogen surface
  2. C1 proteins associate and bind to antibody
  3. Activated C1s cleaves C4
  4. C4b binds to pathogen surface and associates with C1 proteins
  5. C4b binds C2 so C1s can cleave C2 = C4b2b complex formed
  6. C4b2b cleaves C3 many times. C3b may bind to C4b2b or directly to pathogen
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15
Q

What is required to initiate the classical pathway and how does it do this?

A

C1q

Interacts with bound antibody at the Fc portion (or less likely binds directly to pathogen)

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16
Q

What do lectins bind to?

A

Carbohydrates

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17
Q

What is mannose?

A

Major component of microbial cell walls, especially fungal

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18
Q

Which other activation pathway is the mannose-binding lectin pathway most similar to? How does it differ?

A

Classical pathway

But activated by mannose-binding lectin which has a similar role to C1s (C4 cleavage)

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19
Q

What initiates the alternative pathway?

A

Spontaneous cleavage of C3 (hydrolysis)

20
Q

Describe the alternative pathway.

A
  1. C3 undergoes spontaneous hydrolysis to form C3(H20) which binds to factor B
  2. This binding allows factor D to cleave factor B to create C3b(H20)Bb complex
  3. C3b(H20)Bb cleaves C3
21
Q

What do all three complement activation pathways result in the formation of?

A

C3b

22
Q

What roles does C3b have?

A

C5 convertase –> MAC and anaphylatoxin formation

Binds directly to pathogen surface –> opsonisation

23
Q

What are the three outcomes of the complement cascade?

A

Recruitment of inflammatory cells and increased vascular permeability

Opsonisation

MAC/killing of microbe

24
Q

What are anaphylatoxins and what do they do?

A

“a” molecules following cleavage of complement proteins, trigger inflammation

Increase vascular permeability by acting on endothelial cells –> allows extravasation of immunoglobulin and more complement

Chemoattractant to macrophages, PMNs, leukocytes

25
Q

What is opsonisation and why is it important?

A

Flagging microbes to aid phagocytosis

Many microbes have evolved coats/capsules (carbohydrate mainly) to evade phagocytosis/recognition

26
Q

What complement molecules are involved in the membrane attack complex?

A

C5b

C6, C7, C8, C9

27
Q

Describe the formation of the MAC.

A
  1. C5b associated with C6 and C7 = C5b67
  2. C5b67 binds membrane via C7
  3. C8 binds complex and inserts into cell membrane
  4. 1 - 16 C9 molecules bind to complex at C8 and polymerise to form a pore in the membrane
28
Q

How big is a MAC?

A

~15nm high and 10nm in width

29
Q

Which lymphoid cell is involved in innate immunity?

A

NK cell

30
Q

What is the most common myeloid innate immune cell?

A

Neutrophil/polymorphonuclear leukocyte

31
Q

What are PRRs?

A

Pathogen recognition receptors

Recognise pathogen-associated molecular patterns (PAMPs)

32
Q

Give examples of PAMPs.

A

C/G-rich DNA

Double-stranded RNA

Oligosaccharides

Lipoproteins

33
Q

Give three examples of PRRs.

A

Toll-like receptors

C-type lectin receptors

NOD-like receptors

34
Q

What does recognition of a pathogen typically lead to?

A

Phagocytosis

Secretion of inflammatory mediators and cytokines

35
Q

Which cell links the innate and adaptive immunity?

A

Dendritic cells

36
Q

What is a cytokine?

A

Small glycoprotein (~17kDa)

37
Q

Give examples of pro-inflammatory cytokines.

A

IL-1α

IL-1β

TNF-α

Interferon-γ

38
Q

What are the functions of pro-inflammatory cytokines?

A

Induce many of the effects associated with inflammation, including:

Macrophage activation

Stimulate inflammatory mediator release

Activate adaptive immunity

Trigger pyrexia

39
Q

Give examples of anti-inflammatory cytokines.

A

IL-4

TGF-β

40
Q

What are the functions of anti-inflammatory cytokines?

A

Antagonistic to pro-inflammatory cytokines

Mediate adaptive humoral immunity response

41
Q

What are growth factors and colony stimulating factors important for?

A

Immune cell development and increasing secretions

42
Q

What cell changes are growth factors responsible for?

A

Cell growth

43
Q

What cell changes are colony stimulating factors responsible for?

A

Differentiation

44
Q

What are the functions of chemokines?

A

Attract/recruit immune cells to site of inflammation/infection

45
Q

Which receptors do mucosal chemokines commonly act through?

A

CCR6 receptors

46
Q

When are type 1 interferons produced and why?

A

Produced by all cells in response to viral infection to render surrounding cells non-permissive to infection (quiescence)

Also trigger inflammation for removal of infected cells

BDS2 PMI (21 decks)

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