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Immunology > Chapter Two > Flashcards

Chapter Two Flashcards

1
Q

What is the response to an initial infection?

A

innate immune cells become activated by pattern recognition receptors (PRRs) that detect molecules called pathogen-associated molecular patterns (PAMPs)

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2
Q

What are the 5 agents that cause disease?

A
  1. viruses 2. bacteria 3. fungi 4. protozoa 5. helminths (worms): 4 & 5 = parasitology 1-3 = microbiology
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3
Q

What are the characteristic features of each pathogen that must be considered?

A
  1. mode of transmission 2. mechanism of replication 3. mechanism of pathogenesis - the means by which its causes disease & the response it elicits from the host
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4
Q

What are the extracellular sites of infection?

A

interstitial spaces, blood, lymph, epithelial surfaces

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5
Q

What are the intracellular sites of infection?

A

cytoplasmic, vesicular

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6
Q

What is the problem if a extracellular pathogen has a polysaccharide capsule?

A

allows them to resist englufment but this can be overcome by the complement system

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7
Q

How does the body fight extracellular infection?

A

complement, phagocytosis, antibodies, antimicrobial peptides, IgA

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8
Q

How does the body fight intracellular infection?

A

NK cells, cytotoxic T cells, T cell & NK cell dependent macrophage activation

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9
Q

What are the direct mechanisms of tissue damage by pathogens?

A

exotoxin production, endotoxic, direct cytopathic effect

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10
Q

What are the indirect mechanism of tissue damage by pathogens?

A

immune complexes, anti-host antibody, cell-mediated immunity

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11
Q

What is the body’s first barrier against infection?

A

epithelial surfaces - prevent pathogens from crossing epithelia & colonizing tissues

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12
Q

What are B-defensins & cathelicidins?

A

differentiated keratinocytes in the stratum spinosum which are incorporated into secretory organelle called lamellar bodies - a form of specialized physical and chem barrier that provides innate defense in different locations

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13
Q

What does the ciliated respiratory epithelium do?

A

propels the overlying mucus layer for clearance of environmental microbes

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14
Q

What are lysozymes?

A

produced by Paneth cells in the gut , specialized epithelial cells in the base of crypts in the small intestine that secrete many antimicrobial proteins into the gut

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15
Q

What is phospholipase A2?

A

produced by Paneth cells in the gut, a highly basic enzyme that can enter the bac cell wall to access & hydrolyze phospholipids in the cell membrane, killing the bac

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16
Q

What is peptidoglycan?

A

antimicrobial protein that is an alternating polymer of N-acetylglucosamine (GlcNAc) & N-acetylmuramic acid (MurNAc) strengthened by cross linking peptide bridges

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17
Q

What are some antibacterial enzymes?

A

lysozyme & A2 - secreted in tears & saliva & by phagocytes

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18
Q

What is lysozyme & what does it do?

A

glycosidase that breaks a specific chemical bond in the peptidoglycan component of bac cell wall

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19
Q

What are the 3 classes of antimicrobial peptides in mammals?

A
  1. defensins 2. cathelicidins, 3. histatins are all secreted by epithelial cells & phagocytes
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20
Q

What are defensins?

A

small cysteine-rich cationic proteins found in both vertebrates & invertebrates that are amphipathic & disrupt the cell membranes of microbes

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21
Q

How are defensins, cathelicidins, and RegIII proteins activated?

A

proteolysis

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22
Q

What are histains?

A

antimicrobial proteins produced in oral cavity by parotid, sublingual, & submandibular glands. short, histidine-rich, cationic peptides are active against pathogenic fungi

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23
Q

What do RegII proteins contain?

A

C-type lectin domain (CTLD) aka carbohydrate-recognition domain (CRD)

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24
Q

What does LPS (lipopolysaccharide) block?

A

pore forming activity of RegIII alpha -> explains selective bactericidal activity against gram positive but not gram negative bacteria

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25
Q

What is the complement system?

A

collection of soluble proteins (30) present in blood & other blood fluids mainly produced by the liver

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26
Q

What is opsonization?

A

part of the complement systems - coating a pathogen w/ antibodies and/or complement proteins

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27
Q

Does the complement system need antibodies to work?

A

no

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28
Q

What do complement proteins do when there is no infection?

A

circulate in inactive form only become activated in present of pathogens or antibody bound to pathogens

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29
Q

What is the goal of the complement system?

A

“kill” pathogen directly or facilitating its phagocytosis & induces inflammatory responses that help to fight infection

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30
Q

What are the 3 complement system pathways?

A
  1. classical 2. alternative 3. lectin
31
Q

What is characteristic of the classical pathway?

A

antibody-triggered & discovered first

32
Q

What is characteristic of the alternative pathway?

A

can be activated by the presence of the pathogen alone

33
Q

What is characteristic of the lectin pathway?

A

most recently discovered. activated by lectin-type proteins that recognize carbs. uses soluble receptors that recognize microbial surfaces to activate the complement cascade

34
Q

What are the phases of the complement system?

A
  1. pattern recognition trigger 2. protease cascade amplification/C3 convertase 3. inflammation 4. phagocytosis 5. membrane attack
35
Q

What is the sequence of functional protein classes in the complement system?

A

C1, C4, C2, C3, C5, C6, C7, C8, C9

36
Q

How are cleaved proteins named?

A

a = smaller fragment b= larger fragment (C2 only exception)

37
Q

What are C1q, C1r, & C1s?

A

not cleavage products of C1 but are distinct proteins that together comprise C1

38
Q

What is different about naming proteins in the alternative pathway?

A

designated by different capital letters: factor B & factor D. also have addition of a & b for large and small fragment

39
Q

What does C3b do?

A

recognizes features of microbial surfaces & acts as opsonin; marks them for destruction allowing phagocytes that carry receptors for complement to take up and destroy the C3b-coated microbe. can also bind to C3 convertases & form C5 convertase

40
Q

Why is C3 convertase important?

A

activation of C3 for covalent bonding to microbial surfaces by cleaving it into C3a & C3b & exposing a highly reactive thioester bond in C3b

41
Q

What is C3b degraded into? How does this happen?

A

degraded by a serum protease into inactive smaller fragments called C3f and C3dg

42
Q

What is the role of C5 convertase?

A

C5a & C5b: peptide mediators of inflammation, membrane-attack proteins (MAC complex)

43
Q

What do microorganisms have on their surface?

A

repeating patterns of molecular structures known as pathogen-associated molecular patterns (PAMPs)

44
Q

What is true about the carbohydrate side chains on yeast & vertebrate glycoproteins?

A

terminated w/ different patterns of sugars

45
Q

What does MBL & ficolins do?

A

form complexes w/ serine proteases & recognize particular carbohydrates on microbial surfaces

46
Q

What is mannose-binding lectin (MBL)?

A

oligomeric protein built up from monomer that contains an amino-terminal collagen-like domain & carboxy-terminal C-type lectin domain (collectin). synthesized in the liver

47
Q

What are ficolins? (Fi+Col+Lin)

A

group of oligomeric lectin w? subunits consisting of both: 1. collagen like long thin stretches 2. fibrinogen like globular domain w/ lectin activity usually specific of N-acetylgucosamine

48
Q

What is C3 convertase in the lectin pathway?

A

C4b2a

49
Q

How is the classical pathway initiated?

A

activation of C1 complex & is homologous to lectin pathway

50
Q

What is C1/C1 complex? Why is it important?

A

pathogen sensor that interacts directly w/ some pathogens but can also interact w/ antibodies: allows classical pathway to function both in innate immunity & adaptive immunity

51
Q

Describe the makeup of the C1 complex.

A

C1q is larger subunit = pathogen sensor. C1r & C1s = serine proteases

52
Q

What does activated C1s act on in the classical pathway?

A

C4 and C2 (then C3)

53
Q

What is C3 convertase in the classical pathway?

A

C4b2a

54
Q

How does C1q attach to the surface of pathogens?

A
  1. binding directly to cell walls & polyanionic structures (e.g. lipteichoic acid on gram-positive bac) 2. binding to C-reactive protein (CRP)
55
Q

What is C-reactive protein (CRP)?

A

acute phase protein in human plasma that binds to phosphocholine residues in bac surface molecules

56
Q

What is the main function of C1q?

A

bind to constant (Fc) regions of antibodies that have bound pathogens via their antigen-binding sites: links effector functions of complement to recognition provided by adaptive immunity

57
Q

How does the alternative pathway work?

A

amplification loop for C3b formation that is accelerated by properdin in the presence of pathogens

58
Q

What are the 2 ways the alternative pathway can be activated?

A
  1. C3b binds factor B 2.spontaneous hydrolysis (‘tickover’) of thioester bond in C3 to form C3(H2O)
59
Q

What kind of bond is in C3?

A

thioester

60
Q

What is the C3 converstase in the alternative pathway?

A

C3bBb

61
Q

What is the C3 convertase in the fluid phase of the alternative pathway?

A

C3(H2O)Bb

62
Q

What does properdin (factor P) do in the alternative pathway?

A

stablizes C3 convertase on pathogens surfaces. made by neutrophils & stored in secondary granules

63
Q

What are the proteins of the alternative pathway?

A

C3, Factor B, Factor D, P

64
Q

What determines the extent of complement activation?

A

membrane & plasma proteins that regulate the formation & stability of C3 covertases

65
Q

How do we protect our own cells?

A

complement activation will proceed only on the surface of pathogens due to negative regulatory proteins (complement control proteins) present in plasma & in host cell membrane to protect healthy host cells: 1. complement receptor 1 (CR1) 2. decay accelerating factor (DAF) 3. membrane cofactor of proteolysis (MCP)

66
Q

How is C5 convertase activity generated?

A

surface bound C3 convertase deposits large numbers of C3b fragments on pathogen surfaces & generates C5 convertase activity

67
Q

What makes C5b different from C3b and C4b?

A

not covalently bound to the cell surface

68
Q

What does the production of C5b initiate?

A

assembly of terminal complement components

69
Q

How is ingestion of complement-tagged pathogens by phagocytes mediated?

A

receptor for the bound complement proteins. distribution & function of cell surface receptors for complement proteins

70
Q

Why is C5a important?

A

(anaphylatoxin) can enahnce phagocytosis of microorganisms opsonized in an innate immune response

71
Q

How is a local inflammatory response initiated?

A

small complement fragments (especially C5a)

72
Q

What do terminal complement proteins do?

A

polymerize to form pore in membrane that can kill certain pathogens. assembly of MAC generates a pore in lipid bilayer membrane

73
Q

How do pathogens fight about against complement proteins?

A

produce several types of proteins that can inhibit complement activation via “co-evolution”

Immunology (8 decks)

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