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Immunology Midterm > Quiz 1 Part 3 > Flashcards

Quiz 1 Part 3 Flashcards

1
Q

Explain how innate immunity works to destroy an EXTRACELLULAR pathogen

A

normal response—macrophage sends out cytokines to recruit neutrophils to help engulf the pathogens.

Works on BACTERIA AND VIRAL PATHOGENS

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2
Q

Explain how innate immunity works to destroy an INTRACELLULAR pathogen

A

Neutrophil CANNOT engulf an intracellular virus. Virus is doomed once infected by a virus. because viruses thrive and replicate inside cell

NK killer cells (natural killer) recognize the infected cell due to morphological changes. NK cell kills both the virus AND the host cell

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3
Q

do bacteria replicate internally or externally?

A

usually externally

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4
Q
A
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4
Q

What are the 2 phases of the innate immune response

A

-immediate (available at all times. managed by resident macrophage)

-induced (needs to be activated. When resident macrophages become overwhelmed, they recruit neutrophils through cytokines)

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5
Q

what is the first line of defense?

A

physical barriers (skin, at places of entry - skin, gut, lungs, eyes/nose/oral cavity)

all have epithelial cells joined by tight junctions. bacteria cannot get in without cut

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6
Q

Besides the presence of epithelial cells, explain how the skin, gut, lungs, and the eyes/nose/oral cavity all have mechanical barriers

A

skin and gut — longitudinal flow of air/fluid

lungs - movement of mucus by cilia (phlegm)

eyes/nose/oral cavity - tears, nasal cilia

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7
Q

Explain what the skin, gut, lungs, and eyes/nose/oral cavity all have in common for a chemical barrier

A

antimicrobial peptides

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8
Q

Explain how the skin, gut, lungs, and the eyes/nose/oral cavity all possess the same microbiological barrier

A

their normal microbiota (“good” bacteria. bacteria are very territorial and will destroy invaders)

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9
Q

What does the term “microbiota” mean?

A

cohorts of microorganisms (microbes) in specific body regions. they’re usually very good at keeping pathogens out. exception: when we take antibiotics

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10
Q

Name 3 benefits of the microbiota

A

-process digested food
-provide essential vitamins/growth factors
-PROTECT AGAINST INVASION OF PATHOGENS

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11
Q

Is our microbiota always constant?

A

NO - fluctuates depending on age, diet, and health status. Microbial populations change in response to illness or treatment with antibiotics

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12
Q

Does every person have the same combinations of “good” bacteria in their microbiome?

A

no! we’re all different

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13
Q

what is meant by “commensal” microorganims? what is another name for them?

A

the bacteria that are either “goof” or neutral to the human population.
another name = endogenous flora

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14
Q

the colon is colonized by large populations of ____ bacteria.
Give an example of when these bacteria would be killed?

A

commensal
many of them are killed when we take antibiotics

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15
Q

Why is it so important to always take the full course of antibiotics?

A

because taking the antibiotics kills both the good AND bad bacteria. if we stop taking the antibiotics prematurely, the bad bacteria could gain a foothold over the commensal bacteria and cause further disease. We want to make sure ALL THE BACTERIA IS KILLED

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16
Q

What does HMP stand for?

A

the Human Microbiome project

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17
Q

What was the purpose of the human microbiome project?

A

it was an effort to sample and analyze the genome of microorganisms from five sites on the human body:

-nose
-oral cavity
-skin
-gastrointestinal tract
-urogenital tract

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18
Q

What is the complement system ?

A

a system for “tagging” pathogens/pathogenic material for destruction

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19
Q

The complement system consists of…

A

a collection of plasma proteins made by the LIVER (>30 members)

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20
Q

Where do the plasma proteins of the complement system circulate?

A

in blood, lymph, and extracellular fluids

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21
Q

If infection is NOT present, these plasma proteins circulate in the blood, lymph, and extracellular fluid as _________

A

zymogens

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22
Q

When and how are zymogens activated?

A

presence of an INFECTION triggers proteolytic cleavage and thus activation of the complement proteins

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23
Q

Which protein is by far the most important in the complement system?

A

C3

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24
Q

Explain what is happening in the “fixation of the complement”

A

C3 gets cleaved into C3a and C3b.

C3a is a cytokine that recruits phagocytes (neutrophils)

C3b is the “tag” that covalently bonds to the bacterium. It opsonizes by coating the bacteria in C3b which enhances the ability of neutrophils and macrophages to phagocytize the bacterium

25
Q

explain the 2 possible routes of C3 after it is cleaved

A

normally, C3 contains a sequestered thioester bond (-s-carboxyl) that is stabilized within the hydrophobic interior of the C3 protein.

When C3 is cleaved, the thioester bond ON C3b becomes exposed and subject to nucleophilic attack by the surrounding water molecules OR by the amino and hydroxyl groups contained on the surface of the pathogen.

MOST C3b molecules are attacked by water and remain in a soluble, inactive hydrolyzed form.

SOME C3b become covalently bound to the pathogen. The closer the C3b is to the pathogen’s surface, the more likely it will be attacked by it instead of water

26
Q

What are the 3 pathways of complement activation?

A
  1. Alternative pathway
  2. Lectin pathway
  3. Classical pathway
27
Q

All 3 pathways lead to……

A

COMPLEMENT ACTIVATION - cleavage of C3 into C3a and C3b

28
Q

Of the 3 pathways, which is the first to act and explain its role

A

alternative pathway
-the surface of the pathogen stimulates the cleavage of C3

29
Q

Of the 3 pathways, which is the 2nd to act and explain its role

A

lectin pathway
-mannose-binding lectin binds to the pathogen surface which stimulates the cleavage of C3

30
Q

Of the 3 pathways, which is the last to act and explain its role

A

classical pathway
-the C-reactive protein (innate immune system) or antibody (adaptive immune system) binds to a specific antigen on the pathogen surface

31
Q

Name 3 potential results of the cleavage of C3 into C3a and C3b that all ultimately lead to the death of the pathogen

A

-recruitment of inflammatory cells (due to C3a)

-opsonization of pathogens which facilitates the uptake and killing by phagocytosis (bc of coating of C3b)

-Perforation of plasma cell membranes (the pores cause cell lysis)

32
Q

Which enzymes actually do the cleaving of C3 into C3a and C3b?

A

C3 Convertases

33
Q

What is the full term for the C3 protein?

A

“complement protein 3”

34
Q

The capital C in C3 indicates that it is….

A

an intact protein

35
Q

The little letters of C3a and C3b indicate that,,,

A

that they are proteolytic fragments of the C3 protein

36
Q

Explain what iC3 is and how it is formed

A

C3 is made in the liver and secreted into the aqueous environment of the bloodstream in an inactive form (with the thioester sequestered within the hydrophobic interior of the protein)

slowly, the C3 protein changes its conformation and exposes its thioester bond, subjecting it to nucleophilic attack

the thioester bond will either be attacked by a hydroxyl group or an amino group (usually it is attacked by water because it is so plentiful in the aqueous environment of the blood).

This attack by water gives a form of C3 called iC3 (C3(H2O))

This iC3 molecule is used to form the SOLUBLE C3 convertase (soluble because C3 has been hydrolyzed and the thioester group can no longer bond to the membrane of a bacterium)

37
Q

Where is the nucleophilic attack and production of C3 accelerated?

A

near the surface of a microbe or pathogen

38
Q

What happens after iC3 is formed?

A

iC3 binds to factor B. This makes factor B susceptible to cleavage by the protease factor D

39
Q

Factor D cleaves Factor B into……

A

Bb and Ba

Bb is the larger portion that remains attached to iC3

40
Q

What is the name for the soluble C3 convertase?

A

iC3Bb

41
Q

What happens after factor D cleaves factor B?

A

iC3Bb cleaves C3 into C3a and C3b

The cleavage of C3 exposes the thioester bond on C3b, causing it to bind to the membrane of the pathogen and “tag” it

42
Q

Explain what the alternate C3 convertase is and how it’s made

A

The alternate C3 convertase is made when the C3b that has already “tagged” the pathogen binds factor B. factor B get cleaved by factor D, creating the alternate C3 convertase:
C3bBb

43
Q

What happens after the alternate C3 convertase has been made?

A

C3bBb cleaves a C3 molecule into C3a and C3b.

Since C3bBb is BOUND to the surface of the pathogen, the thioester bond on C3b is VERY likely to make a covalent bond with the surface of the pathogen and “tag” it, instead of being hydrolyzed by water

This causes opsonization — amplifies the “tagging” process since each C3b molecule that binds to the surface can bind factor B, become C3bBb, and cleave more C3’s into C3b and C3a

44
Q

As a recap, name the SOLUBLE C3 convertase and the ALTERNATIVE C3 convertase

A

soluble C3 convertase = iC3Bb

alternative C3 convertase = C3bBb

45
Q
A
46
Q

What is the general name of the proteins that regulate complement activity?

A

complement control proteins

47
Q

Complement control proteins either ____ or ____ C3b

A

stabilize or degrade

48
Q

What are the 2 categories of complement control proteins?

A
  1. Soluble plasma proteins that interact with C3b on human and microbial cells
  2. MEMBRANE proteins ON HUMAN CELLS that prevent compliment fixation
49
Q

Why do we not want C3b on our human cells?

A

because C3b tags the cell for destruction through phagocytosis

50
Q

What is the name of the plasma protein that stabilizes C3bBb

A

properdin (factor P)

51
Q

By stabilizing the alternative C3 convertase, what is properdin accomplishing?

A

factor P is preventing the degradation of C3bBb, keeping it bound to the membrane longer. This causing it to continually cleave C3 molecules and increase the speed and efficiency of complement activation

52
Q

What is Factor H and what does it do?

A

Factor H is a plasma protein that degrades C3b.
It facilitates the cleavage of C3b into iC3b through factor I.

This essentially decreases the number of convertase molecules attached to the pathogen surface

53
Q

What will happen in patients who have a deficiency of factor I?

A

These patients will have unregulated levels of C3bBb. This is harmful because it is wasting C3 molecules in the blood and extracellular fluid.

When faced with infection, these patients fix abnormally small amounts of C3b on the pathogen surface, resulting in less efficient bacteria clearance through phagocytosis.

54
Q

What is the purpose of factor H and factor I working together to cleave C3b into iC3b?

A

converting C3b into iC3b prevents C3b from binding to factor B and becoming an alternative convertase and thus amplifying the amount of C3b on the pathogen.

The iC3b is useful because it is still recognized as a “tag” on the pathogen, but cannot bind to factor B and become an alternative C3 convertase (C3bBb)

55
Q

Which 2 proteins are part of the 2nd category of complement control proteins? (the ones that are membrane bound and prevent complement fixation on human cells)

A

DAF and MCP

56
Q

Explain what DAF does

A

DAF is a membrane bound protein that binds to the C3b component of the alternative C3 convertase (C3bBb) which displaces Bb and inactivates the C3b portion.

57
Q

Explain what MCP does.

A

MCP is a membrane bound protein that also binds to the C3 portion of C3bBb. The difference is that MCP binding to C3b makes C3b susceptible to cleavage by factor I, converting it to iC3b

58
Q

Explain how a pathogen can evade the complement system.

A

Factor H has a binding affinity for sialic acid. Eukaryotes have sialic acid on their surfaces while prokaryotes naturally do not.
Thus, some pathogens produce sialic acid on their surface to “mimic” a eukaryotic cell which brings factor H in, to then recruit factor I and inactivate C3b (the “tag” to destroy the cell by phagocytosis)

59
Q
A

Immunology Midterm (8 decks)

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