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Immunology Midterm > Quiz 2 Part 1 > Flashcards

Quiz 2 Part 1 Flashcards

1
Q

What is the role of the CR1 receptor

A

CR1 is a receptor protein present on the surface of macrophages. It helps the macrophage bind to tagged microbes AND improve phagocytic efficiency

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2
Q

What exactly does the CR1 receptor bind to on either side?

A

CR1 is a receptor on the surface of the macrophage. It recognizes the C3B tag on the bacterial surface

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3
Q

What is the term for the newly engulfed area in the macrophage that contains the bacterium (with C3b tags bound to the CR1 receptors)?

A

a phagosome

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4
Q

What happens to the contents inside the phagosome?

A

lysosomes fuse with the phagosome and form a “phagolysosome.”
The lysosome releases hydrolytic enzymes which destroys the contents of the phagosome

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5
Q

What are CR3 and CR4?

A

2 more complement receptors on the surface of macrophages.
They bind iC3b on the surface of the pathogen which facilitates opsonization and engulfment

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6
Q

iC3b is….

A

inactive as a convertase but active as a tag

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7
Q

As the immediate innate immune response develops, ____ plays the biggest role by far

A

C3b

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8
Q

Besides complement fixation on the pathogen surface, what else does C3b do?

A

it initiates a cascade of complement reactions involving terminal complement components (C5-C9)

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9
Q

Explain where the complement cascade begins and ends

A

the complement cascade begins in the cytosol and end with the formation of the MEMBRANE-ATTACK COMPLEX

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10
Q

What does the membrane attack complex do?

A

forms pores in the plasma membrane of the pathogen

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11
Q

how is the alternative C5 convertase formed

A

When the alternative C3 convertase (C3bBb) binds to a C3b fragment, forming the C5 convertase:
C3b2Bb

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12
Q

What does the alternative C5 convertase do?

A

C3b2Bb binds a C5 molecule and cleaves it into C5b and C5a

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13
Q

What are the respective roles of the newly cleaved C5b and C5a?

A

C5a is a potent cytokine which stimulates effector cells (similar role to C3a)

C5b is used to initiate formation of the MEMBRANE ATTACK COMPLEX

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14
Q

Explain what happens to C5b after it’s cleaved from C5

A

C5b binds to C6 and C7. This exposes a hydrophobic portion on C7 which causes the entire complex to bind to the membrane.

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15
Q

What happens after the C5, C6, and C7 complex binds to the membrane of the pathogen?

A

C8 binds to the complex, forming an initiation complex. C8 also has a hydrophobic portion which sticks into the membrane

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16
Q

What happens after C8 comes in?

A

C9 binds to the complex and polymerizes to generate a pore

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17
Q

After C9 polymerizes, what happens?

A

a pore is formed in the pathogen membrane. Osmotic pressure causes everything to rush into the cell and causes it to explode

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18
Q

After the pore causes the cell to explode, what happens to all of the pieces from the destruction floating around?

A

dendritic cells can take these pieces to the lymph node through an afferent lymphatic vessel and induce the adaptive response. (if macrophages and neutrophils cannot engulf all the pieces)

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19
Q

What are the 2 parts of the destructive portion of innate immunity (after tagging)

A

engulfment or explosion by means of the membrane attack complex

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20
Q

Why is C3 important in forming the membrane attack complex?

A

because without C3, the alternative C5 convertase could not be formed, which is responsible for cleaving C5 to form C5b, which initiates the assembly of the membrane attack complex

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21
Q

What are the respective functions of C6, C7, and C8 in the formation of the membrane attack complex?

A

C6 - binds to and stabilizes C5b and forms a binding site for C7

C7 - binds to C5b6 and exposes a hydrophobic portion on itself that permits it to attach to the plasma membrane of the pathogen

C8 - Bind to C5b67 and exposes a hydrophobic portion on itself that inserts into the plasma membrane

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22
Q

Between C5-C9, which has the highest concentration in our serum?

A

C5

23
Q

What happens in the terminal complement pathway?

A

Formation of the membrane attack complex which forms a pore in the plasma membrane of the pathogen and causes explosion (lysis)

24
Q

Is the terminal complement pathway regulated?

A

yes

3 soluble proteins prevent the association of C5b with C6 and C7 (S protein, clusterin, Factor J)

2 surface proteins that prevent the recruitment of C9 (HRF, CD59)

25
Q

Which are more so found in/on human cells–

-The soluble proteins that regulate the terminal complement pathway or…

-The surface associated proteins

A

surface associated (CD59 HRF)

26
Q

Why do we have these surface associated proteins (HRF and CD59) on our cells?

A

because we don’t want the C5b678 complex to bind to C9. If this happens, C9 will polymerize and form a pore in OUR OWN CELLS, causing destruction

27
Q

What are C3a and C5a referred to as and why?

A

Anaphylatoxins.
This is so because they are both potent cytokines which act to increase inflammation.
If there is too much of them, anaphylactic shock can occur

28
Q

Which is more potent - C3a or C5a

A

C5a

29
Q

Which kinds of cells do C3a and C5a recruit?

A

phagocytes, endothelial cells, and mast cells

30
Q

Which cells contain granules of histamine? What does histamine do?

A

basophils and mast cells contain granules of histamine.
The degranulation of mast cells and basophils releases histamine which results in increased blood flow and vascular permeability (for effector cells to get in)

31
Q

What is particularly important about C5a?

A

C5a DIRECTLY INCREASES ADHERENCE of neutrophils and monocytes (immature macrophages) to vessel walls, and promotes the chemotaxis of these cells, and induces expression of CR1 and CR3

32
Q

Recap: what do CR1 and CR3 do

A

they’re both bound to the surface of a macrophage.
CR1 helps to bind tagged microbes and improve phagocytic efficiency
CR3 binds iC3B on the surface of the pathogen which stimulates phagocytosis

33
Q

Increased permeability due to the action of the anaphylatoxins allows what to leave blood vessels?

A

complement components and plasma proteins to leave the blood vessels and migrate to the site of infection.

Also migration of neutrophils and monocytes from the blood to the infected tissue is increased

34
Q

the coagulation system is part of the ___ immune system

A

innate

35
Q

Explain what the coagulation system is

A

the formation of blood clots to fight infection.
Microbes can become physically trapped in the clot and it also prevents more pathogens from entering through the open wound

36
Q

What are platelets

A

cell fragments that migrate to the site of infection and clump together to form a clot

37
Q

what factors do platelets release to promote inflammation?

A

prostaglandins
hydrolytic enzymes
growth factors
bradykinin (vasodilator)

38
Q

Pathogens secrete proteases. What can these proteases do?

A

breakdown human tissue, help to spread the infection, and inactivate antimicrobial agents

39
Q

Why do we have a lot of protease inhibitors in our serum?

A

some pathogens adapt to acquire cell surface proteases. these are dangerous because proteases breakdown human tissue, help to spread infection, and inactivate antimicrobial agents

40
Q

Give an example of an important protease inhibitor in our serum

A

alpha2-macroglobulins

41
Q

Explain the structure and function of alpha2-macroglobulin

A

alpha2-macroglobulin contains a thioester group (like C3)
The molecule has “bait” inside of it to bring the protease inside of it. once the protease binds to the bait and cleaves it, alpha2-macroglobulin undergoes a conformational change which enshrouds the protease and covalently bonds to it. This inactivates the protease

A macrophage can then bind to this complex and engulf it

42
Q

Which cells have receptors for alpha2-macroglobulin?

A

hepatocytes
fibroblasts
macrophages

43
Q

give an example of an antimicrobial peptide

A

defensin

44
Q

Explain the structure of defensins and why this is benficial

A

defensins are amphoteric. This is useful because they can stick their lipophilic portion into the cell membrane to aid in forming a pore

45
Q

Where are defensins secreted and produced?

A

defensins are secreted at mucosal surfaces and produced by neutrophils

46
Q

What are the 2 kinds of defensins and where are they produced?

A

alpha defensins – produced by immune cells

beta defensins – produced by epithelial cells of the skin, respiratory, and urogenital tracts

47
Q

Explain how defensin cells are able to bind to a pathogen

A

defensins have a specificity for different pathogens (ie: gram-positive/gram-negative)

48
Q

What does defensin do after it sticks it’s lipophilic portion into the pathogen’s membrane?

A

it forms a pore. Fluid rushes in and lyses the pathogen

49
Q

What is the main source of defensins in the small intestine?

A

paneth cells (contain granules)

50
Q

What are pentraxins?

A

small, planar, multimeric plasma proteins. They bind pathogens and target them for destruction

51
Q

What are the 2 subfamilies of pentraxins?

A

Short (SAP- serum amyloid P) - made by hepatocytes

Long (PTX3) - produced by myeloid, endothelial, and epithelial cells

52
Q

Which pentraxin has all 4 types of pathogens (parasites, bacteria, fungi, and viruses) as their ligands?

A

SHORT PENTRAXIN (Serum amyloid P)

53
Q

Long pentraxin (PTX3) has which ligands?

A

bacteria, viruses, and fungi

54
Q
A

Immunology Midterm (8 decks)

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