Immunology Lecture 10 Flashcards

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1
Q

Define complement.

A

Heat labile component of blood plasma.

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2
Q

What are the three major functions of complement?

A

Defence against bacterial infection
Augmentation of the antibody response
Waste disposal

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3
Q

Do complements require antibodies to act? Are they specific?

A

No antibodies required, are non-specific.

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4
Q

What kind of reaction is the complement activation?

A

Sequential cascade.

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5
Q

Name the three pathways of complement activation, and their activation requirement.

A

Classical - requires antibodies
Alternative - requires endotoxins/polysaccharides
Lectin - requires mannose-binding protein

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6
Q

What are mannose-binding proteins released by?

A

Macrophages after phagocytosis.

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7
Q

Describe the classical complement activation sequence in detail.

A

Antibody unforked end binds to the C1 complex, activating it.
C1 complex splits C2 into C2a and C2b, and C4 into C4a and C4b.
One C2a/b and one C4a/b fragment merge to form the enzyme C3 convertase.
C3 convertase hydrolyses C3 into C3a and C3b.
C3b converts C5 into C5a and C5b.
C5b, with one C6-8 and many C9s, forms a MAC - membrane attack complex, punching a hole in the membrane.

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8
Q

Which complements form the MAC?

A

C5b, C6, C7, C8, and many C9s.

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9
Q

What is required for C3 hydrolysis? What differs between the classical and alternative complement activation pathways?

A

A C2 and C4 fragment merging to form C3 convertase.

However, it can be hydrolysed without this enzyme. That is the alternative pathway.

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10
Q

What is the controlling factor of complement activation?

A

C3 cleavage by C3 convertase, rate is slow unless infection present.

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11
Q

What is the function of C3a and C5a?

A

Cause mast cells to release histamines, inducing inflammation.
C5a also attracts phagocytes.

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12
Q

Define opsonisation.

A

When C3b coats a pathogen, enhancing phagocytosis.

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13
Q

Name 4 phagocytic cells.

A

Monocytes
Macrophages
Neutrophils
Dendritic cells

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14
Q

Define toll-like receptors, where they are found, and what they recognise.

A

Found on phagocytic cells. Recognise pathogens using TLRs, which recognise PAMPs on the pathogen surface - pathogen associated molecular patterns.

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15
Q

Can a TLR recognise many PAMPs?

A

No, each has a limited range.

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16
Q

Do self cells have PAMPs?

A

No.

17
Q

What happens when TLRs are activated?

A

Induces genes such as cyotkines, chemokines, and phagocytic genes.

18
Q

How does the innate immune system differentiate self from non-self?

A

Using TLRs.

19
Q

What happens after a pathogen is phagocytosed?

A

The bacteria is internalised as a phagosome.
Fuses with a lysosome forming a phagolysosome, and digested.
Phagolysosome is merged with cell membrane to discharge indigested material.

20
Q

What are cytokines?

A

Major control proteins for both specific and non-specific immune responses.

21
Q

Do cytokines have unique functions?

A

No, their functions can overlap.

22
Q

What relationship do cytokines have with stem cells?

A

Are involved in differentiation of stem cells to immune cells.

23
Q

Are cytokines autocrine, paracrine, or endrocrines?

A

All three.

24
Q

Are cytokines required in high concentrations to have an effect?

A

No, they are very effective at low concentrations.

25
Q

How do cytokines act?

A

Bind to specific cellular receptors to induce genes, such as fever.

26
Q

What is a natural killer cell?

A

Large, non-phagocytic granular cell.

27
Q

What do NK cells act on?

A

Malignant and infected cells.

28
Q

How do NK cells appear under a microscope?

A

Exactly like a lymphocyte.

29
Q

How do NK cells act?

A

They recognise antibosies on the cell surface, and also recognise the lack of MHC class 1.

30
Q

How can NK cells kill cancer cells?

A

They lack MHC class 1 markers, which NK cells can recognise the lack of.