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Cancer immunology > Antibodies therapies > Flashcards

Antibodies therapies Flashcards

1
Q

How are t-cells different than b-cell repertoire in terms of maturation?

A

T-cells don’t have affinity maturation, they are born with the same potential repertoire

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2
Q

What are the effector functions of t-cellS?

A

Kill cells through cytotocity or cytokines or recruit other immune cell types to kill the cells

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3
Q

What do b-cells do when they meet an antigen and how?

A

Recognize conformation determinants with the antibodies on their surface that are specific, they develop affinity maturation when producing more antibodies

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4
Q

Effector functions of b-cells?

A

Opsonization, neutralization, complement activation and ADCC

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5
Q

What are antibodies made up of? What links them? How many antigen binding sites?

A

variable region and constant regions that are made up two heavy chains and two light chains. Disulphide bonds
2 antigen binding sites

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6
Q

What happens when they don’t add reducing agent with papain what happens?

A

There is more fragments in the constant regions compared to adding reducing agent

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7
Q

What is the importance of FC regions?

A

They give the antibody it’s class

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8
Q

What’s the first antibody b-cells produce?

A

IGM and IgD

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9
Q

What does class switch depend on?

A

The strength of signal

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10
Q

What are the structural differences between IGA, IGM, IGE,IGG? Where is the IGA found?

A

IGM-pentameric
IGE,IGG-monomeric
IGA-dimeric mucous

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11
Q

Which antibodies are good at activating complementation?

A

IGG,IGM

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12
Q

What is the half life of antibodies?

A

10-20 days

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13
Q

What is IGE good at activating?

A

High affinity to basophils and mast cells

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14
Q

How do b-cells affinity mature?

A

The antibody that binds to antigen it’s strength depends on the activation of b-cells and if re-encounters the antigen it will mutate it’s binding site and the antibodies with the best affinity binding are selected for

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15
Q

What does the interaction between the epitope and antigen depend on?

A

Electrostatic forces, van der waals, hydrogen bonds,shape, hydrphobic forces

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16
Q

What is the tradeoff between multimeric and monomeric antibody structure? What is it good for?

A

Affinity and how easily it transports.

Binds to multiple antigens

17
Q

How are antibodies made?

A

T helper cells bind to b-cells after it binds to antigen and the t-cell secrete cytokines that makes b-cells to be activated and release antibodies

18
Q

What are thibgs to consider when targetting tumour?

A

Unique epitope

Overexpression of antigens on tumour cells and less on normal cells

19
Q

How do b-cells mature?

A

They bind to t-cells and t-cells secret IL-4, which makes them proliferate, they also express CD40L which allows the b-cells to class switch through somatic hypermuation, then the b-cell mature and produce plasma antibody secreting cells and memory cells

20
Q

Which isotype class do TH1 and TH2 induce and what cytokines?

A

th1-IGG2A and IGG3 by ifn-gamma and TGF-b

TH2-IGG1 and IGE by il-4

21
Q

What are ethe different pathways that activate complementation pathway?

A

Classical-antibidy- antigen complex
alternative pathway-pathogen surface
lectin pathway-lectin opsonize the surface of pathogen

22
Q

Explain complementation

A

So soluble c2-c4 cascade of cleavage will activate and recrut the next c protein in the cascade. C3 convertase can mediate inflammation via c3A, and c5a or it can induce killing through recruiting C5-C9 sequentially they form a membrane bound pore and depolarize until cell dies. It can opsonize just by c3 convertase and C3B binding to complement receptor on phagocyte

23
Q

What do CD16, CD32, CD64 and fceRI fcar do? Where are they found?

A

CD16- is activating induces killing, found on macrophage, mast cells, natural killer cells, neutrophils.
CD32-inhibition if the uptake of signalling, found on macrophage, mast cells and b-cells
CD64-activating of killing, and uptake of signalling. Found on dendritic cells and macrophage
fceRI-binds to IGE secrete granules
fcar-bind to IgA and IgM uptakes them to different tissues

24
Q

How does opsinization work?

A

C3B binds to complement receptor on the bacteria and antibody also binds to the surface of bacteria, while the antibody recognizes the FC receptor on the macrohphage and binds to, C3B will bind to cR1 on the surface of the macrophage and then the antibody with the bacteria is engulfed and lysed with lysosomes

25
Q

How does ADCC work?

A

The antibodies bind to the antigens on the cell surface of pathogen and binds to FC receptors(CD16) on NK cells and they release signals that killthe cells

26
Q

What are other fc mediated responses?

A

Inflammatory responses, phagocyte recruitment

27
Q

What is the difference between active immunization and passive?

A

Active- administer immunogen

Passive-create anti-bodies in vitro and adminester it inot patients

28
Q

What are the pros and cons in active immunization?

A

Low cost, polyclonal
Difficult to control response
Difficult to target self antigen

29
Q

What are the pros and cons in passive immunization?

A

Its expensive very few good tumour antigen

Very reproducible and good response to self antigens

30
Q

What are some alternative solutions?

A

Chimeric antibodies
transgenic animals
human monoclonal antibodies(plasmacytoma and immunize humans)

31
Q

Give examples of monoclonal antibodies being used to treat cancer

A

Avastin-neutralizes VEGF used to treat CRC
Retuximab- Activate the complement pathway and bind to NK cells
Pantimumab-Targets HER1 it blocks growth factor receptor and induces apoptosis

32
Q

What are the mechanisms of actions of antibody therapies

A

adcc
Complement mediated lysis
neutralization
apoptosis

33
Q

What are other approaches in cancer therpay?

A

Rdiotherapy-less toxic
antibody drug conjugates-gets cleared quickly but reduces toxicity
Prodrug
toxin targeting

34
Q

What rae the positives and negatives of radioimmunotherapy?

A

Gets cleared quickly, biodistribution, number of cells binding to antibody
less toxic to normal cells

35
Q

Positives and negatives of antibody drug conjugates. What is an example what did it bind to?

A 
Less toxic to normal cells
heterogenity of response of tumour
number of drug per cell for killing
number of cells binding to AB
mylotarg to CD33 on leukimia cells

Cancer immunology (7 decks)

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