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Immuno block 4 > Lecture 1 > Flashcards

Lecture 1 Flashcards

1
Q

environmental factors that cause cancer?

A

carcinogens, radiation trandormation of viruses

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2
Q

example of benign tumor

A

glandular tissue. e.g adenoma

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3
Q

example of malignant (metastatic) tumor?

A

adenocarcinoma, breast cancer, prostate cancer

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4
Q

to a tumor to become established it needs to do what?

A

need to have a mechanism to evade immune mediation

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5
Q

indirect evidence that immune system stops most cancers

A

immune depleted people get more cancer
in vitro evidence
lymphoid infiltrate around tumors cerrelate with better prognosis
animal model with immune deficient.

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6
Q

degree of foreigness?

A

the amount that a molecule/antigen differ from person own molecules. for tumors, they arise from own cells, so immune system generally dont recognize self to fight it.

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7
Q

elimitaion phase of cance mediated by which cell?

A

CD4 and NK,

also gamma delta nad CD8

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8
Q

equilibrium phase

A

tumor cells acquire mutations and become resitant to CTL and NK cells

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9
Q

why are cancer cells so poorly immunogenic?

A

because they arise from one own’s self. not very foreign.

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10
Q

mostimpottat effectors for survailance of tumors

A

CD8 and CTL mediated lysis

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11
Q

3 mechanisms of killing by ctl and nk cells

A
  1. most efficient: perforin and granzymes (induce apoptosis in minutes)
  2. when Fas ligand is expressed on the surgace of CTLs and NK cells) FasL/Fas induces target cell apoptosis
  3. Tumor necrosis factor (TNFs) cell surface-expressed TNF-alpha (24 hours apopt.)
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12
Q

2 main class of antigens that recognises tumors

A
  1. Tumor specific antigens (TSA): unique cancer clone-specific Tumor antigens (ex. chemical/ radiation induced cancers)
  2. Tumor associated Antigens (TAA): over-expressed normal proteins, or Re-expressed normal proteins.
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13
Q

TSAs (tumor specific antigens)

A

expressed only by cancer cells, but not normal cells of that tissues, regardless of stage of differentiation. example: E6, E7 proteins of HPV virus in cervical cancer cells.

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14
Q

Tumor associated antigens TAAs

A

over-expressed normal proteins, re-expressed normal proteins

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15
Q

2 ways a mutation can give rise to epitope?

  1. mutated anchor residue of MHC?
  2. Mutated epitope residue?
A

1: mutated anchor residue of MHC: a point mutation in a self peptide allows binding of a new peptide to mhc.
2: Mutated epitope residue: a point mutation in a self peptide creates a new epitope for recognition by T cells.

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16
Q

number one TSA indicator?

A

Mutated protein . meaning that this is a protein that is produced only by the cancer cancer cell as the result of a mutation. This protein becomes an antigen and is presented to immune cells to build an immune response

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17
Q

tumor associated antigen think of what?

A

Re-expressed protein,

Over-expressed protein

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18
Q

PSA?

A

specific for protate not prostate cancer (TAA)

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19
Q

mechanism of tumor evasion?

A
  1. (HLA class I): downregulation of mhc1 molecule, lead to evasion of CTL cells, but becomes vulnerable to NK cells (kills cells that stops expressing MHC1).
  2. antigen-loss variants (evasion of antibody and CTL resposnses
  3. Lack of costimulatory molecules (80/86) induction of Tcell anergy
  4. TGF beta production: inhibition of cell mediated response and induction of regularory Tcells (Treg) in the tumor environment.
  5. Expression of FasL on cancer cell surface. this induces T-cell apoptosis.
  6. Secretion of mucopolysaccharide: will work as a physical barrier against infiltrating lymph cells and delays the expression of tumor specific antigens.
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20
Q

mechanism to avoid MHC1 and NK cells?

A

KKG2D, killing activating receptor (KAR) on some NK cells

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21
Q

MIC-A and MIC-B

A

are stress induced proteins recognized by NK cells via KAR and by gamma delta Tcells via gamma delta TCR

22
Q

IFN-alpha

A

NK cell activation

23
Q

IFN-gamma

A

activate CTL, up regulates HLA

24
Q

IL-2

A

stimulates T cell and NK cell proliferation

25
Q

BCG

A

vaccine for microbacterium TB. promotes inflammation (adjuvant effect) can prevent tumor even though it is not very effective against tb.

26
Q

challenge to vaccine against tumors?

A

tumor cells can be antigenically heterogenous, because of accumulation of mutation as the tumor grows.

27
Q

DNA vaccine for cancer?

A

encoding tumor antigen,

28
Q

ADCC (antigen dependent cytotoxic cell

A

antibody bind to antigen and NK cells bind to Fc region of antibodies

29
Q

why use a only a FAB of antibodies to killing cancer

A
  1. wont allow NK cell to bind to them on its Fc region,

2. small can penetrate tumor and deliver deep into tumor much better than a complete antibody

30
Q

why use a only a FAB of antibodies to killing cancer

A
  1. wont allow NK cell to bind to them on its Fc region,

2. small can penetrate tumor and deliver deep into tumor

31
Q

ximab

A

chimeric monoclonal antibody. human/foreign

32
Q

zumab

A

humanized 90-95%.

only the CDRs are not human, everything else is human,

33
Q

mumab

A

fully human from transgenic mice or phage display (made in vitro)

34
Q

TSA or TAA recap?

  1. carcinoembryonic antigen
  2. mutated p-53
  3. tyrosinase in melanocytes
  4. HPV oncoprotein
  5. prostate specific protein (PSA)
  6. CD20 on B cell lymphoma
A
  1. TAA
  2. TSA
  3. TAA
  4. TSA
  5. TAA
  6. TAA
35
Q

Immune surveillance theory?

A

when the immune system responds to a tumor, it does in two different types of responses. (TSA and TAA)

36
Q

most important immune cells to eliminate cancer cells?

A

CD8 and NK cells

37
Q

why Th 1 cells important to fight cancer cells?

A

because tumors are very poorly immunogenic, need Th-1 to activate CTL cells

38
Q

what happens if immune cells can’t fight cancer cells?

A

because the tumor cells will acquire mutations and become resistant to the CTL and NK cells.

39
Q

how can a cancer cell spread?

A

a cancer cell can:

  1. become immune to the killing of CTL and NK and multiply unchallenged
  2. recruit regulator cells and (Treg) which will turn off the immune cells fighting the cancer cells.
40
Q

why arent macrophages very effective to fight cancer cells?

A

because cytokines in tumor environment (IL-10 and TGF-B) promote monocyte differentiation into tumor-associated macrophages (TAMs) that promote angiogenesis and supress cell-mediated responses.

41
Q

what will monocytes differentiate into in the presence of IL-10 and TGF-B from the cancer environment?

A

immuno-supressive macropahges

42
Q

how can a point mutation result in new epitopes?

A
  1. Mutation on a peptide binding motif. a normal cell presents self peptides bound to MHC molecules, but a mutation in a self protein allows the biding of a new peptide to MHC molecules, this gives rise to a new peptide to be presented and recognized by Tcells as antigens because they were not present in the thymus during Tcell maturation.
  2. or mutation can affect a Tcell receptor contact resudue (CDR3)
    in both cases they are tumor specific because they are mutations on protein synthesis
43
Q

DNA viruses associated with human cancers?

A
  1. Papilomavirus (Warts)
  2. Hep B virus (liver cancer)
  3. Epstein-Barr virus (Burkitt’s lymphoma (cancer of Bcells)
44
Q

RNA viruses associated with human cancer?

A

Human T-cell leukemia virus type 1 (HTLV-1) causes (adult T-cell leukemia)
2. Human immunodeficiency virus (HIV) and
human herpes 8 (HHV8)

45
Q

what else can give rise to tumor specific antigens?

A

mutations and

translocations

46
Q

products of oncogenes, tumor suppressor genes ex. Ras mutations. TAA or TSA?

A

TSA, anytime see mutation TSA

47
Q

over-expressed genes ex. tyrosinase. TAA or TSA?

A

TAA.

48
Q

differentiation antigens normally in tissue of origin. ex. prostate specific antigen PSA. TSA or TAA?

A

TAA. specific for protate not the cancer.

49
Q

Ig idiotypes on B cells? TSA or TAA?

A

TSA. specific for the cancerous B cell.

50
Q

vaccination against cancer?

A

HBV, HPV, tumor cells with co-stimulatory molecules like CD80, CD86

Immuno block 4 (2 decks)

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