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Exam Flashcards

1
Q

Causes of cancer

A

Radiation
Chemicals
Viruses
Aging

Mutation in gene

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2
Q

Tumour specific antigens

A

overexpressed by tumour
can lead to anti-tumour immunity

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3
Q

Tumour specific antigen used for

A

used in diagnosis
target in immunotherapies

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4
Q

Immune system aware of developing tumour

A

yes, have tumour specific antibodies and T cells

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5
Q

Immune surveillance of tumours

A

immune system survey body for development of malignancy and eliminate tumours as they arise

immuno suppresed develop tumors quickly

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6
Q

Melanoma kidney

Cancer in transplant

A

Transplant patient has higher rate of cancer then general public

lady free from cancer, kidney transplanted, both got cancer

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7
Q

immune system fight aginst tumour cells

A

some tumour regress sudennly
In lab, cytotoxic t cells and NK cells kill tumour cells

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8
Q

how cytotoxic T cells attack tumour

A

Tumour antigen in MHC class I
perforin, granzyme and FAS ligand interaction

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9
Q

In cancer

Why immune system ineffective

A

tumour antigen not presented (ignorance)
T- cell unresponsive (anergised)
too little too late
unable to enter tumour

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10
Q

cytokines secreted by tumour

A

TGFbeta - immunosupressive
VEGF - development of BV

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11
Q

cytokines secreted by regulatory cell

A

TGFbeta
IL-10

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12
Q

how does cancer evad immune system

A

immunosuppressive
hide via no MHC class I
dosnt release danger signals to start inflammation

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13
Q

3 E’s of immunoediting

A

Elimination
Equilibrium
Escape

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14
Q

immunoediting

Elimination

A

innate cells recognise tumour
DC transport antigen to LN
tumour specific T-cell eliminate tumor cells

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15
Q

immunoediting

Equilibrium

A

cant completely eliminate tumour
tumour cells left avoid killng by genetic altration

lose tumour antigen
downreg MHC class I
secrete soluble factor

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16
Q

immunoediting

Escape

A

Tumour cell completely avoid immune killing

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17
Q

aim of immunotherapy + types

A

boast immune system to kill cancer
-vaccination
-cytokines
-checkpoint blockade

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18
Q

Cytokine therapy

A

Interferons: stim NK, T cells and macrophages
TNF: directly kill tumour (used in conj w/ IFNy)
IL-2: Promote cytotoxic T, NK and macrophages

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19
Q

Cancer vaccine

A

tumour antigen
specific types of cancer, underwhelming

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20
Q

CAR

A

Chimeric antigen receptor

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21
Q

DC vaccines

A

expose to antigen, genetically modify and activate.
But tolerance occur if im DC given to patient

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22
Q

Anti-tumour antibody

A

monoclonal antibody that target tumour antigen.
have trouble getting into tumour

Rituximab for B-cell lymphoma CD20

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23
Q

cancer pov

Checkpoint molecules

A

Prevent excessive inflammation
tumours can take advantage of this

24
Q

first checkpoint molecule

A

Cytotoxic T lymphocyte-associated molecule 4 (CTLA-4)
inhibit T-cell activation and proliferation

compete with CD28 for B7 on APCs

25
Q

Anti-PD-1 vs Anti CTLA4

A

PD-1: less toxic, long term remission, possible cure

26
Q

stem cell vs progenitor cells

A

stem cells divide for lifetime
progenitor is already more specific

27
Q

Source of stem cells

A

Adult: largest reservoir BM
Cord blood: umbilical cord (small amount)
Embryonic: fertilized embryos, early phase

28
Q

different graft source

A

Autologous: patient own
Syngeneic: idential twin
Allogeneic: someone else

29
Q

Autologous

A

must not have evidence of disease
mortality low
Relapse high
no GVSHD but also no GVST

30
Q

Allogeneic

A

Matched unrelated
- high mortality
- GVHD
- lower relapse due to GVST
Matched related

31
Q

Matched related donor chances of being related

A

25%
the more siblings, the better the chance

32
Q

key event for stem cell transplant

A
  1. Donor selection: typing 6-10 HLA antigen
  2. Harvest stem cell from donor
  3. Preparative regimen for patient: chemo + radiation
  4. Stem cell intravenous infusion into patient
  5. Pos transplant suppotive care: auto 100 days, allo 180 days
33
Q

Preparative regimen for patient

A
  1. Myeloablation (high dose of chemo +/- radiation)
    - eliminate malignancy
    - generate immunosupp to allow engraftment
    - decrease host vs graft
  2. Stemcell infusion
  3. Maintain with immunosuppressant drugs
34
Q

non-myeloablative conditioning

for low dose chemo

A
  • better for slow growing cancer or older patients
  • immunosuppress enough to allow engraftment
  • less injury to organs
  • higher relapse
35
Q

Mixed chimerism

A

2 set of genetically different cells co-existing

36
Q

Donor prep

A

BM: Given granulocytes colony stimulating factor (G-CSF) to amp stem cell
PB: growth factor
Cord: umbilical cord and placenta

37
Q

what happends to transplated cells

A

“reverse migration” goes back to BM which in empty after chemo
recognise adhesion molecules and growth factor in stroma
proliferate untill BM full

38
Q

Factors for GVHD

A

immunologically competent donor graft
histo-incompatibility
immunologically incompetent host

39
Q

where does GVHD occur

A

starts in skin first, rash to dermatitis, blisters to necrosis
gastrointestinal shows diarrhra, malaise and vomiting

40
Q

MHC antigen

A

main antigen in graft rejection
* upregulation of class I and II on APC and tissue during inflammation
* becomes target antigen by allo-specific T cells
* casue fast and strong rejection by allo-specific T cells

41
Q

minor histocompatibility antigen

A

slower and weaker rejection
* ABO group antigen
* Tissue specfic antigen (vascular endothelial cells)

42
Q

graft vs cancer malignancy effects

A

lower relapse in patients who got GVHD
higher relapse in those withiut GVHD (twin donation, T depleted BM)

43
Q

Direct presentation

A

Donor APC

44
Q

Indirect presentation

A

Recipient APC

45
Q

what cytokines released by tissue due to chemo and other infection

A

IL-1, IL-6 & TNFa
DAMPS

46
Q

Model for GVHD

A

tissue damage from chemo: IL1&6 > inflammation >IL12 and IFNy > tissue damage
infection > inflammation > tissue damage

47
Q

Primary immunodeficiencies

A

abormalities of immune system
genetic causes

48
Q

Bruton’s disease

A

X-linked agammaglobulinaemia, mutation in bruton tyrosine kinase > stop development in pre-B stage
* few B cell in blood or lymph
* decrease immunoglobin

49
Q

6 Main type of immune related functional deficiency

A
  1. Phagocytic deficiencies
  2. Complement def
  3. T cell mediated (cellular) def
  4. B cell mediated (antibody) def
  5. combined immunodeficiencies
  6. disorders of immune dysregulation

65% antibody def

50
Q

Phagocytic deficiencies

A

Neutrophils
any age
e.g. Chronic granulomatous disease and leukocytes adhesion deficiency

51
Q

Chronic granulomatous disease

A

impact neutrophil phagocytosis and dectruction of pathogen

52
Q

IGAM in CoV19

A

IgM: First responder
IgA: in mucous secretion (where CoV enters)
IgG: isotype switching occurs later

53
Q

3 different spike protein

A

RBD
S1
Ectodomain(S2P)

54
Q

spleen and Lymph nodes in COVID-19

A

germinal centres lost in lymph and spleen (isotype switch)
loss of white pulp in spleen (where T&B cells are )

55
Q

Biphasic course for COVID 19

A
  1. viral 2. host inflammatory

imm (3 decks)

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