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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
Anti-PD-1 vs Anti CTLA4
PD-1: less toxic, long term remission, possible cure
26
stem cell vs progenitor cells
stem cells divide for lifetime progenitor is already more specific
27
Source of stem cells
Adult: largest reservoir BM Cord blood: umbilical cord (small amount) Embryonic: fertilized embryos, early phase
28
different graft source
Autologous: patient own Syngeneic: idential twin Allogeneic: someone else
29
Autologous
must not have evidence of disease mortality low Relapse high no GVSHD but also no GVST
30
Allogeneic
Matched unrelated - high mortality - GVHD - lower relapse due to GVST Matched related
31
Matched related donor chances of being related
25% the more siblings, the better the chance
32
key event for stem cell transplant
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
Preparative regimen for patient
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
non-myeloablative conditioning | for low dose chemo
* better for slow growing cancer or older patients * immunosuppress enough to allow engraftment * less injury to organs * higher relapse
35
Mixed chimerism
2 set of genetically different cells co-existing
36
Donor prep
BM: Given granulocytes colony stimulating factor (G-CSF) to amp stem cell PB: growth factor Cord: umbilical cord and placenta
37
what happends to transplated cells
"reverse migration" goes back to BM which in empty after chemo recognise adhesion molecules and growth factor in stroma proliferate untill BM full
38
Factors for GVHD
immunologically competent donor graft histo-incompatibility immunologically incompetent host
39
where does GVHD occur
starts in skin first, rash to dermatitis, blisters to necrosis gastrointestinal shows diarrhra, malaise and vomiting
40
MHC antigen
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
minor histocompatibility antigen
slower and weaker rejection * ABO group antigen * Tissue specfic antigen (vascular endothelial cells)
42
graft vs cancer malignancy effects
lower relapse in patients who got GVHD higher relapse in those withiut GVHD (twin donation, T depleted BM)
43
Direct presentation
Donor APC
44
Indirect presentation
Recipient APC
45
what cytokines released by tissue due to chemo and other infection
IL-1, IL-6 & TNFa DAMPS
46
Model for GVHD
tissue damage from chemo: IL1&6 > inflammation >IL12 and IFNy > tissue damage infection > inflammation > tissue damage
47
Primary immunodeficiencies
abormalities of immune system genetic causes
48
Bruton's disease
X-linked agammaglobulinaemia, mutation in bruton tyrosine kinase > stop development in pre-B stage * few B cell in blood or lymph * decrease immunoglobin
49
6 Main type of immune related functional deficiency
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
Phagocytic deficiencies
Neutrophils any age e.g. Chronic granulomatous disease and leukocytes adhesion deficiency
51
Chronic granulomatous disease
impact neutrophil phagocytosis and dectruction of pathogen
52
IGAM in CoV19
IgM: First responder IgA: in mucous secretion (where CoV enters) IgG: isotype switching occurs later
53
3 different spike protein
RBD S1 Ectodomain(S2P)
54
spleen and Lymph nodes in COVID-19
germinal centres lost in lymph and spleen (isotype switch) loss of white pulp in spleen (where T&B cells are )
55
Biphasic course for COVID 19
1. viral 2. host inflammatory

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