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Immunology 7070 > Lecture 10 - Rouff > Flashcards

Lecture 10 - Rouff Flashcards

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1
Q

Define transplantation.

A

The process of taking cells, tissues, or organs (called a graft) from one individual and placing them into a different individual.

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2
Q

How long have tissue transplants been performed?

A

Since the 1940s

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3
Q

What are the three kinds of graft types?

A

Syngeneic
Allogeneic
Xenogeneic

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4
Q

What is a syngeneic graft?

A

When the donor and recipient are identical to one another like with identical twins or inbred mouse strains.

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5
Q

What is an allogeneic graft?

A

Where the donor and recipient are from the same species but are different genotypes.

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6
Q

What is a xenogeneic graft?

A

Where the donor and recipient are from different species

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7
Q

What is the main concern when transplants are performed? What is the main factor in this problem?

A

Transplant rejection.

The immune response of the recipient to the donor tissue.

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8
Q

By which immune system is graft rejection mediated?

Why?

A

The adaptive immune system.
It is specific.
It develops a memory.
It depends on lymphocytes.

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9
Q

What evidence is there to show that graft rejection is an adaptive immune response?

A

Prior exposure to donor MHC molecules leads to a faster graft rejection.
Ability to reject a graft can be transferred between individuals via lymphocytes from a sensitized individual.
Depletion or inactivation of T cells results in reduced rejection rates.

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10
Q

How can graft rejection be ‘inherited’?

A

The MHC is heritable and it is on the MHC that the rejection takes place.

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11
Q

How do leukocytes recognize allografts?

A

T cells recognize the MHC (HLA) and since they are set to recognize non-self they recognize the non-self MHC.

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12
Q

What, specifically, do T cells recognize directly in an allogenic graft? Which T cells can do this?

A

The unprocessed allogenic MHC molecule.

CD8 and CD4

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13
Q

What, specifically, do T cells recognize indirectly in an allogenic graft?

A

The processed peptide of allogenic MHC molecule bound to self MHC molecule on host APC. Only CD4+ T cells. CD8s cannot do indirect recognition.

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14
Q

How do CD4+ T cells directly damage the allograft?

A

They release cytokines to damage the graft by delayed-type hypersensitivity (type IV).

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15
Q

How can we assess T cell mediated response to a graft before transplant?

A

Mixed lymphocyte reaction (MLR).

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16
Q

What is mixed lymphocyte reaction?

A

MLR is when T cells from one individual are cultured with the leukocytes from another. The magnitude of T cell response in the reaction is proportional to the extent of the MHC difference between the two individuals.

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17
Q

What are the kinds of graft rejections?

A

Hyperacute
Acute
Chronic

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18
Q

Describe hyperacute graft rejection and its mechanisms.

A

Activates complement system and causes tissue damage, inflammation, and thrombosis. Occurs within minutes due to preformed antibodies to either blood groups or prior exposure to alloantigens.

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19
Q

How can you avoid hyperacute graft rejection?

A

Pretest donor for blood type and antibodies.

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20
Q

Describe acute graft rejection and its mechanisms.

A

Alloreactive antibodies or CD8+ T cells cause parenchymal damage, interstitial inflammation, and endothelialitis. Occurs within days or weeks and is the principal cause of early graft failure.

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21
Q

What roles do alloantigens play in acute rejection?

A

B cell recognition of alloantigens
Antigen presentation to CD4+ cells
Alloantigen specific antibody production

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22
Q

Describe chronic graft rejection and its mechanisms.

A

CD4+ T cells release cytokines to cause chronic delayed type hypersensitivity and intimal smooth muscle cell proliferation causing a tightening of blood vessels in the graft. This can take months to years to occur.

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23
Q

What kinds of therapies are there against graft rejection?

A

Mostly immunosuppressive strategies.

  • Block lymphocyte proliferation
  • Deplete T cells by promoting phagocytosis or complement-mediated lysis
  • Inhibit T cell activation
  • Block T cell cytokine production/expansion
  • Inhibit macrophage cytokine secretion
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24
Q

Which drug is commonly used to treat graft rejections by blocking T cell cytokine production and expansion?

A

Cyclosporine A

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25
What can happen to a recipient of poorly matched blood donations?
The preformed antibodies in the recipient will bind to the donor cells and activate the complement system leading to massive cell lysis. The RBCs etc. migrate to the liver, spleen, and kidneys causing failure and intracellular coagulation which can be life threatening
26
Who is the universal blood donor? | Who is the universal blood acceptor?
O- | AB+
27
What does bone marrow contain that makes it a highly sought after transplant? What does it treat?
hematopoietic stem cells (HSCs) that can be used to treat leukemia and hematopoietic defects (like sickle-cell)
28
What can happen in the recipient if they receive a poorly matched bone marrow transplant?
The T cells from the DONOR GRAFT will attack the recipient tissues leading to graft versus host disease.
29
How many new cases of cancer are there per year?
In 2010 it averaged about 90,000 cases/yr, most resistant to treatment
30
What are the four major types of cancer?
Carcinoma Sarcoma Leukemias Lymphoma/myeloma
31
What is carcinoma? What percentage of cancers are carcinomas?
A cancer arising from epithelial tissue such as glands, breasts, skin, and linings of urogenital, digestive and respiratory cancers (89.3% of all cancers)
32
What is a sarcoma? What percentage of cancers are sarcomas?
A solid tumour of the muscles, bone, and cartilage that arise from embryological mesoderm (1.9% of all cancers)
33
What is leukemia? What percentage of cancers are leukemias?
A disease of the bone marrow causing excessive production of leukocytes (3.4% of all cancers)
34
What is lymphoma/myeloma? What percentage of cancers do they encompass?
Disease of the lymph nodes and spleen that cause excessive production of lymphocytes (5.4%)
35
What kind of factors can contribute to the etiology of cancer?
Genetic and environmental factors
36
Name some genetic factors that may contribute to the higher likelihood of getting cancer.
Mutations Tranlocations Amplification Altered proliferations (any changes in cell proliferation)
37
Name some environmental factors that may contribute to the higher likelihood of getting cancer.
``` UV light Chemicals Viral infections Alterations in tumor suppressor genes Conversion of proto-oncogenes to oncogenes ```
38
What kind of cells initiate cancer?
Virtually any cell in the body can act as a cancer initiating cell.
39
How does the immune system detect cancer cells?
Some lymphocytes are able to infiltrate (better response to treatment). While the cancer is usually self initiated and we cannot really recognize self studies show that immunodeficient mice exhibit higher rates of spontaneous and chemcially induced tumours showing that our bodies may get cancer and be rid of it before we know.
40
How does the immune system control tumor cell growth?
T cell immune responses are tumor antigen specific.
41
What are the different types of tumour antigens?
Mutated self protein Product of oncogene/mutated tumor suppressor gene Overexpressed/aberrantly expressed self protein Oncogenic virus
42
What kinds of mutated self proteins would the immune system recognize?
Mutations mediated by carcinogens/radiation | Mutations in the MHC (recognized as foreign)
43
What kinds of oncogene product proteins would the immune system recognize?
Mutates Ras, Bcr/Abl or mutated p53 (tumor suppressor)
44
What kinds of overexpressed/aberrantly expressed self proteins would the immune system recognize?
Overexpressed normal proteins like Gp100 or tyrosinase (found in melanomas) Cancer-specific antigens (MAGE, PSA)
45
What kinds of oncogenic viral proteins would the immune system recognize? How does the immune system recognize these?
Papilloma virus E6 and E7 EBNA viral proteins in EBV lymphomas Hep B in liver cancer Immune system already recognizes them as foreign
46
How does the innate immune system respond to tumors? Why is this important?
NK cells and macrophages can kill cultured tumor cells without Ag specificity. This is important when tumor cells do not express MHC molecules.
47
Describe adaptive immune surveillance of cancers.
CD8+ T cells patrol the body and recognize oncogenic viral proteins or mutant proteins in association with MHC-I molecules.
48
What components do CD8+ T cells need in order to act against the tumor antigens?
CD8+ T cells APCs CD4+ T cells Co-stimulatory cytokines
49
What is cross priming and the anti tumor T cell response?
Tumor cells and antigens are ingested by an APC which is able to present to both CD4 and CD8 cells. The CD4+ cells are able to release cytokines IL2 and 21 which allow CD8+ differentiation of tumor specific T cells.
50
There are often tumor variants in the human body which are kept in check by the immune system. What would need to be suppressed in order to allow these to proliferate further?
T cell and IFN gamma suppression would allow them to grow more rapidly.
51
What are the three Es of cancer?
Elimination - cancer surveillance Equilibrium - cancer persistence Immune Exhaustion - cancer overcoming the immune system
52
What kind of mechanisms can cancer use to escape the immune system?
``` Reduction of immunogenicity Tolerizing T cells Antigenic modulation Tumor-induced immune suppression Tumor-induced privileged site ```
53
How does cancer lower the body's immunogenicity?
By mutating host molecules like p53 or MHC-I so T cells do not recognize the antigen.
54
How does cancer tolerize T cells?
Tumor antigen is treated as self antigen and APCs take up and present 'self' without costimulation creating anergic response.
55
How does cancer modulate antigens?
Antibodies against tumor antigens induces endocytosis and degradation of the Ag. Immune selection of antigen-loss variants is the result.
56
How does cancer suppress the immune system via tumors?
Tumors secrete factors like TGFbeta (an anti-inflammatory cytokine) which directly inhibits T cell function and suppresses it.
57
How does cancer create tumor-induced privileged sites?
Tumors secrete factors that create physical barriers via matrix factors. The immune system loses physical access to tumors.
58
How can immunotherapy be used against cancers?
Monoclonal antibody therapies | Vaccines
59
How are monoclonal antibodies used against cancers?
Anti CD20 antibodies can treat B cell malignancies Anti Her2/Nue to treat breast cancer (overexpressed in tumors) Anti VGF to treat colon cancer
60
How are vaccines used to treat cancer?
Works against tumors caused by oncogenic viruses
61
Which two viruses have vaccines to avoid cancer proliferation?
Hepatiti B and HPV
62
What is one of the new ways that people are trying to inhibit cancer cell proliferation?
Checkpoint inhibitors for PD-1, PD-L1, and CTLA-4

Immunology 7070 (15 decks)

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