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Host Defense Exam 2 > Manipulation of the Immune Response > Flashcards

Manipulation of the Immune Response Flashcards

1
Q

Why are multiple vaccinations “boosters” needed?

A

Vaccines often don’t stimulate the immune system strongly enough to confer protective immunity. Each booster leads to a greater and longer lasting response by the immune system

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2
Q

What is the composition of DTaP?

A

Diphtheria toxoid, tetanus toxoid and an inactivated pertussis bacteria

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3
Q

What is the advantage of combining the pertussis bacteria with the diphtheria and tetanus toxoids?

A

The presence of the bacteria stimulates an improved response to the toxins (presumably by upregulating B7 expression by antigen presenting cells).

Side effect: it produces more inflammation and discomfort at the site of injection

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4
Q

Name 4 different antigen sources for vaccines

A

Killed/inactivated pathogen
Toxoid
Viral subunits
Live attenuated virus

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5
Q

What type of immunity must be produced for intracellular infections?

A

Cell mediated immunity

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6
Q

What type of cytokine must be produced for fungal infections?

A

IL17

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7
Q

What type of response must be generated against toxins and organisms that resist phagocytosis?

A

B cell responses

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8
Q

What type of response must be generated against viruses?

A

Both T and B cells should coordinate to fight off viruses

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9
Q

What are the pros and cons of dead/inactivated pathogens?

A

Pros: safe, more stable than attenuated antigens
Cons: Weaker cell mediated response, boosters required + sometimes contaminants are present

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10
Q

What are the pros and cons of live attenuated pathogen vaccines?

A

Pros: better cell-mediated responses
Cons: Reversion- risk of infecting immunocompromised people, less stable

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11
Q

What are the pros and cons of using molecular components for a vaccine?

A

Pros: no living pathogen, very stable
Cons: fewer epitopes, weaker cell mediated response

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12
Q

What is the “basic tenet of tumor immunology”?

A

Malignant cells are “different” and can be recognized by immune cells. Malignant cells can be attacked by immune effectors thru recognition of tumor associated antigens which are; mutant proteins, overexpressed proteins or modified “altered-self” proteins

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13
Q

If the immune system can recognize and destroy tumor cells, then why does cancer grow?

A

Either 1) the tumor cell is not recognized by the immune system or 2) it has developed a mechanism to thwart activation of an immune response to it

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14
Q

What makes up tumor antigens?

A

Tumor antigens are usually self-proteins modified or selectively over-expressed by a tumor

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15
Q

What is GP-100?

A

GP-100 is the melanocyte specific antigen- antibodies against GP-100 will eliminate all melanocytes (both melanoma and healthy melanocytes)

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16
Q

Name three vectors for the delivery of tumor-specific antigens

A

1) Retroviral
2) Conventional adjuvants (alum)
3) Dendritic cells

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17
Q

Tumor cells are poorly immunogenic so immunogenicity must be increased. Name three methods to increase the immunogenicity of tumors

A

1) Addition of adjuvants
2) Use of gene-engineered tumor cells - cytokines
3) Co-stimulatory molecules B7

18
Q

What are the cell mediated immune responses against tumor cells?

A

CD4+ T cells: produce cytokines and help CD8+ T-cells and B cells with their effector function

CD8+ T cells: direct lysis/killing of antigen-expressing cells

19
Q

What are the B cell -mediated immune responses against tumor cells?

A

Ab production

20
Q

What are the granulocyte-mediated immune responses against tumors?

A

Ab-dependent cytotoxicity (ADCC)

21
Q

What are the macrophage-mediated immune responses against tumors?

A

Cytokine-induced killing

Antibody-dependent cytotoxicity

22
Q

What are the natural-killer cell-mediated immune responses against tumors/

A

Direct lysis of tumor cell targets

Ab-dependent cytotoxicity

23
Q

What are the cytokine-mediated immune responses against tumors?

A

Direct tumor killing (TNF-alpha)

24
Q

What are the antibody-mediated immune responses against tumors?

A

coating of tumor cells –> Antibody-dependent cytotoxicity

25
Q

How does “antigenic loss” allow tumors to escape immune killing?

A

Downregulation of recognizable antigen targets means that CD4+ and CD8+ T cells cannot recognize the tumor any longer and mount a response against it

26
Q

Other than downregulation of specific antigens, how can a tumor cell evade recognition by the immune system?

A

Loss of MHC class I/antigen processing

  • MHC class I expression
  • TAP etc (for processing/loading)
  • Loss of CD8+ T cell recognition
27
Q

What can tumor cells secrete to avoid the immune system?

A

Inhibitory cytokines

-TGFbeta, IL-10, DCs, T regs

28
Q

What is Rituximab?

A

Anti-CD20 monoclonal antibody
Eliminates B-cell lymphoma cells expressing CD20. Works synergistically with chemo or radiation

Recognizes B cell marker regulating B cell activation, induces growth arrest and apoptosis in vitro

29
Q

What is herceptin?

A

Anti-Her2 monoclonal antibody
Works synergistically with radiation therapy
Recognizes EGF-like receptor regulating cellular proliferation (ERBB2) and induces growth arrest and apoptosis in vitro

30
Q

What are TILs?

A

Tumor infiltrating lymphocytes

31
Q

How are TILs generated?

A

Culture lymphocytes with tumor fragments to sensitize them against the tumor antigens, infuse back into patient

You are infusing the patient’s own T-cells so reactivity is not a problem

32
Q

TILS are most effective against what type of tumors?

A

Highly immunogenic tumors- melanoma in particular

33
Q

What is the main drawback of TILs?

A

Lack of persistence of transferred cells –> only confers passive immunity

34
Q

What are the four components of a CAR T cell?

A

Variable region of the heavy chain
Variable region of the light chain
CD8+ transmembrane region
CD3+ signaling component (zeta subunit)

These are all combined in a retroviral vector

35
Q

Describe the production of CAR T cells

A

1) Leukocytes are collected from donor blood
2) T cells are transfected with the chimeric receptor retrovirus and activated
3) Cells are grown/expanded
4) Cells are selected for a re-transfused into the patient

36
Q

How do CAR-T cells kill their target cells?

A

CAR’s recognize antigen on the tumor cells, are activated and induce apoptosis through the death receptor pathway, release pro-inflammatory cytokines, and release cytotoxic granules

37
Q

What are the two immune checkpoints that tumors have co-opted to down regulate the immune response to a tumor?

A

CTLA-4 and PD-1

38
Q

How can antibodies against CTLA-4 and PD-1 help in tumor destruction?

A

Tumor cells express CTLA-4 and PD-1 to block the activation of T-cells.

Antibodies against CTLA-4 and PD-1 block this and the T cells are activated normally now

39
Q

What are CTLA-4 and PD-1 usually used for?

A

They are checkpoints to prevent over-reaction

They act on T cells and NK cells

40
Q

What is PD-1? Where is it normally expressed?

A

PD-1 = Programmed cell death protein-1

Expressed on T-cells

41
Q

What is the normal purpose of PD-1? How is co-opted by tumor cells?

A

PD-1 binds two ligands- PD-L-1 and PD-L-2

PD-1 functions as an immune checkpoint, playing an important role in down regulating the immune response by preventing the activation of T-cells and by promoting apoptosis

Normal homeostasis, PD-1 reduces autoimmunity and promotes self tolerance. However, tumors can upregulate PD L1/2 on their surface, neutralizing cytotoxic T cell tumor attack

42
Q

What is Nivolumab

A

Mab against PD-1

Host Defense Exam 2 (11 decks)

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