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Host Defense Exam 2 > Manipulations of the Immune System > Flashcards

Manipulations of the Immune System Flashcards

1
Q

Contrast active and passive immunity.

A 
active = activates immune response; immunological memory
passive = direct transfer of antibodies; no memory
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2
Q

Why are boosters needed?

A

to achieve protective levels of immunity, requires 3 exposures

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3
Q

What are the components of the DTaP vaccine?

A
  • diphtheria
  • tetanus
  • acellular pertussis
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4
Q

Describe the role of pertussis bacteria in the DTaP vaccine.

A
  • adjuvant
  • upregulates B7 on APCs
  • increased inflammation and pain at site of injection
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5
Q

Define inactivated vaccine.

A
  • toxins/pathogens are killed by heat or chemicals
  • epitopes maintained, but cannot reproduce in the host
  • requires boosters
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6
Q

List some requirements for safe vaccines.

A
  • low toxicity
  • herd immunity
  • long lasting immunity (boosters)
  • inexpensive
  • induces immune response (antibodies, T cells)
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7
Q

List antigen sources for vaccines.

A
  • killed/inactivated
  • toxoid
  • viral subunit
  • live attenuated
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8
Q

What type of immune response is required for intracellular infections?

A

TMMI (Cell Mediated)

- think: Th1, IFNg, macrophages, proinflammatory

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9
Q

What type of immune response is required for fungal infections?

A

IL17

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10
Q

What type of immune response is required of infections that avoid phagocytosis?

A

B cells

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11
Q

What type of immune response is required for viral infections?

A

T and B cells

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12
Q

List pros and cons of inactivated vaccines.

A

Pros:

  • safer
  • more stable than attenuated

Cons:

  • weaker cell mediated response
  • boosters required
  • contains contaminants
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13
Q

List pros and cons of live attenuated vaccines.

A

Pros:
- better cell-mediated response

Cons:

  • reversion
  • causes infection in immunocompromised patients
  • measles, encephalitis
  • less stable
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14
Q

List pros and cons of vaccines using molecular components.

A

Pros:

  • very stable
  • no living pathogen

Cons:

  • fewer epitopes
  • weaker cell-mediated response
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15
Q

List some tumor antigen sources and examples.

A 
Tumor antigens are usually self-peptides that have been modified or are overexpressed
- cell-type specific
=> GP-100 (melanocytes)
=> CD33 (AML)
=> CD20 (B cells)
  • shared
    => HER2/neu (breast cancer)
  • viral
    => HPV
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16
Q

Describe specific antigen vaccines.

A
  • used for tumors with well-defined antigens
  • ex: GP100 (widely expressed in tumors)
  • delivery with adjuvant, viral vector, or through DCs
17
Q

Describe whole tumor vaccines.

A
  • must increase immunogenicity b/c tumor cells are poorly immunogenic
  • add adjuvant, cytokines, B7
  • must prime T cells in vitro
18
Q

List ways tumors evade the immune system.

A
  • downregulation or loss of antigen variant being attacked by T cell => loss of antigen-specific T cells and B cells
  • loss of MHC Class I expression, TAP (for antigen processing)
  • inhibitory cytokine release
  • downregulation of immune checkpoints CTLA4 and PD1
19
Q

Describe tumor passive immunotherapy.

A
  • antibodies against tumor cell
    => anti-CD20 for non-hodgkins lymphoma
    => anti-HER2/neu for breast cancer
  • in vitro activated T cells
20
Q

Define Rituxan.

A
  • anti-CD20 monoclonal antibody therapy
  • high response rate in B cell lymphomas
  • works synergistically with chemotherapy and radiation
  • recognizes B cell marker to regulate B cell activation
  • induces growth arrest and apoptosis
21
Q

Define Herceptin.

A
  • anti-HER2 monoclonal antibody therapy
  • works synergistically with chemotherapy and radiation
  • recognizes EGF-like Receptor (ERBB2) to regulate cell proliferation
  • induces growth arrest and apoptosis
22
Q

Define TILs.

A

Tumor Infiltrating Lymphocytes (TILs)

  • passive tumor therapy
  • patient’s T cells are isolated, activated, and retransferred
  • specific for that tumor
  • most effective for highly immunogenic tumors (can be boosted with Tumor specific antigen vaccination)
  • cons: cells don’t last forever, specificity
23
Q

Define CARs.

A

Chimeric Antigen Receptors

  • passive tumor therapy
  • infusion with modified T cells expressing genetically engineered CAR
  • components = Vh/VL from TAA antibody + TCR intracellular domains + zeta chain
  • steps: leukapheresis + transduction with CAR T cells => expansion => infusion + chemotherapy
  • activation of CAR leads to release of granzymes and proinflammatory cytokines => apoptosis induction in tumor cell
24
Q

Describe the use of CTLA4 monoclonal antibodies in tumor therapy.

A
  • Typically, CTLA4 is expressed on T cells after B7:CD28 activation to interact with B7 and inhibit immune response
  • using CTLA4 mab blocks CTLA4 from binding to B7 and allows immune response to continue (good for killing tumors)
25
Q

Describe the use of PD1 monoclonal antibodies in tumor therapy.

A

Programmed Cell Death Protein

  • Typically, PD1 binds to PD1L and PD2L to inhibit antigen-specific T cell response => prevents autoimmunity and induces T cell apoptosis
  • tumor cells upregulate PD1/2L to induce T cell apoptosis
  • PD1 mab blocks the death signal and allows T cells to continue the immune response

Host Defense Exam 2 (11 decks)

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