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Immunology/Microbiology > Immunomodulation > Flashcards

Immunomodulation Flashcards

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1
Q

When is immunomodulation up-regulated?

A
  • cancer -> increase action of cytokines, APCs, Abs
  • infectious diseases -> increase adaptive and innate immunity
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2
Q

When is immunomodulation down-regulated?

A
  • autoimmune disease -> limit cytokine action, increase regulatory T cells, prevent T cell activation
  • transplantation -> increase regulatory T cell
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3
Q

What is tumor infiltrating leukocytes therapy?

A
  • remove T cells -> activate then -> give them back
  • can lead to bystander death
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4
Q

What is chimeric antigen receptor therapy?

A
  • inject DNA into T cells to express a receptor for specific Ag -> return T cells to patient
  • can lead to cytokine storms
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5
Q

What are the characteristics of monoclonal antibodies?

A
  • expensive to produce
  • single Ab species
  • bind to single specific site
  • recognize particular protein form
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6
Q

What are the characteristics of polyclonal antibodies?

A
  • cheap to produce
  • mixed pop. of Abs
  • bind to different areas of target
  • tolerant of small changes in protein structure
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7
Q

What is the main difference between cancer treatment vaccines and normal vaccines?

A

cancer vaccines are meant to treat NOT PREVENT

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8
Q

How are cancer treatment vaccines made?

A

from tumor, tumor-associated Ags, & dendritic cells

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9
Q

Where do the antibodies and effector cells bind in antibody-dependent cell cytotoxicity?

A
  • Abs bind to Fab region
  • effector cells bind to Fc region
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10
Q

What are immune checkpoints in immunotherapy?

A

slow down immune response

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11
Q

What are the types of immunotherapy?

A
  • immune checkpoints
  • T-cell transfer therapy
  • monoclonal Ab
  • treatment vaccine
  • immune system modulator
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12
Q

What are examples of immune checkpoints?

A
  • CTLA-4 on T cells -> binds to B7 on APCs
  • PD-1 on T cells-> binds to PD-1L on tumor cells
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13
Q

What can happen if CTLA-4 and PD-1 are inhibited?

A

increase immune response

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14
Q

What are the 2 types of T cell transfer therapy?

A

tumor infiltrating leukocytes (TIL) & chimeric antigen receptor (CAR)

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15
Q

What is TIL therapy?

A
  • remove T cells, activates them, returns to patient
  • can cause bystander death
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16
Q

What is CAR therapy?

A
  • remove T cells, inject DNA into T cells to express receptor for specific Ag, returned to patient
  • can lead to cytokine storms
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17
Q

What is a monoclonal antibody?

A
  • expensive to produce
  • single Ab species
  • only bind single specific site
  • recognize particular protein form
18
Q

What is a polyclonal antibody?

A
  • cheap to produce
  • mixed population of Abs
  • bind to different areas of target
  • tolerates small changes in protein structure
19
Q

How are cancer treatment vaccines different from other vaccines?

A

meant to treat disease not prevent it

20
Q

How can cancer treatment vaccines be made?

A
  • patient tumor
  • tumor associated Ags
  • patient dendritic cells
21
Q

How can you decrease the immune response?

A

increase action of CTLA-4

22
Q

What is antibody-dependent cell cytotoxicity?

A
  • Ab bind to target at Fab region -> effector cells bind to Fc region
  • release cytotoxic granules to induce apoptosis
  • ex: perofrins & granzymes
23
Q

What occurs in the initiation classical complement system?

A
  • IgM or IgG bind to microbes
  • some microbes lyse or are killed by infiltrating cells
24
Q

What is neutralization?

A
  • Abs block/neutralize inefectivity of microbes -> prevent infection/spred
  • Abs block action of microbial tocins
25
Q

What is opsonization?

A
  • enhance phagocytosis by coating microbes
  • important with encapsulated bacteria
26
Q

What are superantigens?

A
  • toxin
  • released by bacteria that bind MHC class 2 and TCR
  • results in massive cytokine release
  • NOT processed internally -> act on OUTSIDE of cells
27
Q

What are the characteristics of protein M?

A
  • produced by strepto. pyogen
  • highly anti-phagocytic and prevents C3b from binding
  • B cells bind to ti -> only IgM response
28
Q

What are the characteristics of protein A?

A
  • produced by staphy. aureus
  • prevents IgG from binding
29
Q

What is involved in anti-viral immunity?

A
  • innate: interferon & matural killer cells
  • adaptive: Abs & CD8+ T cells
30
Q

What is viral immune evasion?

A
  • some viruses down-regulate MHC class 1
  • herpes has factors to block cytokines & interfere with TAP
  • HIV causes immunosuppression by destroying CD4+ T cells
31
Q

What are some repsonses to viruses that can cause disease?

A
  • rhino & influenza -> increased cytokines leads to fever
  • coxsackie B & epstein-barr virus -> autoimmune diseases
32
Q

What is the role of innate response in anti-fungal immunity?

A

neutrophils & macrophages phagocytize fungi

33
Q

What is the role of adaptive response in anti-fungal immunity?

A
  • CD4 T cells destroy fungi
  • TH1 response -> protective
  • TH2 response -> exacerbate infections
34
Q

What is the response for protozoa & worms?

A
  • protozoa (unicellular) -> TH1
  • worms (multicellular) -> TH2
35
Q

What role does plasmodium play in parasite immune evasion?

A
  • antigenic variation
  • induction of blocking Abs
36
Q

What role does trypanosoma cruzi play in parasite immune evasion?

A

bind to macrophages & inhibit IgM production

37
Q

What is severe combined immunodeficiency (SCID)?

A
  • defect in both T & B cells maturation
  • difficulty with humoral immunity and CMI
38
Q

What is DiGeorge Syndrome?

A
  • defect in T cell maturation
  • difficulty with viral infections
39
Q

What is Bruton agammaglobulinemia?

A
  • defect in B cell maturation
  • difficulty with extracellular bacterial infections
40
Q

What is chronic granulomatous disease?

A
  • increased bacterial infections
  • phagocytic cells can phagocytize pathogens but NOT kill them
41
Q

What is lymphocyte adhesion defiency disease?

A
  • increased bacterial infections
  • phagocytic cells work but NOT leave the vessel

Immunology/Microbiology (18 decks)

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