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ADV. Human Phys > Test 4 Study Guide Part 7 > Flashcards

Test 4 Study Guide Part 7 Flashcards

1
Q

Coreceptors:

  • Helper T-cells have which coreceptor?
  • How does this effect them?
  • Cytotoxic T-cells have which coreceptor?
  • How does this effect them?
A
  • Helper T-cells have which coreceptor?
    CD4
  • How does this effect them?
    can only be activated by MHC-2 presenting cells
  • Cytotoxic T-cells have which coreceptor?
    CD8
  • How does this effect them?
    Can only kill MHC-1 antigen presenting cells
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2
Q

What happens after T Helper cell activation by binding with a MH2?
- What molecule effects cytotoxic t-cells?

A

Turn into effective Th1, Th2 or other specialties.
B-cell differentiation into plasma cell
cytotoxic T-cell proliferation
- What molecule effects cytotoxic t-cells?
(interleukin-2)

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3
Q

FAS:

  • Stands for?
  • FASL and FAS?
  • Where will FASL be found?
A
  • Stands for?
    First Apoptosis Signal
  • FASL and FAS?
    FAS receptor on T-cells, FAS ligand activates FAS and causes apoptosis
  • Where will FASL be found?
    In a few days into infection T - cells make FASL to kill themselves
    Immune privileged sites (Eye, testes)
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4
Q

Mechanisms to defend the testes:

A

Sertoli cells have tight gap junctions.

Sertoli cells produce FASL

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5
Q

Mechanisms to defend the anterior chamber of the eye:

A

Coating of interior of the eye with FasL

Secretion of different cytokines which inhibit inflammation

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6
Q

How do tumor cells use FasL?

A

Not all but some produce it to protect them from the immune cells by triggering apoptosis of lymphocytes

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7
Q

Severe Combined Immunodeficiency Disease:

  • other name?
  • Cause of disorder:
  • Define:
A
  • other name?
    Bubble boy disease
  • Cause of disorder:
    inherited, WBC stem cells lack adenosine deaminase
  • Define:
    Lack antibody-mediated and cell-mediated immunity
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8
Q

Adenosine deamanise is involved in what condition?

A

A lack of this causes Severe Combined Immunodeficiency Disease

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9
Q

Treatment for Severe Combined Immunodeficiency Disease:

A

Gene therapy with retrovirus.

- many developed leukemia

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10
Q

Infection with one disease protects from another closely related one

A

Cross reactive immunity:

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11
Q

Edward Jenner and cow pox (vaccinia) vaccine:

A

Milk maid exposed to cowpox -> immunity to small pox

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12
Q

Edward Jenner and cow pox (vaccinia) vaccine:

A

Milk maid exposed to cowpox -> immunity to small pox

Innoculate orphan with vaccinia (cow pox) -> infect small pox -> protected orphan

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13
Q

Louis Pasteur anthrax vaccine:

A

Heated anthrax -> lost virulence (attenuated), antigenicity maintained -> inoculated sheep -> they survived

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14
Q

Four types of adaptive immunity:

A

Naturally acquired active immunity
Naturally acquired passive immunity
Artificially acquired active immunity
Artificially acquired passive immunity

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15
Q

Naturally acquired active immunity:

A

Get infected and recover

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16
Q

Naturally acquired passive immunity:

A

Placenta: IgG transfer into plasma

Breast Feeding: IgA and some IgG into gastrointestinal tract (does not enter circulation from GI tract!)

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17
Q

Artificially acquired active immunity:

A

Vaccination

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18
Q

Artificially acquired passive immunity:

A

Gamma globulin shots (IgG injection)
Intravenous immunoglobulin
Antiserum/antitoxin (target and neutralize a toxin)
Antivenom shots (antitoxin)
RhoGam (Rh system, antibodies against big D antigen)

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19
Q

Response time:

  • Primary response:
  • Secondary response:
A
  • Primary response:
    5 - 10 days
  • Secondary response:
    ~ 2 hours
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20
Q

Secondary response is dependent on what?

A

Memory B cells
Memory T cells (lesser extent?)
NOT CAUSED BY RESIDUAL ANTIBODIES, exists without them

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21
Q
  • B- cells inherent there specificity in a massive library
  • Each B cell produces one of these antigen options
  • When the B-cell finds the antigen it is specific for, it multiplies
  • These progeny/clones become plasma cells and memory cells, which respond to infection
A

Clonal Selection Theory:

22
Q

What are the most abundant lymphocytes in adult?

When do these lymphocytes reduce in levels?

A

Long-lived T cells of different subtypes, specific for the antigen that caused their generation
About age 70

23
Q

Germinal centers:

- Formation:

A
  • Formation:

B-cell is activated, becomes the center of a massive dividing group of clones, both b memory cells and plasma cells

24
Q

Advantages of germinal centers:

A

Somatic hypermutation occurs here
Plasma cells are longer lived
Plasma cells have faster replication
Plasma cells have better antibody production

25
Q

Somatic hypermutation:

A

Occurs in germinal centers. An activated B cell has a higher mutation rate as it continues to divide.
This results in plasma cells which make antibodies which are either slightly more or less effective against the invader

26
Q

Vacca:

A

Latin for cow.

Start of vaccination because of cow pox

27
Q

Salk vaccine:

A

1st polio vaccine
inactivated virus
- Only inactivated salk type vaccines are used in the US

28
Q

Sabin vaccine:

A

Oral live attenuated polio vaccine. Caused about 100 polio cases a year in the US, but is no longer used

29
Q

Three ways to make a vaccine:

A
  • Live viruses (attenuated virulence):
  • Killed virulent viruses:
  • Recombinant viral proteins
30
Q

Adjuvants:

- How do they work?

A

Act as PAMPs or DAMP to bind to pathogen recognition receptors of dendrites.
Enhances adaptive immune response.
Therefore enhances vaccine ‘strength’

31
Q

Fetal self recognition:

A

Fetus originally capable of targeting self antigens.

Continuous exposure early in fetal and postnatal life results in toleration of an antigen

32
Q

Antibodies targeting the body are called?

T-cells targeting the body are called?

A

Autoantibodies

Autoreactive T cells

33
Q

Mechanisms of self-antigen removal:

A
  • Clonal Deletion:
    lymphocytes recognizing self-antigens are destroyed
  • Clonal Anergy:
    lymphocytes recognizing self-antigens are prevented from becoming inactive (regulatory t cells)
34
Q

Thyroid gland:

  • Imune privilege status?
  • Protein that is hidden self antigen:
A
  • Imune privilege status?
    Immune privileged
  • Protein that is hidden self antigen:
    Thyroglobulin
35
Q

Central Tolerance:

  • Define:
  • Controlled by:
A
  • Define:
    Regulation of potential self targeting lymphocytes in thymus or bone marrow.
  • Controlled by:
    Apoptosis, clonal deletion, or anergy
36
Q

Peripheral Tolerance:

  • Define:
  • Controlled by:
A
  • Define:
    Regulation of potential self targeting lymphocytes outside thymus or bone marrow.
  • Controlled by:
    Anergy (provided partly by regulatory T lymphocytes)
37
Q

Forbidden clones:

A

Auto-reactive T Cells, which are kept in check by regulatory T cells.

38
Q

Person’s ability to develop active immunity is called:

A

Immunological competence

39
Q

Immunological competence:

  • When does it occur?
  • What helps in the meantime?
  • What might happen if immune competence occurred in utero?
A
  • When does it occur?
    ~1 month post-parturition
  • What helps in the meantime?
    Passive immunity from IgG that crosses the placental
  • What might happen if immune competence occurred in utero?
    Fetus could target mom
40
Q

The fetus is immune to the same antigens as the ____:

How long is breast feeding recommended?

A

Mother

Exclusively breast milk for 6 months at least (then it can continue)

41
Q

Intravenous immunoglobulin:

  • Source:
  • Example of:
  • Treats:
A
  • Source:
    Pooled plasma from thousands of people.
  • Example of:
    Artificial passive immunity
  • Treats:
    First used: combat microbial infections in immunodeficient individuals
    Now used: Treat autoimmune conditions, immuno-comprimised cancer patients
42
Q

Polyclonal antibody:

  • What is it?
  • Why/how is it made?
A
  • What is it?
    Antibodies in a variety of specificities, some of which have optimal specificity, others of which have poorer specificity
  • Why/how is it made?
    Due to somatic hypermutation activated B cells undergoing clonal expansion will produce slightly modified forms. Some with higher affinity and some with low. Polyclonal antibodies include all of these.
43
Q

Monoclonal antibodies:

  • What is it?
  • Three letter designation:
  • Why/how is it made?
A
  • What is it?
    Pure antibody with optimal antigenic specificity
  • Three letter designation:
    MAB
  • Why/how is it made?
    Myeloma and plasma cell -> fused -> form hybridoma -> immortalized cell line producing monoclonal antibody
44
Q

Hybridoma:

A

Immortalized plasma b cell for antibody production.
Made by:
- myeloma (cancerous cell) fused with plasma B cell

45
Q 
- Define:
monoclonal antibody against HER2 receptors of invasive breast cancers
- Treats:
invasive breast cancers
- Is a type of:
Artificially acquired passive immunity
A

Herceptin:

  • Define:
  • Treats:
  • Is a type of:
46
Q

Avastin:

  • Define:
  • Treats:
  • Is a type of:
A 
- Define:
monoclonal antibody which block VEGF (vascular endothelial growth factor) from binding to its receptors
- Treats:
Cancer. Colorectal, lung, kidney, brain.
- Is a type of:
Artificially acquired passive immunity
47
Q

Natural Killer Cells:

  • Target:
  • Mechanism of action:
  • Inhibitory receptors:
A
  • Target:
    Cancer/virus (
  • Mechanism of action:
    (receptor recognition mechanism unexplained, but does not use MHC)
    Cell-mediated (perforins and granzymes)
    Destroy on sight, no delay for verification
  • Inhibitory receptors:
    MHC inhibits them, stopping them from killing normal host cells.
48
Q

How do NKCs get reinforcements?

A

Cytokine release to bring in acquired immune cells

49
Q

Three categories of disease of the immune system:

A

Autoimmune diseases
Immune complex disease
Allergy (hypersensitivity)

50
Q

Who gets autoimmune diseases more often?

- Why?

A

Women
2x as likely as in men
- Why?
Andy thinks its from escaped fetal cells

51
Q

Six reasons for the failure of self tolerance:

A

1: Immune system exposed to antigen not normally in circulation
2: Self-antigen combines with foreign antigen (or hapten) altering it
3: Antibodies against other antibodies
4: Antibodies produced against foreign antigens may cross-react with self-antigens.
5: Self antigens may be presented with MHC-2 complexes to helper T lymphocytes
6: Inadequate activity of regulatory (suppressor) T lymphocytes

ADV. Human Phys (51 decks)

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