Ch. 17 - Adaptive Immunity: Specific Defenses of the Host Flashcards

1
Q

Describe Adaptive Immunity
(AKA? When does it develp? How is it aquired? Recognition, memory, immune response, line of host defense)

A
  • AKA: “Specific” Defenses of the Host
  • Develops later in life to handle a specific microbe
  • Aquired through infection or vaccination (results in immune response)
  • Specific recognition and response to a specific microbe
  • Has immunological memory
  • Slower Immune response
  • Consists of 3rd line host defenses
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2
Q

Define: Immunology

A

study of host defenses against foreign substances (antigens)

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3
Q

Define: Antigen (Ag)
Provide examples

A

substance that stimulates a certain immune reponse in the form of antibody production
- pathogens, foreign substances, vaccines (injection of a foreign particle)

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4
Q

Define: Antibody (Ab)

A

protective/globular proteins (quartenary structure) made by the host in reponse to certain antigens

AKA “immunogoblins” (Ig)

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5
Q

What cell(s) are involved in adaptive immunity?

A

B cells and T cells (Lymphocyte <- Agranulocyte)

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6
Q

Compare Humoral Immunity from Cell-Mediated (Cellular) Immunity
Include function and examples

A

Humoral Immunity
- attacks antigens OUTSIDE the cell (extracellular Ag)
- ex: extracellular pathogens, toxins (in the blood)

Cell-Mediated (Cellular) Immunity
- attacks antigens that ENTERED the cell (intracellular Ag)
- ex: animal viruses present inside host cell

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7
Q

TRUE or FALSE: The Humoral Immune Response and Cell-Mediated Immune Response do NOT work together.

A

False, both of them work together to help rid of the Ag

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8
Q

Compare the Humoral Immune Response from the Cell-Mediated (Cellular) Immune Response

A

Humoral Immune Response

  • involves B cells (B cell -> plasma cell -> Ab)
    -> indirectly make antibodies (Ig) that help destroy antigens (Ag)

Cell-Mediated (Cellular) Immune Reponse

  • produces T cells
    -> recognizes part of antigen (that got fragmented) by phagocyte and migrated to surface -> destory antigen
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9
Q

Describe the development of B cells and T cells

A

Both derive from Stem cell (parent cell)

If stem cell passes through red bone marrow = B cell
If stem cell passes throguh thymus = T cell

Both B and T cell will migrate to lymphoid tissue (speen, lymph nodes)

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10
Q

Which immune response is being turned on if antibodies are being produced?

A

Humoral Immunity

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11
Q

Antigens are substnaces that cause the production of ______

A

antibodies (Ig)

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12
Q

Generally describe the structure of antigens (Ag)

hint: what is on an antigens surface?

A

Antigens (Ag) have external components on its surface called, antigenic determinants, which antibodies (Ab) interact and bind to

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13
Q

Antibodies ________ and interact with ___________ _________ of the antigen and will bind to the antigen to form the _________________

A

recognize
antigenic determinants
Ag-Ab complex

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14
Q

TRUE or FALSE: Antibodies directly destroy antigens

A

False, antibodies DO NOT destroy the antigen, but will help by tagging the antigen for destruction

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15
Q

Describe the structure of an Antibody (Ab)

A

four protein subunits form a “Y shape”
-> two identical light chains and two identical heavy chains joined together

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16
Q

Compare the Variable Region from the Constant Region of Antibodies (Ab)

A

Variable Region
- located at end of arms (arms = variable)
- is the part that binds to antigenic determinants

Constant Region
- is the stem
- five classes of Ig: IgG, IgM, IgA, IgD, IgE

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17
Q

Describe this immunoglobulin class: IgG

(Include: Structure, Location, Characteristics, Function)

A

Structure:
- Monomer (1 unit)

Location:
- Blood
- Lymph
- Intestine

Characteristics:
- Long-lived = several (3) weeks (other Ig only few days)
- Crosses placenta via Transplacental Passage
-> Mom can give her IgG to fetus, which helps with survival

Function:
- Long term protection
- Enhances phagocytosis
- Neutralizes toxins and viruses

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18
Q

Describe this immunoglobulin class: IgA

(Include: Structure, Location, Function)

A

Structure:
- Dimer in secretions (2 unit), and sometimes Monomer

Location:
- Mucous membrane surfaces
- Secretions (tears, saliva, breast milk)

Characteristics:
- x

Function:
- Prevents microbial attachment of pathogens to mucous membranes (attach to pathogen before they can attach to mucous membrane and cause disease)

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19
Q

Describe this immunoglobulin class: IgM

(Include: Structure, Location, Characteristics, Function)

A

Structure:
- Pentameter (5 units)

Location:
- Blood

Characteristics:
- Largest antibody (Ab)

Function:
- Primary response to infection; first antibody to be made
- Causes agglutination (clumping) of pathogen
-> to gather pathogen in one area for efficient phagocytosis

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20
Q

Describe this immunoglobulin class: IgD

(Include: Structure, Location, Function)

A

Structure:
- Monomer

Location:
- Blood
- Lymph
- B cells

Characteristics:
- x

Function:
- May be involved in self-tolerance
-> ability to tolerate yourself so you don’t attack yourself
-> vs. loss of cell tolerance = your immune system attacks you = autoimmunity

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21
Q

What can be said about the stage of infection (is it late or early) if a patients blood results show high IgM and low IgD?

A

If high in IgM, it indicates that it is an new infection because IgM are the first antibodies to be made due to first time exposure to an Ag/vaccination (primary immune reponse)

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22
Q

Describe this immunoglobulin class: IgE

(Include: Structure, Location, Function)

A

Structure:
- Monomer

Location:
- On Mast cells
- On Basophils
- Blood

Characteristics:
- x

Function:
- Causes release of histamine from mast cells/basophils (allergies)
- Destruction of parasitic worm infections

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23
Q

Name the order of immunoglobulins (antibodies) from most abundant to least abundant found in the BLOOD

A

IgG

IgA

IgM

IgD

IgE

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24
Q

Name the order of immunoglobulins (antibodies) from most abundant to least abundant found in the BODY

A

IgA (because you have a lot of mucous membranes that line tissue)

IgG

IgM

IgD

IgE

25
Q

Define: Clonal Selection

A
  • process of B cell activation
  • surface Ig on B cell surface recognizes a specific Ag (based on specific antigenic determinant) -> this B cell now gets selected
26
Q

Define: Clonal Expansion

A
  • “selected” B cell proliferates (make many copies) into clone of activated B cells that can now differentiate into:
    -> memory B cells -> plasma cells -> antibodies
    (can either become B cell or plasma cell first)
27
Q

Describe, in detail, Clonal Selection and Clonal Expansion of B cells

A
  • mature B cells contain immunoglobulins against a specific pathogen
  • surface Ig (of B cell) recognizes a specific antigen (based on specific antigenic determinant) and becomes “selected” ; Clonal Selection
  • Selected B cell will proliferate (make many copies) of the activated B cell - Clonal Expansion
  • They will either become a memory cell or plasma cell (if memory cell first, it will become plasma cell -> Ab)
  • Plasma cells secrete immunoglobulins into BV
28
Q

When an Ab binds to the antigenic determinant of an Ag it forms an Ag-Ab complex, which is also known as…

A

Immune Complex

29
Q

What can immune complex formations result in?

A

NOAAA

  • Neutralization
  • Opsonization
  • Agglutination
  • Activation of Complement
  • ADCC (Antibody-Dependent Cell Mediated Cytotoxicity)
30
Q

Describe the result of this immune complex formation: Agglutination
Include: Ig involved and How does the Ag get destroyed

A

Ig involved
- IgM

How does Ag get destoryed?
- IgM causes clumping to gather Ag in one location
-> Phagocyte can engulf them all at once

31
Q

Describe the result of this immune complex formation: Opsonization
Include: Ig involved and How does the Ag get destroyed

A

Ig involved
- IgG

How does Ag get destoryed?
- IgG coat the surface of the Ag
-> attracts phagocyte -> engulfs Ag

32
Q

Describe the result of this immune complex formation: Neutralization
Include: Ig involved and How does the Ag get destroyed

A

Ig involved
- IgG
- IgA (monomer)

How does Ag get destoryed?
- IgA (monomer) lines mucousa -> prevents Ag from attaching to mucosa
- IgG captures midstream Ag -> prevents Ag from attaching to mucosa

33
Q

Describe the result of this immune complex formation: Activation of Complement
Include: Ig involved and How does the Ag get destroyed

A

Ig involved
- IgG
- IgM

How does Ag get destoryed?
1. Immune complex forms (between IgG/IgM and Ag)
2. Complement proteins bind to stem of Ab (IgG/IgM)
3. Complement protein lyses pathogen

34
Q

What lines of defenses do you see complement proteins involved in?

A

2nd and 3rd line of defenses
(Complement System, Humoral Immunity?)

35
Q

Describe the result of this immune complex formation: ADCC (Ab-Dependent Cell-Mediated Cytotoxicity
Include: Ig involved and How does the Ag get destroyed

A

Ig involved
- IgE

How does Ag get destoryed?
1. IgE attaches to parasitic worm = immune complex formed
2. Eosinophil/macrophage/NK cell attaches to Ab stem region
3. Releases digestive enzymes on worm
4. Parasitic worm dies

36
Q

B cells destroy _______ antigens, while T cells destroy _______ antigens

A

extracellular
intracellular

37
Q

TRUE or FALSE: Tₕ cells can recognize intracellular Ag that do not migrate to the infected cells’ surface.

A

False, if an intracellular Ag is not processed and presented to the infected cell’s surface, then it can hide from the immune system. It MUST get fragmented and migrate to the cell surface for Tₕ cells to recognize it.

38
Q

Name the 5 types of T cells

A

Helper T cells (Tₕ)
Cytotoxic T cells (T꜀); AKA Killer T cells
Regulatory T cells (Tᵣ)
Delayed Hypersensitivity T cells (T𝒹)
Memory T cells

39
Q

Describe the function of this T cell: Helper T cell

A
  • activate cytotoxic T cells (T꜀) involved in CMI
  • activate memory B cell (T-dependent B cells) to produce Ab
40
Q

Describe the function of this T cell: Cytotoxic T Cell

A
  • destory target cells ON CONTACT
    ->T꜀ cell bind to infected cell (that has Ag fragment on surface)
    -> T꜀ cell releases perforin (digestive)/enzymes
    -> makes lesions and destory infected cell

AKA Killer T cells

41
Q

Describe how Helper T cells and Cytotoxic T cells work together to destory an infected host cell.

A
  • Infected host cell contains fragmented Ag on its surface
  • Helper T cell (Tₕ) binds to fragmented Ag
    -> releases cytokines
  • Cytokines activate Cytoxic T cells (T꜀)
  • Cytotoxic T cell (T꜀) attaches to the fragmented Ag on infected host cell
  • Cytotoxic T cell releases perforin/enzymes and destroy pathogen

Helper T cell MUST ATTACH FIRST AND RELEASE CYTOKINES in order for Cytotoxic T cells to activate and know where to go

42
Q

Compare T-independent cells from T-dependent cells

A

T-independent cells

  • B cells that are NOT dependent on Helper T cells to make Ab

T-dependent cells

  • B cells that ARE dependent on Helper T cells to make Ab
    -> B cell must be activated by Helper T cells
    -> usually memory B cells
43
Q

Describe the function of this T cell: Regulatory T Cell

A
  • supresses/turns-off immune reponse when it is not needed
    -> Without this, your immune system would attack itself and result in autoimmunity
44
Q

Describe the function of this T cell: Delayed Hypersensitivity T Cells

A
  • produces a delayed, exaggerated immune reponse that can occur days to years later

Ex: Person who touched posion ivy will not experience an immune respone (ex: rash) until days later

45
Q

Describe the function of this T cell: Memory T Cell

A
  • promote a faster and stronger immune reponse than the primary immune response as a result of the second encounter with the same Ag
46
Q

Antigen Presenting Cells can as as _____

A

phagocytes

47
Q

Fully describe the function of this cell that is involved in CMI: Antigen Presenting Cells (APCs)

Include: How its eliminates the intracellular pathogen

A
  1. Ag passes through lymphoid tissue of GI tract; APCs are located here
  2. Engulf Ag -> Ag fragments -> fragmented Ag migrate to surface and presents it to Helper T cell
  3. APC and Helper T cell releases cytokines
  4. Cytokines activate Cytotoxic T cells and/or Memory B cells
    -> When Cytotoxic T cells activated, it attaches to presented Ag on phagocyte surface and releases perforins/enzymes to destory infected host cell
    -> When Memory B cells activated, it makes Ab (memory B cell -> plasma cell -> Ab)
48
Q

Why are Helper T cells called helper cells?

A

releases cytokines that activate Cytotoxic T cells (to destroy infected host cell) and activates memory B cells (to make more Ab against Ag)

49
Q

Give two examples of APC’s and what is their function/location?

A

Macrophages
- activated by cytokines/ingestion of pathogen
- migrate to lymphoid tissue in GI tract, engulf, and present fragmented Ag to Helper T cell

Dendritic Cells
- found in skin
- engulf and degreade pathogens and present to Helper T cell

50
Q

What kind of T cell(s) can bind to APC?*

A

Helper T cells
Cytotoxic T cells

51
Q

What other cells are involved in Cell Mediated Immunity (besides T cells)

A

Antigen Presenting Cells (APC)
NK cells

52
Q

TRUE or FALSE: NK cells belong to adaptive immunity

A

False, NK cells belong to innate immunity (formed elements) and B lympocytes and T lymphocytes belong to adaptive immunity. However, NK cells are involved in adaptive immunity

53
Q

Name the role/function of NK cells in adaptive immunity

A

involved in destruction of:
- extracellular parasites/worms
- tumor cells
- animal virus-infected cells (intracellular pathogens)

54
Q

Describe how immunological memory works

A
  1. Immune system encounters pathogen for the 1st time
  2. Makes memory cells (ex: memory B cells) in case immune system seem same pathogen in future
  3. Immune system encounters same pathogen for the 2nd time
  4. Memory cells made earlier take notice
55
Q

Differentiate between Primary Immune Response and the Secondary Immune Response

A

Primary Immune Response
- due to first-time exposure to Ag/vaccination
- IgM made first and peaks first (high IgM and low IgG)
- will produce memory (B) cells for future activation

Secondary Immune Response
- occurs after 2nd exposure to same Ag
- Class switching: high IgG and low IgM
- more rapid and stronger immune reponse than primary; lasts many days (can skip clonal selection and expansion)
- Memory cells produced earlier (from initial exposure) are activated by secondary exposure

56
Q

Define: Antibody titer

A

amount/concentration of Ab’s in the serum

57
Q

A graph showing the antibody titer in serum shows that there is high IgG that peaked first and there is low IgM. What can be said about the immune reponse (is it a primary or seondary immune reponse).

A

Secondary immune reponse, because of class switching where there is high IgG and low IgM. There is a stronger, faster immune reponse because you can skip clonal selection and expansion and memory cells produced earlier are activated

58
Q

Compare and Contrast the different ways of acquiring adaptive immunity

A

Natural = natures course
Artificial = involves needles
Active = get Ag -> make Ab
Passive = get Ab (did not make Ab)

Naturally aquired Active immunity
- results from infection (you make Ab)

Naturally aquired Passive immunity
- Transplacental (IgG) or via Breast milk (IgA); baby got Ab from Mom

Artificially acquired Active immunity
- injection or vaccination (inject Ag to make Ab)

Artificially acquired Passive immunity
- injection of Ab

59
Q

Which way of acquiring adaptive immunity is involved in the administration of these drugs: adalimumab and secukinumab

A

artificially acquired passive immunity

adalimumab and secukinumab