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BSCI 2150 > Week 13.2 Adaptive Immunity > Flashcards

Week 13.2 Adaptive Immunity Flashcards

1
Q

How can blood serum from an infected person help another infected patient fight the infection?

A

Serum contains a high concentration of antibodies of that specific infection produced from plasma cells

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2
Q

Antigen

A

A molecule that is not normally found in the body that stimulates the production of antibodies

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3
Q

Epitope

A

Region of an antigen that antibodies interact with (pathogens can have multiple antigens with multiple epitopes)

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4
Q

Dendritic cells

A

phagocytic cells of innate immune response that function to activate the adaptive immune response

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5
Q

Steps of dendritic cell phagocytosis

A
  1. Bacterium is engulfed into dendritic cell and is encased in a phagosome
  2. Lysosomes fuse with the phagosome and digest bacterium
  3. Immunodominant epitopes are associated w/ MHC II and presented on cell surface
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6
Q

Two types of MHC found on our cells

A
  1. MHC I
  2. MHC II
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7
Q

MHC I

A

found on all nucleated body cells

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8
Q

MHC II

A

found only one macrophages, dendritic cells, and B cells

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9
Q

What happens after dendritic cell is activated?

A

The dendritic cell brings the antigen to the lymph nodes and presents them to MHC II receptors on T cells

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10
Q

What are T cells?

A

white blood cells involved in the regulation of other immune cells and the destruction of infected/tumor cells

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11
Q

T-cell receptor?

A

-a membrane-bound protein that binds to antigens similar to an antibody
-have variable regions that are produced through genetic recombination
-binds to antigen on MHC

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12
Q

CD4/CD8 on T cells

A

coreceptors that bind to the MHC protein on the antigen-presenting cell (dendritic cells)

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13
Q

CD28 on T cells and B7 on antigen-presenting cell

A

checks to make sure TCR binding is real

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14
Q

CD8 naive T cell

A

recognizes antigens on MHC I complex and develops into cytotoxic T cells and T-memory cells

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15
Q

Cytotoxic T cells?

A

Will travel to infected tissue and kill infected cells using perforin and granzymes to induce apoptosis (same as NK cells)

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16
Q

Difference between NK cells and Cytotoxic T cells?

A

What they’re asking about host cell

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17
Q

What do cytotoxic T cells ask host cell?

A

Is this cell expressing an antigen that my TCR binds to (are you sick with this specific illness?)
-Yes: Kill
-No: DON’T kill

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18
Q

CD4 naive T cell

A

recognizes antigens on MHC II and develops into helper T cells (TH0, TH1, TH2, THreg, TH17)

19
Q

What helper T cells activate B cells?

A

TFH, TH1, and TH2

20
Q

What two homogenous antibodies on naive B cells serve as antigen receptors (or B cell receptors)?

A

IgM and IgD

21
Q

What is an antibody?

A

A Y-shaped protein produced by B cells with variable and non-variable regions

22
Q

Fragment of antigen binding (antibody)

A

variable proteins that will interact w/ antigen
-top part of antibody (light chain and top part of heavy chain)

23
Q

Fragment of crystallization (antibody)

A

constant region that is structural and will interact w/ immune cells
-bottom part of heavy chain of antibody

24
Q

Sequence variation in the antigen binding site will…

A

create a pocket with different chemical properties

25
Q

Four major forces that help create pockets in antigen binding sites

A
  1. Hydrogen bonding
  2. Electrostatic forces (charges)
  3. Van der waals
  4. Hydrophobic/hydrophilic interactions
26
Q

How are unique antibodies produced?

A

By inducing point mutations in hypervariable regions of the heavy and light chain genes

27
Q

What happens when an antigen bind to a BCR?

A
  1. The B cell internalizes the BCR and antigen
  2. The antigen is degraded and parts are expressed on the MHC II
  3. A helper T cell that has been exposed to the same antigen binds to the antigen on the B cell’s MHC II w/ its TCR
28
Q

What happens after the B cell is activated by the T cell?

A

The B cell proliferates quickly and introduces new mutations to the daughter cells to improve antibody affinity
-More T helper cells will present the antigen to the new B-cells
-If antibody doesn’t match = apoptosis
-If affinity improves = proliferate

29
Q

What two cells do B cells differentiate into?

A

Plasma cells and memory B cells

30
Q

Plasma cells (effector B cell)

A

produce 2000 unbound antibodies per second for 4-5 days before they die

31
Q

Five mechanisms that antibodies use to destroy pathogens

A
  1. Agglutination
  2. Neutralization
  3. Opsonization
  4. Antibody-dependent cellular cytotoxicity
  5. Complement activation
32
Q

Agglutination

A

Clumps of agglutinated cells are easier to fight because a phagocyte can kill many pathogens at one time

33
Q

Neutralization

A

Antibodies block a pathogen’s ability to infect
Ex: an antibody might bind to a surface protein on a virus; if that protein is required to infect a cell, the virus can no longer infect the cell bc the protein is blocked

34
Q

Opsonization

A

Phagocytic cells can use Fc receptors to bind to IgG-opsonized pathogens and initiate attachment

35
Q

Antibody-dependent cellular cytotoxicity

A

If a pathogen is too large to phagocytize, antibodies can bring NK cells into close proximity where it will release extracellular cytotoxins

36
Q

Complement activation

A

Antibodies help INITIATE the classical pathway of the complement system

37
Q

T-cell-dependent B cell activation steps summarized

A
  1. Antibody on naive B cell BCR contacts a matching antigen
  2. B cell internalizes BCR and antigen
  3. B cell presents antigen pieces on MHC II
  4. Matching T-helper cell activates B cell
  5. Hypermutations improve antibody affinity
  6. B cell proliferates into plasma cells and memory B cells
  7. Class switching
  8. Response
38
Q

T-cell-independent activation

A

PAMP and TLR interactions can also activate B cells

39
Q

If plasma cells produce antibodies, what are memory B cells’ function?

A

Memory B cells retain the antibody sequence (hence “memory”) to produce a faster and more effective response to future infections w/ the same antigens

40
Q

Long-lived plasma cells

A

After initial infection, some plasma cells become long-lived plasma cells (and don’t die after 4-5 days)

41
Q

Where are long-lived plasma cells found?

A

In the bone marrow; they secrete circulating antibodies for months to years

42
Q

What if circulating antibodies isn’t enough to fight off infection?

A

Then memory B cells in the spleen and lymph nodes (secondary lymphoid organs) come into contact w/ the antigen and proliferate into plasma cells

43
Q

What happens to memory B cells during second exposure to an infection?

A

Some memory B cells will go through a second round of somatic hypermutations to try and improve antibody affinity

44
Q

How can memory T cells be reactivated?

A

By antigen presenting cells in the lymph nodes

BSCI 2150 (11 decks)

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