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
Four major forces that help create pockets in antigen binding sites
1. Hydrogen bonding 2. Electrostatic forces (charges) 3. Van der waals 4. Hydrophobic/hydrophilic interactions
26
How are unique antibodies produced?
By inducing point mutations in hypervariable regions of the heavy and light chain genes
27
What happens when an antigen bind to a BCR?
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
What happens after the B cell is activated by the T cell?
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
What two cells do B cells differentiate into?
Plasma cells and memory B cells
30
Plasma cells (effector B cell)
produce 2000 unbound antibodies per second for 4-5 days before they die
31
Five mechanisms that antibodies use to destroy pathogens
1. Agglutination 2. Neutralization 3. Opsonization 4. Antibody-dependent cellular cytotoxicity 5. Complement activation
32
Agglutination
Clumps of agglutinated cells are easier to fight because a phagocyte can kill many pathogens at one time
33
Neutralization
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
Opsonization
Phagocytic cells can use Fc receptors to bind to IgG-opsonized pathogens and initiate attachment
35
Antibody-dependent cellular cytotoxicity
If a pathogen is too large to phagocytize, antibodies can bring NK cells into close proximity where it will release extracellular cytotoxins
36
Complement activation
Antibodies help INITIATE the classical pathway of the complement system
37
T-cell-dependent B cell activation steps summarized
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
T-cell-independent activation
PAMP and TLR interactions can also activate B cells
39
If plasma cells produce antibodies, what are memory B cells' function?
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
Long-lived plasma cells
After initial infection, some plasma cells become long-lived plasma cells (and don't die after 4-5 days)
41
Where are long-lived plasma cells found?
In the bone marrow; they secrete circulating antibodies for months to years
42
What if circulating antibodies isn't enough to fight off infection?
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
What happens to memory B cells during second exposure to an infection?
Some memory B cells will go through a second round of somatic hypermutations to try and improve antibody affinity
44
How can memory T cells be reactivated?
By antigen presenting cells in the lymph nodes