IM 4 Flashcards

1
Q

how is clonal expansion started?

A

cytotoxic T cell activation with binding of antigen presentation

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2
Q

what is needed for maximal activation of cytotoxic T cell

A

helper T cells (IL-2 and other cytokines) to stimulate full cytotoxic T cell clonal expansion

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3
Q

what is formed from full cytotoxic T cell clonal expansion?

A

effector and memory cells

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4
Q

what do activated effector cytotoxic T cells do?

A

circulate and recognize virus infected cells

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5
Q

what happens with recognition effector cells?

A

release perforin and granzymes

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6
Q

what happens when perforin is released?

A

create channel for intracellular entry (similar to MAC)

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7
Q

what happens when granzymes are released?

A

digestive enzymes enter via perforin created channel

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8
Q

how is perforin and granzymes related?

A

perforin creates channels and granzymes enter the channels

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9
Q

what is the result of cytotoxic T cells?

A

-virus infected cells undergo apoptosis
-lots of cells can be lost depending on how many are infected
-virus released into extracellular where other defenses can attack easier

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10
Q

what is the role of regulatory T cells?

A

suppress immune responses to keep from over-reacting (this provides some balance to immune responses)

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11
Q

what are some possibilities of the mechanism for regulatory T cell?

A
  • Not as many copies made
    * Cytokines drive production from helper T cells
    * Cytokines that increase clonal expansion, we also have cytokines that decrease clonal expansion
    * Negative feedback to IL-2
    * Costimulation activation of
    *basically countering what we’ve done in past slides
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12
Q

how is B cell activation done?

A

variable end antigen binding to antigen (clonal selection) and starting clonal expansion

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13
Q

what does maximal activation for B cells require?

A

helper T cells contributions (IL-2 and other cytokines) to stimulate full B cell clonal expansion

=some effector and memory cells formed

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14
Q

some effector B cells differentiate into…

A

plasma cells that form antibodies for specific antigen

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15
Q

what are antibody mediated attacks?

A

specific formed antibodies being released out into circulation

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16
Q

what’s the difference between B cell proliferation and differentiation?

A

proliferation: B cells make more B cells
differentiation: B cells making plasma cells then antibodies

17
Q

what’s a direct attack for antibody?

A

results directly from antigen-antibody binding

18
Q

what happens with direct attacks antibody?

A

neutralization, agglutination, precipitation

19
Q

what is neutralization?

A

antibody binding antigen blocks antigen attaching to healthy cells or interfering with pathogen chemical reactions

20
Q

what is agglutination?

A

clumping when antibody binds to antigen
(Clumping makes antigen + antibody bigger so phagocytosis can detect it easier)

21
Q

what is precipitation?

A

soluble antibody and soluble antigen form insoluble product (insoluble more visible to phagocytosis)

22
Q

what are indirect attacks for antibody?

A

results from more than just antigen-antibody binding

23
Q

how is enhanced phagocytosis and antibody dependent cellular cytotoxicity (ADCC) related?

A

they have very similar processes

  1. antibody binds to antigen and acts like opsonin
  2. phagocyte or NK cells with correct receptor attaches to stem end of antibody
  3. forms bridge between pathogen and phagocyte or NK cell
    -enhanced phagocytosis: to make phagocytosis easier
    -ADCC: in response to binding NK cell releases cytotoxic chemicals to destroy pathogen
24
Q

what is the primary response for immunity?

A

following first contact to antigen

-slow (several weeks) response
-small numbers of specific antibodies
-limited time in blood

25
Q

what is the secondary response for immunity?

A

subsequent encounter by same antigen

-quicker response
-larger numbers of specific antibodies
-longer time in blood

26
Q

what are secondary responses driven by?

A

stored memory cells

27
Q

what do secondary responses give?

A

greatly enhanced immunity toward subsequent infection

28
Q

what are the 2 types of immunity and their subtypes?

A

active and passive

-subtypes are natural and artificial

29
Q

what is active immunity?

A

exposure to antigen

30
Q

what is active natural immunity?

A

exposure to antigen by chance (ex. out in nature and you come across like touching door handle)

31
Q

what is active artificial immunity

A

deliberate exposure to antigen (ex. vaccine)

32
Q

what is a vaccine?

A

small quantities of living or dead pathogens, toxins, or harmless antigen fragment from pathogen or it’s toxin

33
Q

what is passive immunity?

A

direct transfer of already formed antibodies

34
Q

what is passive natural immunity?

A

antibody transfer mother to infant

35
Q

what happens between mother and fetus/

A

passive natural immunity when lgG moves across placenta

36
Q

what happens in breast-fed child?

A

passive natural immunity when lgA in breast milk can move across intestinal lining (this is important early protections as antibody synthesizing is relatively poor in young)

37
Q

what is passive artificial?

A

antibody transfer from person to person (injection)

-only occurs in dangerous or fatal conditions where there is no time to wait for active immunity

38
Q

what’s the catch with preformed antibodies?

A

they offer immediate protection but have a limited lifespan (weeks or months)