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Biology 116 > Immunity > Flashcards

Immunity Flashcards

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1
Q

timing of adaptive immunity

A

takes several days to prepare (specific immunity); use innate defenses until adaptive is ready

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2
Q

lymphocytes

A

WBCs; in both innate + adaptive immunity; 2 types in adaptive both originating as stem cells in bone marrow; 2 diff dev paths: some remain in BM to dev into B cell, some migrate to thymus to complete dev into T cells

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3
Q

antigen (Ag)

A

any foreign substance that triggers B or T cell response; most Ag = protein or large polysac on the surface of cell; pathogen, blood cells and tissue cells transplants

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4
Q

epitope

A

specific exposed region on surface of Ag molecule; specific part of Ag that binds to Ag receptor on immune cells; each B + T cellw specificity for a specific epitope; recognition = very specific

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5
Q

Y-shaped receptors on B cells

A

4 PPCs: 2 identical heavy chains @ identical light chains linked via disulfide bridge; receptors w transmembrane region near ends of heavy chains anchors receptor in BC pm; constant vs variable regions

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6
Q

constant region on Y-shaped receptor

A

portions of LC + HC

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7
Q

variable region on Y-shaped receptor

A

w/i 2 tips of Y shape; each receptor w 2 identical Ag-binding site; each tip is binding site for specific Ag

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8
Q

diff BC classes

A

5 types of immunoglobulins (Ig) based off of distinct heavy chain constant region; Ig A, Ig G, Ig M, Ig E, Ig D

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9
Q

BC activation

A

no pathogen no danger; BC = inactive; activation when BC Ag-receptor (tips of Y) binds to Ag leads to formation of BC that secretes soluble form of receptor; secretes antibodies; Ab = Ig

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10
Q

antibodies

A

same Y shaped structure BC Ag-receptor; not mem bound; soluble; Ab do actual defense against pathogen not BC; BC simply secrete Ab

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11
Q

T cells

A

TC Ag receptors bind only to fragments of displayed Ag on surface of a HC; HC display on major histocompatibility complex (MHC) molecules = host particles that display Ag

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12
Q

Ag receptor

A

2 diff PPCs: alpha + beta linked via disulfide bridge; C region = rest of mlecule; transmembrane region anchors to TC pm; variable region @ ends of chains w single Ag binding site

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13
Q

recognition of Ag protein by TC

A

happens when pathogen either infects or part of pathogen is phagocytosed by cell; cellular enz cleave Ag into smaller peptide = Ag fragments; Ag fragments bind to MHC molecules w/i cell; MHC + Ag move to cell surface; display of Ag frag on surface; HC = Ag-presenting cell (APC); other immune cells can recognize danger

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14
Q

BC+TC diversity

A

body is ready to respond to unbelievable # of pathogens of Ag entering body; >1 mil diff BCRs; >10 mil diff TCRs

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15
Q

self tolerance

A

IS recognies itself so won’t attack self; self vs non self (foreign); due to surface proteins = biochemically unqiue; everyone is diff

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16
Q

proliferation of BC+TC

A

once specific BC/TC act undergoes multiple CDs clonal selection of large pop of identical cells to fight specific pathogen; clonal selection creates effector cells and memory cells

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17
Q

effector cells

A

take effect immediately to attack pathogen; BC plasma BC; TC cytoxic TC + helper TC; short lived

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18
Q

memory cels

A

long lived; ready to divide if same Ag appears again; give rise to effector cell activation

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19
Q

immunological memory

A

response for long term protection due to some prior infection; body + IS remembers that you were infected previously; primary and secondary immune response

20
Q

primary immune response

A

rxn to 1st exposure to Ag; peak activity 10-17 after exposure; selected BC + TC pops become effectors

21
Q

secondary immune response

A

rxn to same Ag again; faster strong more prolonged 2-7 days after exposure; less Ag needed to sitmulate secondary response; due to memory BC + TC

22
Q

humerol response

A

blood + lymph; Ab

23
Q

cell mediated response

A

infected HC destroyed by specialized TC

24
Q

helper T cells

A

trigger humerol + CM response produce signals to initiate Ab production (humoral); activate TC which kill infected cells (cell mediated): do not directly kil pathogens/infected cell only produce signals that trigger other immune cells

25
Q

helper T cell activated by APCs displaying

A

diff types of APCs: dendritic cells, macrophages, BC; APC displays MHC + Ag fragment on cell surface either displayed MHC I (all cells) or MHC II (only APCs) molecular signature that ensures helper T cell recognizes APC

26
Q

2 parts of helper T cell that bind to APC

A

(1) Ag receptor (TCR) binds to Ag fragment + MHC II displaying Ag (2) CD4 = helper T cell, accessory protein on TC surface also binds to MHC II keeps APC + helper T cell joined together

27
Q

cytokines

A

produced by helper T cell binding to APC stimulating APC; signaling molecules triger help T cells to produce own cytokines; helper T cells gets fully activated and proliferates w ton of clone w same TCR to recognize tons of the same Ag on tons of APCs

28
Q

activated BC

A

activated by activated helper T cell; humerol

29
Q

activated TC

A

activated by activated helper T cell; cell mediated

30
Q

cytotoxic T cell

A

TC use proteins to kill cells already infected by viruses or other intracellular pathogens; ensures pathogen can’t mature any further stops spread

31
Q

cytotoxic TC activaiton

A

HTC signals +APC interactions; infected HC displayed Ag fragments on MHC I on surface; recognition by cytotoxic cytotoxic TC bind (2 parts; (1) Ag receptor (TCR) binds to Ag frag + MHC I (2) CD8 accessory protein on cytotoxic T cell surface also binds to MHC I keeps APC + cytotoxic TC bound together

32
Q

activated cytotoxic TC releases

A

perforin and granzymes

33
Q

perforin

A

forms pores in infected cell’s pm

34
Q

granzymes

A

enter infected cell via endocytosis induces apoptosis; programmed cell death due to activation of self breakdown enz

35
Q

infected cell dies

A

cytotoxic TC released ready to attack another infected cell

36
Q

B cell activation

A

inactive BC engulfs Ag; displays Ag fragments on MHC II (APC); HTC attracted to MHC II + Ag; HTC activates BC; 1000s of plasma BCs effectors cells produce + secretes Ab, memory BC

37
Q

Ab function

A

don’t kill pathogen directly instead bind to Ag and interfer w pathogen activity and/or mark pathogen for inactivation + destruction by other immune cells

38
Q

mechanism of Ab function

A

(1) neutralization (2) opsonization (3) activate complement system

39
Q

neutralizaiton

A

Ab binds all around virus surface virus can’t enter HC

40
Q

opsonization

A

Ab binds all around bac surface; promotes phagocytosis via mo + neutrophils

41
Q

activate complement system

A

Ab binds to Ag on foreign intruder; complement proteins bind to Ab-Ag complex; produces mem attack complex (MAC); pores in foreign cell mem; death of invader

42
Q

active immunity

A

immunity dev following direct exposure to Ag; primary and secondary responses

43
Q

natural active immunity

A

pathogen enters body; “natural encounter”

44
Q

artifical active immunity

A

ex: immunization/vaccination; stimulates same response as natural exposure: make Ab against vacine, booster shot (secondary response), vacine prep (pathogen killed/weakened, still has epitope/Ag not whole thing

45
Q

passive/borrowed immunity

A

ind given Ab actively produced by other ind; temporary immunity bc no memory cells; ex: rabies = inject Ab from people already vaccinated against rabies

46
Q

naturally acquired passive immunity

A

fetus is protected by mom’s IgG as passes through placenta; newborns gets breast milk w colostrum that contains IgG w enough protection to prepare own IS

Biology 116 (27 decks)

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