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Biology 116 > Immunity > Flashcards

Immunity Flashcards

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
helper T cell activated by APCs displaying
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
2 parts of helper T cell that bind to APC
(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
cytokines
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
activated BC
activated by activated helper T cell; humerol
29
activated TC
activated by activated helper T cell; cell mediated
30
cytotoxic T cell
TC use proteins to kill cells already infected by viruses or other intracellular pathogens; ensures pathogen can't mature any further stops spread
31
cytotoxic TC activaiton
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
activated cytotoxic TC releases
perforin and granzymes
33
perforin
forms pores in infected cell's pm
34
granzymes
enter infected cell via endocytosis induces apoptosis; programmed cell death due to activation of self breakdown enz
35
infected cell dies
cytotoxic TC released ready to attack another infected cell
36
B cell activation
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
Ab function
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
mechanism of Ab function
(1) neutralization (2) opsonization (3) activate complement system
39
neutralizaiton
Ab binds all around virus surface virus can't enter HC
40
opsonization
Ab binds all around bac surface; promotes phagocytosis via mo + neutrophils
41
activate complement system
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
active immunity
immunity dev following direct exposure to Ag; primary and secondary responses
43
natural active immunity
pathogen enters body; "natural encounter"
44
artifical active immunity
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
passive/borrowed immunity
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
naturally acquired passive immunity
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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