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Microbiology 1 > Lecture #9 - Adaptive Immunity > Flashcards

Lecture #9 - Adaptive Immunity Flashcards

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1
Q

The Adaptive Immune System

A

Acquired

Very specific

Has a memory component

Consists of two components:

  1. Humoral (antibody mediated) immunity
  2. Cell mediated immunity
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2
Q

The Adaptive Immune System

• Acquired (meaning)

A

NOT born with - instead, develops over course of your life b/c of pathogens your encountering on daily basis

  • Begins as soon as a pathogen is encountered for the very first time
  • Adaptive response will not occur until a pathogen is encountered
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3
Q

The Adaptive Immune System

• Very specific (meaning)

A

• Very targeted to a specific feature of a given bacterium, virus, toxin
- going after something about E.coli, something about HIV or SARS-COV-2 (not random or non-specific)

  • • Immunity to one pathogen will not confer immunity to another
  • NOT cross-reactive responses
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4
Q

The Adaptive Immune System

• Has a memory component (meaning)

A

• Produces a more effective response when a pathogen is encountered for the second time-faster and stronger

  • ~long-term protection b/c it remembers any adaptive interaction that took place before
  • 2nd response is much quicker & will produce higher levels of immune activation, immune response & stronger response overall
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5
Q

The Adaptive Immune System

Consists of two components:

A
  1. Humoral (antibody mediated) immunity
    - B cells are respon. for this
  2. Cell mediated immunity
    - T cells (*specifically cytotoxic ones) are respon. for this
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6
Q

Antibodies:

A

Something YOU make to protect you

• Proteins produced by the immune system that bind and inactivate foreign antigen

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7
Q

Immunogens:

A

Any foreign material that has the ability to active the adaptive immune system
- NOT YOU
- get the attention of adaptive immunity
• Normally protein, polysaccharide, lipid material *=ALL ORGANIC

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8
Q

Epitopes:

A

• The actual portion of the ANTIGEN that binds to the antibody
- each spike protein will be referred to as an antigen & antibodies binding to this are doing so with specific regions referred to as epitope

• A single antigen will have more than one epitope
- each antigen will have their own specific epitope that they bind to, in order to induce protection & nutrilization
• Increases the ability of an antigen to activation the immune system –> immunogenicity
- some antigens so a much better job of activating the immune system then others
– some antigens will be less immunogenic & won’t have same opp. to activate immune system & that means some antigens are better for vaccination then others b/c they’ll be stronger in terms of how they turn on the immune system
• Each epitope requires a distinct antibody

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9
Q

Describe the result of, “A single antigen will have more than one epitope”

A
  • each antigen will have their own specific epitope that they bind to, in order to induce protection & nutrilization
    • Increases the ability of an antigen to activation the immune system –> immunogenicity
  • some antigens do a much better job of activating the immune system then others
    – some antigens will be less immunogenic & won’t have same opp. to activate immune system & that means some antigens are better for vaccination then others b/c they’ll be stronger in terms of how they turn on the immune system
    • Each epitope requires a distinct antibody
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10
Q

Collectively those _____ will bind @ different regions of the _____, which are then gonna allow for subsequent destruction

A

ANTIBODIES

ANTIGENS (Ag)

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11
Q

Hapten:

A

• LOW MOLECULAR WEIGHT compound that is too small on its own to activate adaptive immunity
- not big enough to get the attention of the immune system

• NOT IMMUNOGENIC

  • Can bind to other molecules such as protein in blood and tissues
  • Becomes strongly immunogenic
  • An allergy forms
  • Ex) penicillin
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12
Q

If Hapten are NOT immunogeneic, how do you get them to get attention of immune system?

A

• Can bind to other molecules such as protein in blood and tissues
• Becomes strongly immunogenic
- activates immune system more aggressively & then can develop an allergy
• An allergy forms
• Ex) penicillin

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13
Q

Describe penicillin

A
  • antibiotic used to treat infection
  • penicillin is a HAPTEN that specifically will bind to PROTEINS that are be present in blood & tissues for ex
  • & whole thing gets attention of immune system
  • & is said to be STRONGLY IMMUNOGENIC (allows opp. for immune system to react against penicillin which you don’t want)
  • whole point of penicillin was to help you treat an infection (not to kill off drug & remove from insides of body)
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14
Q

Antibodies (Ab) are…

A

glycosylated protein molecules

- b/c are AA sequences that have sugar groups that are added to various locations

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15
Q

Antibodies (Ab) are AKA

A

Also called IMMUNOGLOBULINS (Ig)

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16
Q

Antibodies (Ab)

Consist of 4 subunits

A
  • TWO identical HEAVY chains
  • TWO identical LIGHT chains
  • CHAINS are assembled creating THREE distinct regions
  • 2 identical variable regions (Fab regions)
  • 1 constant region (Fc region)
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17
Q

Why is the two identical heavy chains called heavy?

A

heavy b/c consist of MANY AA’s, which INCREASES the molecular weight

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18
Q

Why are the two identical light chains called light?

A

light b/c have FEWER AA’s that comprise them, which means they’ll be LOWER molecular weight

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19
Q

Explain the 2 identical variable regions (Fab regions)

A

formed from heavy & light chain that come together

• Provide the specificity of the antibody

  • allow foreign material to initiate a response
    • get bound to that foreign material specifically at that site & if you want to bind a diff kind of foreign matter, you will then need a brand new antibody in order to do it
  • has to be more than 1 antibody when you have foreign material that has diff components or antigens b/c each antibody is so specific

think: same way police has to interact with bad guys (Fab region)

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20
Q

Explain the 1 constant region (Fc region)

A

b/c not an infinite # of possibilities but instead are only 5
- type of Fc region will determine which of the 5 we have

• Allows for INTERACTION (talk) with immune cells
- Fc region allows antibody to be able to send messages & to be able to communicate with other elements of the immune system

• Based on differences in the Fc region there are FIVE different types of antibody

think: in Fc region, police has opp. to interact with other members of the force, to communicate diff types of info they found

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21
Q

Classes of Antibody

A
  1. Immunoglobulin M (IgM)
  2. Immunoglobulin G (IgG)
  3. Immunoglobulin A (IgA)
  4. Immunoglobulin D (IgD)
  5. Immunoglobulin E (IgE)
22
Q

Immunoglobulin M (IgM):

A

• PENTAmeric

  • Five different antibody units form IgM
    • & each antibody has opp. to be able to bind to 2 identical antigens, therefore IgM with 5 of these units can bind to 10 identical antigens

• Always the first antibody to be produced in response to an antigen (infection)

    • PRIMARY ANTIBODY RESPONSE
    • initial that’ll be produced early on that can switch later within the infection

• Found on the surface of B lymphocytes (imp. cells for antibody prod.)

  • think: like advertisement on surface of B lymphocyte that says “hey if you stimulate me to produce antibody, this will be type of antibody flavour/specificity that they will produce for you”
  • Remains in the blood (stuck - b/c so large it can’t leave capillaries, even with those increased pore sizes during periods of inflammation)
    • Unable to enter the tissues

• LOW AFFINITY FOR ANTIGEN
- doesn’t bind strongly

• Very good at AGGLUTINATION
- b/c you can bind 10 Ag (antigen) = all identical

23
Q

Immunoglobulin G (IgG):

A

• MONOMER - only binds to 2 identical antigen

*• MOST PREDOMINANT antibody in the BLOOD

• Also present IN the TISSUES (ex in foot, intramuscular enirv. etc.)

24
Q

If you go to doctor b/c you think you contracted the HIV, they’ll ask you q’s about when you think that might’ve happen but also ask you to come back & get retested. What is the reason?

A

reason: b/c you always begin by producing IgM against foreign material, but what ends up happening when its produced is you switch to another antibody at some point after the initial infection
- for HIV virus you start by producing IgM against virus & then switch to formation of IgG
- if you’ve just been infected, you’re either not producing antibody yet or if you are its always initially IgM
- IgG will be prod. after infection has been taking place for some time - ask you to come back after 3 & 6 months b/c after 3 months post infection, most ppl have already been producing IgG against HIV virus & after 6 months post infection you for sure are likely to be producing IgG against the virus
- any test result before that class switching could potentially be a false neg.

25
Q

Immunoglobulin A (IgA):

A
  • DImeric
  • Secreted at MUCOSAL sites
  • in GI tract, repro tract, respir tract
    • SALIVA, TEARS, MUCOUS
    • in order to protect all these open tracts to outside against infection
  • – really imp. otherwise we’d have more infection at these locations all of the time

• Important DEFENSE AGAINST respiratory, reproductive, digestive tract INFECTIONS

26
Q

How many antigens can Immunoglobulin A (IgA) bind to?

A

to identically 4

b/c dimeric

27
Q

Immunoglobulin D (IgD):

A
  • MONOMER
  • Located on the SURFACE of B cells
  • another ex of an advertisement
  • on its surface if you stimulate this B cell, that’s the type of Fab region you’ll get
    • will secrete something else (not IgD)?

• Important in ACTIVATION of B cells to begin producing antibody against a specific antigen

  • b/c B cells in your body aren’t always producing antibodies & an antibody is protein & its really expensive to make so you don’t want to make it unnecessarily on inside of body
    • critical to be made only when needed, when cell has been told to activate
28
Q

Immunoglobulin E (IgE):

A

• MONOMOR
• Binds to receptors located on the surface of MAST CELLS and BASOPHILES
- Binding of IgE-antigen complex triggers degranulation and histamine release
– ALLERGY

Antibody can attack with Fc fragment & then allergen binds to Fab region (b/c allergen this in response to the allergen bound to IgE, bound to Fc receptor located on the mast cell or basophil)
– HISTAMINES then gets released to outside & causes all the allergic symptoms

29
Q

Allergy shots

A

get doses of something your allergic to injected into you in a controlled setting in an allergents office

  • idea: try to force your body to produce IgG which is antibody you’d produce in muscle or places where you’ve been injected instead of producing IgE
  • still be allergic, still be producing antibodies unnecessarily against something not threatening, but wouldn’t get degranulation of the cell, therefore wouldn’t get symptoms of the allergy b/c its only IgE that has opp. to do that
  • spotty effectiveness
  • done over course of 2 or 5 years but idea can be that it can serve to provide protection so you don’t get allergy symptoms continuously
30
Q

Five major antibody functions:

A
  1. Neutralization
  2. Opsonization
  3. Agglutination
  4. Antibody mediated cytotoxicity
  5. Complement activation
31
Q

Neutralization:

A

• ANTIBODIES BIND (hug) TO ANTIGEN BLOCKING ATTACHMENT SITES
- Prevents bacteria, virus and toxin entry into tissues and host cells (from causing harm, i.e. neutralize & prevent their beh)

think: someone pull fire alarm, & then someone grabs you & hugs so you have no where to go so you’ve neutralized their beh so you’re not able to do what you were gonna do any longer (blocked something that was bad)

32
Q

Opsonization:

A

ANTIBODIES COAT (add bulk) the SURFACE of the bacterial CELL
• ATTRACTS PHAGOCYTES
• Greatly ENHANCES the RATE OF PHAGOCYTOSIS (& lead to destruction of those bact. coated with antibody)
- b/c macrophage is able to attack with it
• PHAGOCYTE has the ABILITY to INTERACT with the Fc region of the antibody

think: tell someone to find you at hockey game but don’t tell them where you’re sitting so to help you, you can put a big fat flashing stick on your head that go 6ft high
- friend quickly scans entire place & spot you in a few secs

33
Q

Agglutination:

A

• Each class of antibody can bind to a minimum of 2 identical antigen units

  • IgM can bind to 10 identical antigens
  • IgA can bind to 4 identical antigens

Together will create:
• CLUMPS together many ANTIGENS
think: absorbant paper towel - get stuck within a region & inturn have protection & no movement of material all over

• ALLOWS PHAGOCYTOSIS to occur more EFFECTIVELY
- aggulation keeps control of a messy situation

34
Q

Antibody mediated cytotoxicity:

A

ATTACHMENT of antibody to parasites RECRUITS EOSINOPHILS

  • EOSINOPHILS ATTACH to the Fc component of antibodies
  • Activated EOSINOPHILS RELEASE REACTIVE OXYGEN SPECIES and HYDROLYTIC ENZYMES
  • PARASITE is DESTROYED
  • large parasite (basically Euk path) is coated with IgE - same way we have IgE on an allergen
  • when those IgE antibodies are attached to surface, eosinophil comes & attaches & that’ll be the trigger for eosinophil to degranulate
  • as eosinophil degranulates, it produces EC enzymes that digest parasite outside cell (rmbr b/c fact their both Euk, you can’t phagocytose the structure, so instead you ECly digest the parasite so its completely taken apart in this setting)
35
Q

Complement activation:

A

• Complement is a system consisting of a SERIES of
(inactive) PROTEINS (in off position) found IN the BLOOD
- each protein is WAITING FOR an ACTIVATION SIGNAL
- Can be ACTIVATED BY ANTIBODY that is BOUND to a bacterial CELL
(complement protein that gets turned on by this & result in destruction of the cell)
– CLASSICAL PATHWAY of complement activation

36
Q

Complement activation create…

A

a number of DIFFERENT IMMUNE RESPONSES when activated

When whole system is on, you end up with a…
• MAC attack complex forms
- plentera of diff. complement proteins that’re all turned on (some identical, some diff)
- a pore that inserts into mem. of a bact cell where you then have opp for material to leak to outside of that cell (cell no longer alive)
– Inserts into the membrane of bacterial
cell FORMING a PORE
– CONTENTS of the cell LEAK and the bacterium DIES

37
Q

Activation of Antibody Mediated Immunity

A

• B CELLS (respon for antibody prod) are (also) antigen presenting cells
- MACROPHAGES and DENDRITIC CELLS also perform ANTIGEN PRESENTATION
- All antigen presenting cells can insert MHC II into the plasma membrane
(also have MHC I b/c they belong inside of the body)

• ANTIBODIES are PRODUCED AGAINST EXOGENOUS ANTIGEN
- Antigen that exists outside of the cell in the surrounding extra-cellular fluid
– Can be bacteria, virus, parasite, toxin, etc.
- Once antibodies are secreted from B cells they can BIND to and NEUTRALIZE/OPSONIZE these EXOGENOUS ANTIGENS
(*antibodies are made for exogenous antigen)

38
Q

All nucleated cells have _____ (in PM)

A

MHC I

(including APCs, liver cells, muscle cells; everything other than RBC’s b/c they have anuclear when mature)

think: everyone at hospital has badge that says they work there

39
Q

MHC I identifies a…

A

self cell

40
Q

If Antigen Presenting Cell

A

also have MHC II within mem - allows opp for antigen presentation
- part of the profession of an APC (something they’ll have in add. to the “hey I belong here MHC I badge b/c it allows them to do their job)

MHC I (b/c belongs to you & has a nucleus)

41
Q

Understanding that they have MHC I & MHC II according to their beh & identity, we need to differentiate 2 things:

A

Exogenous antigen

&

Endogenous antigen

42
Q

Exogenous antigen:

A

foreign material located outside of the cell in extracellular fluid –> presented with MHC II

*activates antibody immunity

43
Q

Endogenous antigen:

A

foreign material located inside of a cell –> presented with MHC I

*activates cell mediated immunity

44
Q

Activation of Antibody Mediated Immunity

• Steps in antibody production:

A
  1. B cell phagocytoses exogenous antigen
  2. T helper cells bind to MHC II-Antigen complex resulting in T helper cell activation
  3. Some of these newly produced B cells will become plasma cells
45
Q

Steps in antibody production:

1. B cell (respon for making antibody & also an APC) phagocytoses exogenous antigen

A

• Digested content in the phagolysosome will not be exocytosed to the extracellular fluid
- Instead it will be COMPLEXED together with MHC II and INSERTED into the plasma membrane

  1. B cell takes in exogenous antigen in ECF
  2. Gets digested (what happens when phagosome (what’s produced with EC material taken up) fuses with lysosome, so you can digest that material in there)
    - rmbr neutrophils vomit out all of the digested content that was phagocytosed
    - APC DON’T vomit out all of that material, instead put it with MHC II (what APCs use for their profession)
    - digested content with MHC II gets inserted into mem & now its “presenting antigen” to other cells of immune system (hence its term as an APC)
    - using MHC II to do it
46
Q

Steps in antibody production:

2. T helper cells bind to MHC II-Antigen complex resulting in T helper cell activation

A

(activating signal will be T helper cell spitting out cytokine)
• The activated T helper cell releases cytokines that bind to receptors on the B cell resulting in B cell proliferation

  1. Cytokines are released from T helper cell in response to TCR contact with MHC II-Antigen complex (T helper cell is active)
  2. Cytokine binds to cytokine receptor in B cell plasma membrane triggering the proliferation of the B cell (Releases cytokines)
  3. Result: A clonal population of the B cells

T helper cells are AKA CD4+
- T cells (the ones HIV infect)
Outcome: cytokine that binds to B cells cytokine receptor causes B cell proliferation (B cells that come from clonal expansion - a pop. of clones of B cell, are all gonna produce the exact same type of antibody against the exogenous antigen that was encountered)

47
Q

Steps in antibody production:

3. Some of these newly produced B cells will become plasma cells

A
  • ACTIVELY TRANSCRIBE, TRANSLATE and SECRETE an IDENTICAL ANTIBODY PROTEIN to the EXTRA- CELLULAR FLUID
    • These antibodies are SPECIFIC to the ORIGINAL EXOGENOUS antigen

• A SMALLER FRACTION of NEWLY produced B CELLS will BECOME MEMORY CELLS

  • These will be used in subsequent encounters with the same antigen
    • They will not produce antibodies during the current response

(with that clonal pop of B cells that was stimulated to be produced by mitosis b/c of this (light brown receptor) binding int., some of those cells will become memory & some will be plasma cells

  • memory cells go on shelf for later, so they basically stay there, so if ever you encounter this foreign material later, those memory cells can activate
  • plasma cells are ones that’ll be used rn in this response to collectively transcribe, translate & secrete antibodies (antibodes made will all be IgM if 1st time, IgG or IgA later depending on when they were encountered & are specific to whatever antigen it was that B cell intially phagocytosed - you end up with a smaller fraction of B cells that are memory cells & larger fraction actively secreting antibody & B cells that’re memory cells don’t secrete antibody rn (will be used in subsequent responses)
48
Q

Primary antibody response:

A

• Occurs the very FIRST TIME a specific ANTIGEN is ENCOUNTERED
- Can be a NATURAL encounter (day to day life - coughed on, touched yourself with something contaminated etc.) OR an ARTIFICIAL encounter (ex: vaccination - abnormal, but puppet response to get outcome we want –> memory)

• Produces a WEAK ANTIBODY MEDIATED RESPONSE
- SLOW PRODUCTION of LOW LEVELS of ANTIBODY

• Results in the PRODUCTION of MEMORY B CELLS: major goal

49
Q

Secondary antibody response:

A

• Occurs every ADDITIONAL time
(after the primary response) a specific antigen is ENCOUNTERED (5th, 6th, 100th etc. as long as its not the 1st time seeing that secondary response)
• Produces a STRONG ANTIBODY MEDIATED RESPONSE
- RAPID production of HIGH LEVELS of ANTIBODY
– So rapid that the pathogen will not be able to establish infection (won’t get sick - antibodies prod so quickly & so early on that it won’t create all illness b/c of memory response protecting you with high levels so fast)
— NO DISEASE occurs

50
Q

Tolerance

A

Tolerance PREVENTS IMMUNE RESPONSES AGAINST SELF-ANTIGENS
- have to understand what belongs & what doesn’t, b/c if you don’t, you mount a response against it an error & start killing yourself –> autoimmune disease)
• ANY immune cells that are found to recognize SELF-ANTIGENS (shouldn’t be there) are DESTROYED early on in development (quickly)
- to GET RID OF THEM before they have an opp to cause any sort of long-term problem (like a deletion response that’s really critical in everything that’s happening here)
- otherwise there’s disease (or if tolerance fails will get disease symptoms)
• Helps to PREVENTS AUTO-IMMUNE DISEASE

51
Q

Cell Mediated Immunity

A

• RECOGNIZES and DESTROYS ABNORMAL CELLS present in the body

  • Cells infected with virus or obligate intracellular bacteria
  • These are ENDOGENOUS antigen (present inside; means WHOLE CELL needs to be destroyed) because they are (infection) present inside of the host cell
  • Involves CYTOTOXIC T CELLS
  • DISEASED host cell will display ENDOGENOUS ANTIGEN in the plasma membrane complexed together with MHC I
  • Cytotoxic T cells will bind to MHC I-Antigen complex using their T cell receptor (TCR)
  • This results in activation of the cytotoxic T cell triggering it to release perforins and granzymes that cause death of the infected host cell

• In order to clear a viral infection BOTH antibody mediated immunity and cell mediated immunity are REQUIRED

52
Q

Got a cell with a problem:

Virally infected liver cell (NOT APC’s)

A

MHC I in mem (b/c nucleated)

  • don’t have MHC II b/c not APCs
  • this viral antigen gets displayed on surface
  • call that (fragment of) endogenous antigen
  • perforins & granzymes kills infected cell

Cytotoxic T cell (AKA CD8+ T cell)

  • with its T cell receptor, it finds this & becomes activated & releases molecules called PERFORINS & GRANZYMES (poke holes inside mem. & kills infected cell so threat is removed)
  • also basis of transplant rejection - which is why person needs to be on immunosuppressent to make sure this doesn’t happen b/c you want that transplant to stick)

End outcome: to destroy virally infected cell, cancer cell etc.

Microbiology 1 (15 decks)

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