Lecture #9 - Adaptive Immunity Flashcards

Question

Immunoglobulin A (IgA):

Answer 1

* 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

Answer 2

to identically 4 | b/c dimeric

Answer 3

* 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

Answer 4

• 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

Answer 5

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

Answer 6

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

Answer 7

• 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)

Answer 8

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

Answer 9

• 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

Answer 10

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)

Answer 11

• 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

Answer 12

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

Answer 13

• 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)

Answer 14

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

Answer 15

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)

Answer 16

Exogenous antigen & Endogenous antigen

Answer 17

foreign material located outside of the cell in extracellular fluid --> presented with MHC II *activates antibody immunity

Answer 18

foreign material located inside of a cell --> presented with MHC I *activates cell mediated immunity

Answer 19

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

Answer 20

• 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

Answer 21

(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)

Answer 22

- 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)

Answer 23

• 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

Answer 24

• 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

Answer 25

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

Answer 26

• 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

Answer 27

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.