Exam 2 Ch. 4-7

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164 Terms

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Where does adaptive immunity occur?

First in secondary lymphoid tissue, then throughout the body

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When does the adaptive immune response occur?

4-7 days after infection, usually subsides 2-3 weeks later

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T and B cells develop from what progenitor?

common lymphoid progenitor

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Antigen receptor of B cells

immunoglobulins

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Antigen receptor for T cells

T-cell receptor

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How does T-cell activation work?

  1. dendritic cell takes up antigen and is activated by PRRs

  2. dendritic cell travels to lymph node

  3. antigen is processed and presented by MHC

  4. dendritic cell interacts with naive T cells, causing them to proliferate and perform their specific functions

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Structure of the T-cell receptor

heterodimer whose chains each have membrane-distal variable domains, membrane-proximal constant domains, transmembrane domains, and cytoplasmic tails

<p>heterodimer whose chains each have membrane-distal variable domains, membrane-proximal constant domains, transmembrane domains, and cytoplasmic tails</p>
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What are the TCR loci?

alpha, beta, gamma, and delta

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What forms the structure of antigen binding sites?

combination of two variable domains

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Somatic recombination

V, J, and sometimes D regions of DNA recombine to produce a new exon for a new protein, increasing diversity dramatically with a small amount of DNA

<p>V, J, and sometimes D regions of DNA recombine to produce a new exon for a new protein, increasing diversity dramatically with a small amount of DNA</p>
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Which chains have D segments in addition to V and J segments?

heavy chain in immunoglobulins and beta chains in TCRs

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TCR signaling happens by association with what?

several additional polypeptides containing ITAMs

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Signaling motifs

small polypeptides that help in the signaling pathways

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MHC molecules

peptide binding specialists that bind a variety of different peptides, not stable when empty

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Beta2 microglobulin

invariant polypeptide found in all class I MHC molecules

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What is the difference in peptide binding ability between class I and II MHCs?

class I can bind to peptides ~9 amino acids long

class II can bind to peptides ~14-20 amino acids long

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Is MHC class I or class II more common on cells?

class I is on all cells

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CD8

coreceptor for T cells that associates with MHC class I

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CD4

coreceptor for T cells that associates with MHC class II

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What is the difference between the structure of antigen binding grooves on MHC class I and class II?

class I groove is made only from the alpha chain

class II groove is made from both alpha and beta chains

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MHC equivalent in mice

H-2

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Mechanism of MHC class I peptide presentation

  1. cytoplasmic proteins digested by the proteasome

  2. peptides transported to the ER where they bind to the peptide-binding site

  3. the complex leaves the ER and travels through the secretory pathway to the plasma membrane where it is presented to T cells

<ol><li><p>cytoplasmic proteins digested by the proteasome</p></li><li><p>peptides transported to the ER where they bind to the peptide-binding site</p></li><li><p>the complex leaves the ER and travels through the secretory pathway to the plasma membrane where it is presented to T cells</p></li></ol><p></p>
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Mechanism of MHC class II peptide presentation

  1. MHC class II are translated and transported to the rough ER where they remain in an inactive state

  2. travel through the secretory pathway to a vesicle where they wait for further action by a phagolysosome

  3. extracellular molecules and pathogens are endocytosed by professional APCs

  4. endosome containing extracellular material matures into a phagolysosme

  5. lysosomal proteases digest proteins

  6. phagolysosome fuses with secretory vesicles containing MHC class II molecules

  7. travel to cell surface where they present peptides generated by digestion 

<ol><li><p>MHC class II are translated and transported to the rough ER where they remain in an inactive state</p></li><li><p>travel through the secretory pathway to a vesicle where they wait for further action by a phagolysosome</p></li><li><p>extracellular molecules and pathogens are endocytosed by professional APCs</p></li><li><p>endosome containing extracellular material matures into a phagolysosme</p></li><li><p>lysosomal proteases digest proteins</p></li><li><p>phagolysosome fuses with secretory vesicles containing MHC class II molecules</p></li><li><p>travel to cell surface where they present peptides generated by digestion&nbsp;</p></li></ol><p></p>
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Proteasome

proteolytic enzyme that degrades intracellular proteins

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What chains are in surface immunoglobulins?

surface immunoglobulins contain 2 heavy chains and 3 light chains

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Structure of B-cell receptor complexes

contain 2 heavy and 3 light chains, transmembrane domains, and small cytoplasmic domains

<p>contain 2 heavy and 3 light chains, transmembrane domains, and small cytoplasmic domains</p>
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What makes up the antigen binding site of antibodies?

combination of V domains of the heavy and light chains

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Contents of the chains of an antibody

each has a single variable domain, one constant domain in the light chain, and 3-4 constant domains in the heavy chain

<p>each has a single variable domain, one constant domain in the light chain, and 3-4 constant domains in the heavy chain</p>
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Hinge region

flexible angle on antibodies that can adapt to bind to a large or small structure

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Where do proteases cleave immunoglobulins?

just above the hinge or just below the hinge

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Fab

fragment of immunoglobulin that binds antibody

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Fc

constant fragment of immunoglobulin

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Fab2

antibody binding fragment resulting from cleavage below the hinge, does not have the constant region and its signaling capabilities

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Other than somatic recombination, what genetic mechanism increases diversity of Ig and TCR genes?

addition of N nucleotides by TdT

addition of P nucleotides

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RAG1 and RAG2

recombination genes in the immune system that recognize heptamer and nonamer sequences with spacers of either 23 or 12 base pairs

<p>recombination genes in the immune system that recognize heptamer and nonamer sequences with spacers of either 23 or 12 base pairs</p>
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Mechanism of V(D)J Recombination

  1. recombinase recognizes recombination signal sequence (RSS)

  2. recombinase brings the 12 and 23 RSS together

  3. recombinase cuts the DNA to produce a hairpin and a circular byproduct by covalently attaching ends

  4. hairpin cleaved randomly by another nuclease

  5. exonucleases, polymerases, and TdT modify the ends until DNA is reconnected by ligase

  6. imprecision leads to addition and deletion of nucleotides

<ol><li><p>recombinase recognizes recombination signal sequence (RSS)</p></li><li><p>recombinase brings the 12 and 23 RSS together</p></li><li><p>recombinase cuts the DNA to produce a hairpin and a circular byproduct by covalently attaching ends</p></li><li><p>hairpin cleaved randomly by another nuclease</p></li><li><p>exonucleases, polymerases, and TdT modify the ends until DNA is reconnected by ligase</p></li><li><p>imprecision leads to addition and deletion of nucleotides</p></li></ol><p></p>
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Positive selection of T lymphocytes

only T cells that have moderate affinity for self-MHC + peptide recieve a survival signal

<p>only T cells that have moderate affinity for self-MHC + peptide recieve a survival signal</p>
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Death by neglect

cell dies because it does not receive a signal to survive

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Negative selection of T lymphocytes

T cells that have high-affinity for self-MHC + peptide receive a death signal to produce tolerance

<p>T cells that have high-affinity for self-MHC + peptide receive a death signal to produce tolerance</p>
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MHC restriction

T-cells only recognize peptides + MHC molecules matching their own self-MHC type

<p>T-cells only recognize peptides + MHC molecules matching their own self-MHC type</p>
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Allogeneic response

immune system attack by a recipient against foreign antigens from a donor of the same species

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Syngeneic

no response when donor A T cells are mixed with donor A APCs

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Allogeneic

strong response when donor A T cells mixed with donor B APCs

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B-cell negative selection

self-reactive B cells are deleted or become anergic

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Anergic

not killed but non-responsive

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Clonal selection

T cells with receptors that recognize the specific pathogen are activated

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Clonal expansion

T-cell proliferation and differentiation results in effector cells that work to eliminate pathogens

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Function and activation of cytotoxic T cells

recognize target, and destroy cells infected with an intracellular pathogen

activated upon engagement of a T cell containing a CD8 corecpetor with an MHC class I APC

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Function and activation of TH1 helper cells

aid in combatting extracellular pathogens by activating macrophages

activated upon engagement of a T cell containing CD4 coreceptor with MHC class II APC

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Function and activation of TH2 helper cells

combat extracellular pathogens by activating B cells, good at combating helminths

activated upon engagement of a T cell containing a CD4 coreceptor with MHC class II APC

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Follicular helper T cell

within secondary lymphoid tissue to promote isotype switching and somatic hypermutation

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isotype switching

B cell changes the type of antibody it produces without changing the target specificity

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Function and activation of TH17 helper cells

combat extracellular pathogens by activating neutrophils

activated upon engagement of a T cell containing CD4 coreceptor with MHC class II APC

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Regulatory T cells

Inactivate self-reactive T cells to promote peripheral tolerance

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Memory T cells

long-lived T cells that promote an adaptive immune response to a pathogen upon subsequent exposure

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Secreting cells and function of IL-2

T cells

T-cell activation

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Secreting cells and function of IL-4

T cells, ILC2s

B-cell activation, T cell activation (TH2)

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Secreting cells and function of IL-10

monocytes, macrophages, T cells

anti-inflammatory

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Secreting cells and function of IL-12

dendritic cells, macrophages

TH1 helper T-cell and NK cell activation

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Secreting cells and function of IL-17

T cells, ILC3s

neutrophil activation

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Secreting cells and function of IFN-γ

T cells, macrophages, NK cells, ILC1s

macrophage activation

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IFN-a/IFN-B

macrophages, dendritic cells, virally infected cells

activation of NK cells, prevents viral replication

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Secreting cells and function of TGF-β

regulatory T cells

anti-inflammatory, peripheral tolerance, T-cell inactivation

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Antibody effector functions

neutralization, opsonization, complement activation, antibody dependent cellular cytotoxicity

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Neutralization (antibody effector function)

inactivation, prevents binding to cells

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Opsonization (antibody effector function)

binds to pathogens to facilitate phagocytosis

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Complement activation (antibody effector function)

activates the complement system to facilitate membrane attack and opsonization

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Antibody dependent cellular cytotoxicity (antibody effector function)

activates NK cells to trigger killing, triggers degranulation of other granulocytes

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Function and production of IgM

antibody isotype that acts as a B-cell receptor on the surface of naive B-cells, neutralizer, complement activator

produced by activated B cells in conjunction with IgD through alternative splicing

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Function and production of IgD

antibody isotype acting as a B-cell receptor on the surface of naive B cells, activates mast cells and basophils

produced by activated B cells in conjunction with IgM through alternative splicing

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Function of IgG

antibody isotype: neutralizes, opsonizes, complement activator, helps form and clear soluble immune complexes, helps activate NK cells in ADCC

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Function of IgE

antibody isotype: binding to antigen causes mast cell degranulation and release of inflammatory mediators, activates mast cells, basophils, and eosinophils

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Function of IgA

antibody isotype: found on mucosal surfaces, neutralizes, delivers pathogens to mucosa-associated lymphoid tissue

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How do we measure cytotoxic T-cell activity?

  1. incubate target cells with radioactive chromium which gets taken up into the cytoplasm

  2. mix effector cells and target cells at different ratios

  3. after a few hours, collect and measure radioactivity in the supernatant

  4. calculate specific lysis

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What cells are in the thymus?

bone-marrow derived cells and radiation resistant epithelial cells

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C-kit

receptor for stem cell factor cytokine

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CD34

marker for stem cells

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CD25

receptor for T cell growth factor IL-2

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AIRE

autoimmune regulator

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Instructive model of MHC restriction

CD8 ligation produces a different signal than CD4 ligation and the signal generated tells the cell what it should become

<p>CD8 ligation produces a different signal than CD4 ligation and the signal generated tells the cell what it should become</p>
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Kinetic signaling model of MHC restriction

all cells reduce CD8 expression on DP thymocytes, TCRs seeing MHC class I signal less and respond by increasing CD8 and turning off CD4, while TCRs seeing class II have unchanged signaling and loss of CD8 continues

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Transgenic

injecting DNA into an embryo results in those embryos sometimes incorporating that DNA

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Function of CD8 cells

become cytotoxic T-cells

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Function of CD4 T-cells

become helper T cells

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Which coreceptor is favored when TCRs recognize class I MHC?

CD8

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Which coreceptor is favored when TCRs recognize class II MHC

CD4

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What type of antigens are presented by MHC class I?

intracellular

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What type of antigens are presented by MHC class II?

extracellular

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Complementarity determining region

where molecules bind to their specific antigen

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CD28

costimulatory molecule on T cells that binds a ligand on APCs

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Function of αβ or δγ subunit

recognize antigen presented to T cell

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Function of CD4

recognize MHC class II molecule, transduction of antigen-binding signal

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Function of CD8

recognize MHC class I molecule, transcution of antigen-binding signal

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Function of CD3δ, CD3ε, CD3γ, CD3ζ

transduction of antigen-binding signal

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Function of CD28

required for co-stimulation of T-cell activation during primary immune response

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Function of CD45

transduction of antigen-binding signal and preferentially activating memory T cells

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Function of CTLA4

downregulate T-cell activation by dampening costimulatory signal

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Mechanism of class I peptide processing and loading

  1. phagolysosome and β-microglobulin find each other to facilitate peptide binding

  2. TAP transports peptides in

  3. ERAP trims peptides so they fit better into the grooves of MHC class I molecules

  4. stable vesicle buds off and is secreted

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Mechanism of class II peptide processing and loading`

  1. MHC class II binds invariant chain

  2. CLIP produced

  3. antigen is phagocytosed to a phagolysosome which fuses with MHC class II vesicle

  4. HLA-DM pulls out any peptides it can, so you are left with high-affinity binding peptides

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How do naive T cells become anergic?

encounter MHC-peptide complexes in the absence of CD28 co-stimulation