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UNIT 6 > IMMUNO > Flashcards

IMMUNO Flashcards

1
Q

primary and secondary immune organs

A

Primary- phagocytes, complement system and barriers like skin
Secondary- T cells, B cells, lymphocytes, macrophages, dendritic cells

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2
Q

the ways in which cell types are identified

A

by: histology (size, shape, stain, nucleus characteristics), enzymes and antibodies that recognize immune cells

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3
Q

antibody and its Fc region

A

flexible specific adaptor due to a high affinity antigen binding site and Fc region in order to neutralize toxins (prevent binding to receptors) and aid in phagocytosis

*Fc regions: located on the opposite end of the antigen binding site and is a place where effector cells or proteins can bind to

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4
Q

antibody and its Fc region

A

flexible specific adaptor due to a high affinity antigen binding site and Fc region in order to neutralize toxins and aid in phagocytosis

*Fc regions: located on the opposite end of the antigen binding site and is a place where effector cells or proteins can bind to

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5
Q

opsonins

A

antibodies that are capable of forming a high affinity bridge to enhance phagocytosis of bacteria found in the extracellular space (opsonization)

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6
Q

complement

A

serum protein that recognizes bound antibody molecules and can result in cell lysis

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7
Q

CD

A

“Cluster of Differentiation”: notation system of antibodies that recognize immune cells

examples:
CD3–> mature T-cells
CD4–> T-helper/regulatory
CD8–> T-cytotoxic

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8
Q

neutrophil

A

the end product of myeloid differentiation that will not divide and contains primary/azurophilic and secondary/specific granules (bactericidal and hydrolytic enzymes of the cell)

make up 60-70% of the circulating white cells (12hrs) and complete its life cycle at the site of inflammation when released from the bone marrow to fight off infection

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9
Q

eosinophil

A

1-3% of the circulating leukocytes (30min half life and 12 day survival in tissues) with the ability to destroy parasitic worms by releasing granule contents due to Eosinophilic Basic Protein (EBP)

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10
Q

macrophages-monocytes

A

derived in the bone marrow and function as effector cells at sites of inflammation phagocytosing bacteria (creating phagosomes and phagolysosomes once the bacteria is degraded) but can exist in a resting state when inflammation is not present

  • intracellular killing: bacteria, yeast, parasites
  • extracellular killing (in vitro): virally infected cells, larger parasites, tumor cells

**binding of bacterial components to signaling receptors induces the synthesis of inflammatory cytokines

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11
Q

pathway of monocyte precursor to immune response initiation

A

monocyte (precursor)–> macrophage–> T-cell activation–> initiation of immune responses

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12
Q

mast cell

A

expels parasites by releasing granules that contain active agents such as histamine

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13
Q

lymphocytes

A

B-cells: expresses immunoglobulin producing antibodies when fully differentiated as a plasma cell (or can become memory cells) and is only able to express a single variable region (idiotype) with the highest affinity to the antigen that undergoes clonal expansion

T-cells (cytotoxic T-cells): helps B-cells through regulating the immune response and acting as an antigen specific effector cell restricted to killing cells with self and foreign antigen limiting target cell types to infected cells and tumor cells (prevents B-cells from attacking our own cells)

  • *some can kill non-self cells associated with transplants
  • *histology: no granules present in cytoplasm
  • *pathogen-reactive lymphocytes proliferate
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14
Q

lymphocytes

A

B-cells: expresses immunoglobulin producing antibodies when fully differentiated as a plasma cell

T-cells (cytotoxic T-cells): helps B-cells through regulating the immune response and acting as an antigen specific effector cell restricted to killing cells with self and foreign antigen limiting target cell types to infected cells and tumor cells

  • *some can kill non-self cells associated with transplants
  • *histology: no granules present in cytoplasm
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15
Q

natural killer cells

A

granular lymphocytes that kill tumor and virally infected cells WITHOUT specificity

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16
Q

what is the pathway that leads to the production of platelets?

A

hematopoietic stem cell–> myeloid precursor–> megakaryocyte–> platelets

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17
Q

what do each end of immunoglobulin molecules do?

A

constant region binds to transmembrane surface and variable region has antigen-binding sites at its tips

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18
Q

proteins that make up immunoglobulin molecules

A

heavy chains and light chains make up constant and variable regions which are attached by disulfide bonds at hinge region and contains carbohydrates

  • variable region is located at Y tips and contains antigen-binding sites
  • light chains are the outside of Y branches
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19
Q

proteins that make up immunoglobulin molecules

A

heavy chains and light chains make up constant and variable regions which are attached by disulfide bonds at hinge region and contains carbohydrates

  • variable region is located at Y tips and contains antigen-binding sites
  • light chains are the outside of Y branches
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20
Q

IgG

A
  • most common
  • longest half life
  • transportation across placenta
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21
Q

IgA

A
  • one form is secreted (resists acid hydrolysis)
  • highly glycosylated
  • monomers/dimers/trimmers
  • capable of transportation across epithelium
  • opsonizing and agglutinating (sticks)
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22
Q

IgM

A
  • primitive
  • potent complement fixation
  • no opsonization-immune cells don’t have IgM receptors
  • greatest molecular mass
  • 4 heavy chain domains without a hinge region
  • J chain
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23
Q

IgE

A
  • responds to parasites
  • allergic reactions
  • few in circulation–>binds to target/mast cells
  • mediates release of granule contents from mast cells
  • mediates changes in vascular permeability
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24
Q

**proteolytic degradation of IgG

A

IgG –(protease cleavage)–> 1 Fc + 2 Fab fragments

Fc= crystallizable and made of constant region repeats
Fab= antigen binding with the variable region
  • –not really important but in the notes—-
  • papain digests hinge region
  • pepsin degrades heavy chain beginning at carboxy terminal and ending at the region of interchain disulfide bonds
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25
Q

proteolytic degradation of IgG

A

IgG –(protease)–> 1 Fc + 2 Fab fragments

Fc= crystallizable and made of constant region repeats
Fab= antigen binding with the variable region
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26
Q

framework residues and hypervariable regions of the variable region of immunoglobulin molecules

A

framework residues: same between proteins and contribute to the folding of the V region producing the antigen binding site

hypervariable region: 3 in each heavy and light chain contributing to the specific antigen binding site and forming a continuous surface to complement a specific antigen; regions are distant in primary sequence (on two chains) but are close together in the antigen binding site

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27
Q

monoclonal antibody

A

bound reversibly to an antigen and the affinity between the two is the sum of all of their interactions expressed by the law of mass action

K= [Ab Ag] / [Ab][Ag]

*have affinity but since they bind to the same epitope, there is no cooperativity and no increase in avidity

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28
Q

why are immunoassays used and what are 4 examples?

A

a process of measuring specific proteins through their properties as antigens or antibodies

examples: ELISA, immunofluorescence, FACS and Western Immunoblot

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29
Q

how do immunoassays work and when are they used?

A

?

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30
Q

cross-reactivity

A

antiserum cross reacts with other antigens besides the specific antigen which may be due to impurities (already present antibody or antigenic contaminating proteins) or common/similar structures (homology) on antigens such as epitopes

could lead to: masking an expected result, false results, lowering of the effective sensitivity of the assay or could have no effect on immunoassay test results

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31
Q

techniques used to eliminate cross reactivities

A
  • absorbtion: using cross reacting material to remove the activity that causes the cross reaction
  • affinity chromatography: a method used to purify antigens using an insoluble support (ex: agarose) and mild denaturant (ex: salt) to wash away unbound molecules and elute specifically bound molecules
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32
Q

techniques used to eliminate cross reactivities

A
  • absorbtion: using cross reacting material to remove the activity that causes the cross reaction
  • affinity chromatography: a method used to purify antigens using an insoluble support and mild denaturant to wash away unbound molecules and elute specifically bound molecules
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33
Q

*preparation of monoclonal antibodies

A
  1. immunize an animal
  2. isolate spleen cells (B-cells which can only live a few days without myeloma cells)
  3. fuse cells to plasmacytoma tumor cells (unlimited growth)
  4. select for hybrids of tumor cells and B-cells
  5. clone hybridomas so each cell grows independently
  6. select the individual clone with specificity you need
  • production of a single clone of one B-cell
  • no heterogeneity (population of antibody molecules identical with the same specificity)
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34
Q

what happens when an immunization if to a specific protein?

A

the clones have individual specificities to all parts of the molecule (epitopes) and to other molecules that have contaminated the immunization preparation

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35
Q

serum sickness

A

immune reaction (antibodies) to injected proteins causing a hypersensitivity reaction

*this is why you cannot use mouse monoclonals to treat humans unless B or T cells are eliminated

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36
Q

chimeric monoclonal antibodies

A

constant regions: human
variable regions: from mouse monoclonal

“-ximab” drugs

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37
Q

human monoclonal antibodies

A

totally made through molecular biology techniques

“-umab” drugs

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38
Q

ELISA

A

*Enzyme-Linked InnumoSorbant Assay:

add an antibody to tube filled with antigen and incubate it, wash away unbound antibody, add second antibody with a covalently-bound enzyme and incubate it, wash away unbound antibody, detect amount of second antibody-enzyme complex by adding a chemical reagent that turns a certain color in its presence

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39
Q

Immunofluorescence

A

used to identify a specific cell type, cellular structure or a pathogen through use of specific antisera, unbound antisera is washed away, a second antibody specific for the first antibody but with a fluorescent molecule is added and binds, the fluorescent molecule emits light when exposed to UV light which can be seen under a special microscope

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40
Q

FACS

A

*Fluorescence Activated Cell Sorter- Flow Cytometry:

machine using lasers with multiple detectors that scan many cells for size and immunofluorescence detecting several antigens an creating a histogram (x-axis: intensity of fluorescence, y-axis: number of cells) and dot plot (top right: both positive, bottom left: both negative)

  • cell sorters: analyzes and sorts based on amount of fluorescence
  • flow cytometers: only analyze cells
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41
Q

*Western Immunoblot

A

electrophoretical separation of mixtures of proteins which are bound to nitrocellulose paper, antibody binds to protein of interest, unbound antibodies are washed away, specific antibodies are detected like the ELISA assay providing information such as: amount of antigen (density of bands), molecular weight (how far bands travel), different forms of antigen

*quantitative and qualitative information

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42
Q

Western Immunoblot

A

electrophoretically separated mixtures of proteins which are bound to nitrocellulose paper, antibody binds to protein of interest, unbound antibodies are washed away, specific antibodies are detected like the ELISA assay providing information such as: amount of antigen, molecular weight, different forms of antigen

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43
Q

titer

A

how much you can dilute blood before loss of activity

44
Q

phases of antibody production in response to an antigen

A
  1. lag/inductive/latent period
  2. exponential increase in antibody concentration
  3. steady state (peak antibody concentration is reached)
  4. decay/decline: small amount of antibody is detected
45
Q

immunologic rememberance response

A

increase in affinity for IgG which persists in blood and response more quickly when the antigen presents itself again

46
Q

*toxin vs. toxoid

A

toxin: will kill you since the amount required for a response is lethal
toxoid: protein is chemically modified so it is antigenically the same but not lethal

47
Q

Hapten-Carrier

A

hapten: small molecule that cannot induce an antibody response on its own and is recognized by the B-cell
carrier protein: helps make hapten immunogenic and is recognized by the helper T-cell or B-cell

48
Q

Hapten-Carrier

A

hapten: small molecule that cannot induce an antibody response on its own and is recognized by the B-cell
carrier protein: helps make hapten immunogenic and is recognized by the helper T-cell or B-cell

49
Q

Antigen Presenting Cells (APC)

A

macrophages and dendritic cells which initiate the interaction with antigen by endocytosis or phagocytosis enhanced with a complement, pre-existing antibody or specific receptors through presentation of antigen as a small peptide (antigen/MHC complex) and a second/co-stimulatory signal (B7 antigen on presenting cell binds to CD28 on T-cell) critical for an immune response (B-cell or T-cell activation and proliferation)

50
Q

Antigen Presenting Cells (APC)

A

macrophages and dendritic cells which initiate the interaction with antigen by endocytosis or phagocytosis enhanced with a complement, pre-existing antibody or specific receptors through presentation of antigen as a small peptide

51
Q

what are two things essential for inducing immunity?

A

presentation of antigen AND co-stimulation

52
Q

what contributes to the loss of many T and B cell precursors

A

most rearranged genes won’t function which is the usual mechanism to bring about diversity in antigen receptors (rearrangement of small pieces of DNA)

53
Q

why does the concept of one gene one protein do not hold for immunoglobulin molecules?

A

they have a constant region and a variable region

  • in the germ line, the constant regions are not next to the variable regions and there are different configurations for Ig gene material compared to the myeloma
  • multiple Vs, Js and Ds (segments which proved that rearrangement occurs) are brought together by signal sequences from enzymes
54
Q

VJD segments of heavy vs. light chains

A

heavy chain: V (38-46), D (23), J (6)
light chain: V (34-38), J (5)

  • of the two light chain possibilities (kappa and lambda), only one is kept active
  • germline DNA undergoes somatic recombination for the segments to be joined (light- VJ joins; heavy- DJ then VDJ joins)
55
Q

how are V, D and J brought together?

A

enzymes (recombinase genes, RAG 1 and RAG 2) are induced in developing B-cells- signal sequences determine which segments can be joined through random, independent combinations

*RAG- grabs one end of the immunoglobulin and pulls it around and together causing a piece of DNA to be irreversibly discarded (section is cleaned and ligated)

56
Q

mechanism of the generation of junctional diversity (pay special attention to what TdT can do)

A
  1. RAG complex cleaves the heptamer to yield DNA hairpins
  2. RAG complex opens hairpins generating palindromic P-nucleotides
  3. N-nucleotide additions by TdT/terminal deoxynucleotidyl transferase (random additions only in heavy chains of B-cells in the pro B stages until an overlap is achieved); repair enzymes repair
  4. strands are paired
  5. unpaired nucleotides are removed by an exonuclease
  6. gaps are filled by DNA synthesis and ligation to form coding joint

***P (in all joining junctions) and N regions made at edit sites by the random additions by TdT may cause DNA to exceed reading frame and stop encoding for the correct AA (results in incorrect IgM which won’t be able to be inserted into the membrane)

57
Q

early pro-B cell to immature B cell

A

heavy chain rearrangement:
(early pro-B) D-J rearrangements on both chromosomes
(late pro-B) V-DJ rearrangement on first chromosome and if nonproductive, then on second chromosome and if nonproductive, then apoptosis

light chain rearrangement:
(pre-B) rearrange K gene on first chromosome and if nonproductive, then on second chromosome and if nonproductive, then lambda gene on first chromosome and if nonproductive, then on second chromosome and if nonproductive, then apoptosis (several changes to rearrange in light chain since heavy chain has already been successful in rearranging)

*immature B cell will express mu and K or mu and lambda signal when rearrangement has ended based on if a productive rearrangement was made with K or lambda gene in light chain rearrangement

58
Q

what causes the switch from IgM to IgD?

A

selective splicing of primary RNA transcripts made of both IgM and IgD constant regions

*splicing control also determines whether a cell synthesizes membrane bound Ig (2 extra exons) or secreted Ig

59
Q

**AID

A

*Activation-Induced Cytidine Deaminase

enzyme that attacks regions allowing for another editing inducing mutations and allowing section of DNA being cut and goes to gamma chain (causes mutations that produce antibody diversity)

  • makes mutations DURING the immune response across DNA causing single base changes
  • responsible for class switching and somatic hypermutation
60
Q

class switching

A

a variable region is joined to a new constant region (except in IgD) which brings about more diversity only with the help of T-cells and during an immune response

  • since the variable region stays the same, class switching does not affect antigen specificity
  • the antibody retains affinity for the same antigens, but can interact with different effector molecules
  • daughter cells can produce antibodies of different isotypes
61
Q

somatic hypermutations

A

targets rearranged gene segments encoding the variable region (gives it the capability to respond to new threats- alters affinity)

*only in immune cells and not transmittable to offspring

62
Q

**B-cell vs. T-cell receptor formation

A
  • most of the mechanisms for their formations are the same except T-cell receptor does not undergo somatic hypermutation
  • also, T-cell will NOT change during the immune response
63
Q

regulation of T-cell proliferation in the thymus

A

T is selected for the elimination of strong self-reacting T-cells (tolerized to self antigens) which occurs in order to prevent autoimmune diseases (also related to transplantations)

  • T-cells become MHC-restricted (peptide is presented by MHC molecule for TCR recognition) and lineage committed since the thymus provides the appropriate microenvironment
  • selection occurs at several stages (positive and negative selection)
64
Q

what would a deficiency in RAG 1 or RAG 2 lead to?

A

inability to make T and B cells leading to immunodeficiency

65
Q

which MHC molecules do CD4 and CD8 lineage T ells recognize?

A

CD4- beta 2 of MHC II

CD8- alpha 3 of MHC I

66
Q

DiGeorge’s Syndrome

A

human T-cell immunodeficiency due to a loss of a TF required for thymic epithelial differentiation

67
Q

embryonic thymic development

A

thymus is formed from the fusion of the 3rd pair of pharyngeal pouch (endoderm) and the cleft (ectoderm)

68
Q

what are the major regions of the thymus and what happens with age?

A

regions: cortex, medulla and cortical-medullary junction

* function decreases as age increases

69
Q

migration of T-cells to and from the thymus

A
  • T-cell precursors (prothymocytes which are not completely committed yet) leave the bone marrow and enter the thymus via blood vessels at the cortico-medullary junction
  • mature T-cells leave the thymus and enter secondary lymphoid tissues (GALT, spleen, lymph node) through venules in the medulla
  • chemokines and sphingosine 1-phosphate signal traffic for cell movement
  • stage is identified by cell surface markers
70
Q

2 major lineages of T-cells

A

gamma:delta and alpha:beta

71
Q

fate of immature thymocytes

A

death by apoptosis if MHC is not recognized

72
Q

pre-T cell receptor

A

2 chains (heterodimer)–> heterodimer with itself (superdimer- more complex)–> signaling components (pre-T cell receptor)–> TCR

73
Q

synthesis of T-cell receptor alpha and beta chains

A
  • alpha: alpha chain locus can sustain many attempts at a functional rearrangement (usage of upstream components to try and create a functional product)
  • its rearrangement will always eliminate the linked delta-chain locus

-beta: two attempts can be made to achieve a productive rearrangement of the beta chain locus

74
Q

early T-cell development mechanism

A

progenitor cell–> proliferation–> double negative T cells commit to T lineage–> rearrange beta genes–(check-point for pre-TCR)–> proliferating double negative pre-T cells–> immature double-positive cells rearrange alpha genes–(checkpoint for TCR)–> mature double positive cells (FULLY FUNCTIONAL TCR)

*all steps occur in cortex except proliferation of progenitor cells which occurs in the medulla

75
Q

double positive thymocytes recognition of self peptides presented by MHC

A 
receptor binds self-peptide:self-MHC class I--> CD8
receptor binds self-peptide:self-MHC class II--> CD4
76
Q

negative selection of alpha:beta T-cells

A
  • by dendritic cells, macrophages and other cells in the thymus in which tight binding will initiate apoptosis and moderate binding allows the cell to live
  • prevents too strong of a recognition
77
Q

ligands

A

self peptide/MHC complexes expressed on stromal and hematopoietic cells

  • self peptides are derived from endogenous (self) sourcses
  • Aire TF plays a key role in regulating the expression of some tissue specific antigens in medullary epithelial cells in the thymus
78
Q

engagement of the TCR by self-MHC:peptide complexes

A

can lead to either further maturation or to cell death

79
Q

Avidity model of T cell selection

A

depends on the affinity of the TCP-peptide/MHC interaction and the density of the peptide/MHC on the thymic epithelial cell

  • avidity determines the total strength of signal delivered which dictates the outcome of the signaling event
  • balance of avidity and signal intensity for positive selection whereas too much avidity= negative selection and too little will cause death by neglect
80
Q

**T-cell repertoire

A

sum of all of the specificities of the mature T cells produced by the thymus and this differs between individuals

*shaped by thymic selection and modified in the periphery throughout life by the encounters with antigens

81
Q

what is needed for suppression of autoreactive T cells by regulatory T cells?

A

interaction with the same antigen-presenting cell

*important for tissue tolerance

82
Q

what will activate the complement and classical pathways

A

pathogens–> complement

antibodies–> classical

83
Q

endotoxin

A

Structure: heat stable hydrophobic lipid rich end and hydrophilic polysaccharide rich end that is antigenic and is the determinant of the O antigen; epitope: 3-4 repeating monosaccharides

Function: produces the toxic LPS which resides in the Lipid A region (we know this since cleaving the polysaccharide from the lipid A will not affect the activity of the endotoxin) responsible for the body’s response to gram negative bacteria

84
Q

*gram negative sepsis

A

endotoxin shock/septic shock due to gram negative bacterial infection causing decreased BP and CO

  • is the response to endotoxins
  • high incidence of DIC (disseminated intravascular coagulation) causing thrombi (due to an enzyme cascade) and eventual depletion of coagulation factors which then causes hemorrhage and necrosis
85
Q

systemic introduction of LPS in low quantities and in high quantities

A

low: *fever, moderate immunostimulation which causes infiltration of neutrophils and macrophages along with increased vascular permeability and swelling
high: *fever, headache, vomiting, endotoxin shock (septic shock)

86
Q

acute respiratory distress syndrome

A

associated with septic shock or gram negative insult to the lungs

87
Q

why is LPS a pyrogen?

A

it causes fever

88
Q

assays used to make sure something is pyrogen-free

A
  • USP rabbit pyrogen test

- LAL- Limulus Amebocyte Lysate

89
Q

pathway leading to survival after LOCAL infection with gram-negative bacteria

A

macrophages are activates and secrete TNF-alpha in tissue–> increased release of plasma proteins into tissue–> increased phagocyte and lymphocyte migration to tissue–> platelet adhesion to BV wall–> phagocytosis of bacterial–> vessel occlusion–> containment of infection–> antigens are carried to lymph nodes–> survival

90
Q

pathway leading to death after SYSTEMIC infection with gram negative bacteria (sepsis)

A

macrophages are activated in the liver and spleen to release TNF-alpha into blood–> systemic edema causes decreased blood volume, hypoproteinemia, neutropenia followed by neutrophilia–> decreased blood volume causes collapse of vessels–> organ failure/septic shock–> death

91
Q

mediators of the LPS response

A

outside the intact organism, LPS is not toxic

inside–> proteins (IL-1 and TNF-alpha) produced by LPS-stimulated macrophages serve as the endogenous mediator which induce blood vessels to become more permeable enabling effector cells and fluid containing soluble effector molecules to enter infected tissue causing inflammation at the site of infection

92
Q

cytokine effects

A

overlapping effects in the cell in which too much would be bad

93
Q

IL-1 beta and TNF-alpha

A

induce blood vessels to become more permeable enabling effector cells and fluid containing soluble effector molecules to enter infected tissue causing inflammation at the site of infection

94
Q

IL-6

A

makes heat by inducing fat and muscle cells to metabolize

95
Q

CXCL8

A

recruits neutrophils guiding them to infected tissue

96
Q

IL-12

A

activates NK cells that secrete cytokines strengthening the macophages’ response to infection

97
Q

tumor necrosis factor

A

induces intravascular coagulation and hemorrhage in the tumor serving as an immunoregulatory molecule while mediating inflammatory processes

*stimulates T and B cells along with inducing fevers just like IL-1

98
Q

anti-TNF-alpha antibodies

A

block the induction of shock induced by LPS

99
Q

TLR

A

toll-like receptors that bind signals inducing signal transduction pathways and production of cytokines

100
Q

what complex recognizes LPS?

A

the TLR4, MD2, CD14 complex which is them broken up by a cascade of P that then produces inflammatory cytokines

101
Q

what does TLR4 homodimer recognize?

A

gram-negative bacteria and is located on the plasma membrane of macrophages, dendritic cells, mast cells and eosinophils

102
Q

interleukin-1

A

cytokine that is secreted by activated and stimulated macrophages that is produces as a pro-cytokine and must be cleaved by caspase 1 (which is activated by the inflammasome) before being released

103
Q

inflammasome

A

inflammation sensitive complex that activates caspase 1

*target of anti-inflammatory drugs

104
Q

superantigen

A

binds to MHC class II and then T-cell receptor and CD28 in which activation occurs and the production of TNF alpha and IL 1 occur

105
Q

toxic shock syndrome

A

produced by staph aureus and causes fever, vomiting, diarrhea, shock and multi-organ dysfunction (due to mediators)

UNIT 6 (6 decks)

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