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HST.175 Immunology > 1) Innate Immunity, Ab+Antigens, Antigen Recep. & Gen. of Div. > Flashcards

1) Innate Immunity, Ab+Antigens, Antigen Recep. & Gen. of Div. Flashcards

1
Q

The 4 themes of Immunology are

1) Generation of (X)
2) (Y) vs. (Z) discrimination
3) Protection by (A) or destruction of non-self
4) (B)

A 
X = Diversity
Y = Self
Z = Non-self
A = Neutralization
B = Memory
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2
Q

Physical Barriers in Innate Immunity

A

Skin, Mucosa

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3
Q

Humoral Innate Immunity (Agglutinins/Collectins): Must be (X) to get effective agglutination

A

X = Multivalent

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4
Q

Humoral Innate Immunity: Antibacterial (X)

A

X = Peptides

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5
Q

Which complement pathway is antibody dependent

A

Classical (Alternative pathway is independent)

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6
Q

What 5 processes does the Complement system engage

A
  1. Bacterial lysis
  2. Phagocytosis
  3. Mast cell activation
  4. PMN recruitment
  5. Clearance of immune complexes
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7
Q

What type of Interferons are produced by both infected and sentinel cells to block further viral replication?

A

Type I Interferons (IFN-Alpha, IFN-Beta)

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8
Q

High levels of type I Interferons induce (X) and (Y)

A 
X = PKR (dsRNA dependent protein kinase)
Y = an Oligo A Synthase
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9
Q

PKR Mechanism
Must bind to (X) in a virally infected cell cytosol to be active. It is able to distinguish between host (X), which do not activate it, and viral (X), which do. When active, often blocks both (Y) and (Z) translation leading to
cell death and blockade of viral replication

A 
X = dsRNA
Y = Viral
Z = Host
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10
Q

Oligo A Synthase Mechanism
Must bind to (X) within cell cytoplasm to be
active. Once activated, the synthase makes oligo A, which can activate an
(Y) degrading enzyme (Z). The (Z) then destroys both viral and host (Y), also leading to cell death

A 
X = viral dsRNA
Y = RNA
Z = RNAse L
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11
Q

Cell Mediated Innate immune Response: Phagocyte subclasses

A

PMNs, Macrophages, etc.

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12
Q

NK cells secrete (X) for macrophage recruitment

A

X = IFN-Gamma

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13
Q

Virally infected cells and tumor cells can have downregulation of MHC-I and (X) can recognize cells with low levels of MHC I and lyse them.

A

X = NK Cells

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14
Q

Recognize heat shock proteins and aren’t MHC restricted

A

GammaDelta T cells

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15
Q

Pattern Recognition Receptors: NOD1

Binds (X) components found on (Y)

A 
X = peptidoglycan
Y = Gram- Bacteria
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16
Q

Pattern Recognition Receptors: NOD2

Binds (X) components found on (Y)

A 
X = peptidoglycan
Y = either Gram+ or Gram- receptors (bacteria)
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17
Q

NLRP family responds to cytosolic PAMPs and DAMPs by forming (X) which create active forms of (Y)

A 
X = Inflammosomes
Y = IL-1 and IL-18
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18
Q

Canonical inflammosome is activated by variety of bacterial products, crystals, ions, extracellular ATP, or other danger signals. NLRP proteins interact to form an
(X) through prionization. Bind to (Y), an adapter, to form the inflammasome, along with procaspase-1, which is inactive. Pro-caspase-1 is cleaved to form active Caspase-1. Caspase-1 cleaves (Z) to induce further inflammation. Inflammasome activation also can lead to inflammatory cell death
(A). Cell death is caused by an effector protein, (B), which pokes holes in the cell membrane

A 
X = Oligomer
Y = ASC
Z = pro-IL-1 and pro-
IL-18
A = pyroptosis
B = Gasdermin D (Gsdmd)
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19
Q

Non-canonical inflammosome: Activated by cytosolic (X) which binds directly to (Y). (Y) directly cleaves Gsdmd which then activates the NLRP3/ASC inflammasome and leads to (Z) production

A 
X = LPS
Y = Caspase-11 (Caspase 4/5 in humans)
Z = IL-1
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20
Q

What Pattern Recognition Receptor binds bacterial peptides which begin with fMet rather than Met?

A

fMet receptor

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21
Q

What Pattern Recognition Receptor recognizes bacterial carbohydrates? (non self sugars on pathogens)

A

Mannose receptor

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22
Q

(X) and (Y) are cytosolic proteins that reside in each cell with a CARD domain and a helicase domain. They are sensors for dsRNA present in infected cells only. They induce (Z) and (A)

A 
X = RIG-I
Y = MDA-5
Z = type I IFN
A = NFkB
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23
Q

Cytosolic DNA Receptors: (X) and (Y)

A

(X) cGAS
(Y) STING

dsRNA binds to cGAS, which makes a cyclic dinucleotide, cycic GMP-AMP (cGAMP). cGAMP causes STING to translocate to the Golgi, where it serves as a scaffold for IRF3. IRF3 goes to the nucleus and stimulates transcription of type I interferons (which induce the antiviral state in neighboring cells), as well as autophagy which helps redirect cytosolic microbes to the lysosome

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24
Q

Cytosolic DNA Receptor (recognizes cytosolic dsDNA, and forms a caspase-1 canonical inflammasome)

A

AIM2

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25
Q

PRRs: Location of TLRs and PAMP/DAMP Ligands

TLRs 1-9

A

Plasma membrane and
endosomal membranes of
dendritic cells, phagocytes, B cells, endothelial cells, and many other cell types

Various microbial molecules including bacterial LPS and peptidoglycans, viral
nucleic acids

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26
Q

PRRs: Location of NOD-like receptors (NLRs) and PAMP/DAMP Ligands

(NOD1/2, NLRP Family [inflammosome])

A

Cytosol of phagocytes, epithelial cells, and other cells

Bacterial cell wall peptidoglycans (NOD1/2)

Intracellular crystals (urate, silica); changes in cytosolic ATP and ion concentrations; lysosomal damage (NLRP family)

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27
Q

PRRs: Location of RIG-like receptors and PAMP/DAMP Ligands

RIG-1, MDA-5

A

Cytosol of phagocytes and other cells

Viral RNA

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28
Q

PRRs: Location of Cytosolic DNA sensors (CDSs) and PAMP/DAMP Ligands

(AIM2, cGAS)

A

Cytosol of many cell types

Bacterial and viral DNA

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29
Q

PRRs: Location of C-type lectin–like receptors (CLRs) and PAMP/DAMP Ligands

(Mannose receptor, Dectin)

A

Plasma membranes of
phagocytes

Microbial surface carbohydrates with
terminal mannose and fructose (Mannose Receptor)

Glucans present in fungal cell walls (Dectin)

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30
Q

PRRs: Location of Scavenger receptors and PAMP/DAMP Ligands

CD36

A

Plasma membranes of
phagocytes

Microbial diacylglycerides

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31
Q

PRRs: Location of N -Formyl met-leu-phe receptors and PAMP/DAMP Ligands

(FPR and FPRL1)

A

Plasma membranes of
phagocytes

Peptides containing N -formylmethionyl
residues

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32
Q

PRRs: Location of soluble receptor (Pentraxins) and PAMP/DAMP Ligands

(C-reactive protein)

A

Plasma

Microbial phosphorylcholine and phosphatidylethanolamine

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33
Q

PRRs: Location of soluble receptor (Collectins) and PAMP/DAMP Ligands

(Mannose-binding lectin, Surfactant proteins SPA and SP-D)

A

Plasma

Carbohydrates with terminal mannose and fructose (Mannose-binding lectin)

Various microbial structures (SP-A, SP-D)

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34
Q

PRRs: Location of soluble receptor (Ficolins) and PAMP/DAMP Ligands

(Ficolin)

A

Plasma

N -Acetylglucosamine and lipoteichoic acid components of the cell walls of gram-positive bacteria

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35
Q

PRRs: Location of soluble receptor (Complement) and PAMP/DAMP Ligands

(Complement proteins)

A

Plasma

Microbial surfaces

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36
Q

PRRs: Location and target of TLR1:TLR2

A

Cell surface, Bacterial lipopeptides

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37
Q

PRRs: Location and target of TLR2

A

Cell surface, Bacterial peptidoglycan (GP Bacteria)

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38
Q

PRRs: Location and target of TLR4

A

Cell surface, LPS (GN Bacteria)

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39
Q

PRRs: Location and target of TLR5

A

Cell surface, Bacterial flagellin

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40
Q

PRRs: Location and target of TLR2:TLR6

A

Cell surface, Bacterial lipeptides

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41
Q

PRRs: Location and target of TLR3

A

Endosome, dsRNA

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42
Q

PRRs: Location and target of TLR7

A

Endosome, ssRNA

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43
Q

PRRs: Location and target of TLR8

A

Endosome, ssRNA

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44
Q

PRRs: Location and target of TLR9

A

Endosome, CpG DNA (viral or bacterial, unmethylated DNA)

45
Q

Phases of Adaptive Immunity

  1. Recognition of (X)
  2. (Y) Activated
  3. Effector phase of antigen elimination
  4. Return to homeostasis with (Z) cells that remain
A 
X = Antigen
Y = Lymphocytes
Z = Memory
46
Q

Two signal theory of adaptive immunity

A

First signal: Antigen
Second signal: (Danger signal), microbial
products or the innate response to microbial products

47
Q

Main defense against extracellular microbes

A

Humoral immunity (B cell produced antibodies)

48
Q

Two types of humoral immunity

A
  1. Active - Your own antibody response (Primary, Secondary)
  2. Passive (transfer of antibodies/cells generated by another host) (Maternal/fetal, Ig Immunization, Transferal of cells)
49
Q

(X): every individual has numerous clones, each of which arose from a single cell with a unique receptor that recognizes a specific antigen

A

X = clonal selection

50
Q

Antibody stucture: (X) heavy chains, (Y) light chains. Variable regions (with (Z)) and constant regions

A 
X = 2
Y = 2
Z = CDRs (Complementarity determining regions)
51
Q

What does papain cleave an Ab into?

A

2 Fab and 1 Fc

52
Q

What does pepsin cleave an Ab into?

A

1 F(ab’)2 and 1 constant tail (pFc’)

53
Q

IgA: (X) immunity. Forms (Y) with (Z)

A 
X = mucosal
Y = dimer
Z = J-chain
54
Q

IgD: Most important as marker of (X) as their receptor

A

X = naive B cells

55
Q

IgE: What is its main purpose?

A

Immediate type hypersensitivity (allergies). Dealing with helminth infections

56
Q

IgG: Seen after the (X) response. Forms (Y)

A 
X = Primary (it is secondary)
Y = Monomer
57
Q

IgM: Initial Isotype (primary response) (seen before (X) to IgA, IgE, and IgG). Forms (Y) with (Z)

A 
X = Isotype switching
Y = Pentamer
Z = J-chain
58
Q

Antibody Function: As non-soluble, membrane bound (X): Recognition of antigen by the (X) leads to B cell activation and proliferation.

A

X = B cell receptor

59
Q

Antibody Function: Soluble, free Ab (List 6 general functions)

A
  1. Neutralization
  2. Classical pathway complement activation
  3. Opsonization
  4. Antibody-dependent cellular cytotoxicity (ADCC)
  5. Agglutination
  6. Immediate type hypersenistivity
60
Q

Antibody Function: Neutralization: Neutralizes toxins or antigens by (X) them (all secreted
Ab)

A

X = binding

61
Q

Antibody Function: Complement pathway (classical).

(X) binds to constant regions of antibodies (Y). (Z) coats microbes and increases opsonization. Small fragments of (A) attract leukocytes to the site of
inflammation. (B) creates holes in microbial membranes, leading to osmotic lysis

A 
X = C1q
Y = IgM, IgG
Z = C3b
A = C3 and C5
B = Membrane Attack Complex
62
Q

Antibody Function: Opsonization: Secreted (X) coats free antigen and (Y) on phagocytes see the bound antigen and phagocytize it (IgG)

A 
X = IgG
Y = FcγR receptors
63
Q 
Antibody Function: Antibody dependent cellular cytotoxicity (ADCC): Binds directly to
antigen on cell and (X)
on NK cells phagocytize
the cell (this is the (Y)
role of NK cells) (IgG)
A 
X = FcγR
Y = adaptive
64
Q

Antibody Function: Immediate type hypersensitivity: (X) is generated after the first exposure to an antigen. (Y) have free (Z) which bind secreted (X) very tightly. When the second exposure to the same antigen occurs, the (X) bound to the MC is crosslinked, leading to degranulation of the (Y) and (A) release (mechanism for allergies, anaphylaxis, etc). (X)

A 
X = IgE
Y = Mast cells and basophils
Z = FcεRI
A = Histamine
65
Q

Anibody Function: Mucosal immunity: (X) is dimerized, binds to a receptor on the (Y) of intestinal cells, is transcytosed to the luminal side of the cell (with some of the receptor removed by (Z)) where it protects against mucosal pathogens.
Interestingly, oral protein often leads to tolerance, not immunity. (IgA, IgM)

A 
X = IgA
Y = blood side
Z = proteolysis
66
Q

Antibody Function: Neonatal Immunity: Maternal (X) crosses the placenta via (Y) to fetus. Additionally, (Z) are in breast milk.

A 
X = IgG
Y = FcRn
Z = IgA and IgG
67
Q

Ab-Antigen Binding: Binding happens at the end of the (X) regions, with the binding site determined by (Y) (CDRs), especially (Z).

A 
X = VH and VL
Y = complementarity determining regions
Z = CDR3
68
Q

CDRs look like fingers reaching toward the antigen and present on both the (X) and (Y) chains

A 
X = Heavy
Y = Light
69
Q

Ab-Antigen Binding: Antigens are delivered to (X) in the (Y)

A 
X = follicular B cells
Y = Lymph node
70
Q

What 2 cell types take up and present antigen in the LYMPHATICS?

A

1) Follicular dendritic cells

2) Subcapsular sinus macrophages

71
Q

What migratory cells take up and present antigen from the periphery in the lymph nodes?

A

Activated dendritic cells

72
Q

Multivalent structures can cluster (X) and give a T-independent signal to activate B cells

A

X = BCRs

73
Q

Small molecules that need to be conjugated to a carrier to get an immune response are called (X)

A

X = Haptens

74
Q

Haptens are (X) (they can be bound by an antibody once the antibody is made). They are not (Y) (They cannot provoke an antibody response on their own)

A 
X = antigens
Y = immunogens
75
Q

All cells have multiple V, D and J segments to be used in (X)

A

X = V(D)J recombination

76
Q

V(D)J recombination: D segments are only on (X) and (Y) genes

A 
X = heavy chain (BCR) genes
Y = beta chain (TCR) genes (TCR-Beta, TCR-Delta)
77
Q

What is the goal of gene rearrangement?

A

Create diverse (10^9) receptors with very few genes

78
Q

Gene rearrangement begins in the developmental stage in (X) and (Y) cells

A 
X = pre-B
Y = pre-T
79
Q

What do V, D, and J stand for?

A 
V = Variable region
D = Diversity region
J = Junctional region
80
Q

What are the two rearrangement events in VDJ recombination?

A

First joining a D to a J and then a V segment to the

fused DJ segment

81
Q

Gene rearrangement control: Each segment must be flanked by a (X)

A

RSS, Recombination Signal Sequence

82
Q

What is an RSS

A

Adjacent to the coding
region is a conserved heptamer (CACTGTG or its reverse complement
CACAGTG) followed by a spacer (see next section) and then a relatively conserved nonamer

83
Q

The spacer in an RSS is either approximately (X) in length or approximately (Y) in length. RSSs with (X) spacers recombine only with RSSs with (Y) spacers. The (X)/(Y) spacer rule
This prevents V-V, D-D, J-J
recombination

A 
X = 12 bp
Y = 23 bp
84
Q

What are the VDJ gene rearrangement sequence (4 steps)

A

1 - Synapsis
2 - Cleavage
3 - Hairpin opening and end-processing
4 - Joining

85
Q

VDJ recombination: STEP 1:
Cleavage of the DNA to create a double stranded break. (X - 2 molecules) form a tetrameric complex that recognizes (Y) and creates a single strand (ss) break (or “nick”) between the (Z) and coding sequence

A 
X = Recombination activating gene-1 (RAG-1) and recombination activating gene -2 (RAG-2)
Y = RSSs
Z = heptamer
86
Q

VDJ recombination: STEP 2: The coding sequence free end displaces the other strand, forming a (X) at
the (Y) end of the coding sequence

A 
X = hairpin
Y = 3’
87
Q

VDJ recombination: STEP 3:

What plays a significant in opening the DNA hairpin?

A

Artemis

88
Q

VDJ recombination: STEP 4:
Junctional diversity is generated by adding or removing nucleotides.
1. Addition of (X) –a random addition of up to (Y) extra nucleotides directed by (Z) in a non-template dependent manner
2. Addition of (A) (these compensate for uneven cleavage of hairpins)

A 
X = N nucleotides
Y = 20
Z = terminal deoxynucleotidyl transferase (TdT)
A = P nucleotides
89
Q

VDJ recombination: STEP 5:
What 3 double strand break repair proteins (enzymes) helps join the newly processed ends?

Without these enzymes, recombination does not take
place and there are no B or T cells

A

DNA PKcs, XRCC4, DNA ligase IV

90
Q

Combinatorial Diversity generated by VDJ recombination and juxtaposition of 2 randomly generated chains (Heavy-light or alpha-beta). How many V, D, and J segments can be combined randomly to make IgG heavy chain?

A

45 V, 23 D, 6 J

91
Q

(X) is the largest contribution to the diversity of antigen receptors. Removal of nucleotides (endonucleases) or addition of N or P nucleotides at the V-D, D-J, or V-J junctions

A

X = Junctional diversity

92
Q

What are the VDJ steps in BCR Heavy and Light Chain rearrangement?

A

Heavy Chain D-J rearrangement
Heavy Chain V-DJ rearrangement
Light Chain V-J rearrangement

93
Q

What are the VDJ steps in TCR alpha and beta chain rearragement

A

TCRβ D-J rearrangement
TCRβ V-DJ rearrangement
TCRα V-J rearrangement

94
Q

There are 2 mechanisms for VDJ Recombination:

1) Segments in SAME orientation recombine by (X)
2) Segments in OPPOSITE orientation recombine by (Y)

A 
X = Deletion
Y = Inversion
95
Q

Adaptive Immune Response

1) Generation of (X) (need to recognize an amazing (X) of antigens) - VDJ recombination and somatic hypermutation
2) Determining (Y) (to identify dangerous pathogens/tumors/etc) - (Z) in development, (A) in the periphery
3) Protection via (B) or destruction of non-self - Destroy pathogens/tumors/etc
4) (C) - Faster response in the future

A 
X = diversity
Y = self v. non-self
Z = Central Tolerance (negative selection)
A = peripheral tolerance and anergy
B = neutralization
C = Memory
96
Q

Innate vs. Adaptive Dichotomies

A

Innate (germline encoded receptors, broad reactivity; agglutinins, complement, phagocytes, NK cells, etc)

Adaptive (receptors generated by DNA
recombination, have specificity and memory; TCR/BCR, etc)

97
Q

What 2 categories are under adaptive immunity?

A

Humoral (B cell produced Ab, etc.) & Cell Mediated (CTLs, etc)

98
Q

What 2 categories are under T cells?

A

MHC I/CD8+ T cells (CTL, intracellular pathogens)

MHC II/CD4+ T cells (helper T cells, TH)

99
Q

What 3 categories are under Helper T Cells

A

Th1 v. Th2 v. Th17

100
Q

2 classifications for lymphoid organs, their purpose, and examples of each

A

Central lymphoid organs (sites of generation): bone marrow and thymus

Secondary lymphoid organs (sites of activation): lymph nodes, spleen,
Peyer’s patches (gut)

101
Q

Morphology of the Thymus

A

Cortex, medulla (T cell development)

102
Q

Lymph node morphology: cortex of primary follicles (X) cells and secondary
follicles ((Y), where response to antigen happens); and
medulla. T cells lie in between follicles in (Z).

A 
X = naïve B
Y = germinal centers
Z = T cell zone/paracortex
103
Q

Spleen morphology: (immunologically relevant) (X) pulp. The area around the arterioles (Y) is the T cell zone and there are
lymphoid follicles with (Z) which are the B cell zones.

A 
X = white pulp
Y = periarteriolar lymphoid sheaths
Z = germinal centers
104
Q

Innate Immunity: NK Cells:
i. Origin: (X).
ii. No rearrangement of (Y) genes
iii. Function:
1. Cell mediated cytotoxicity - e.g. lyse cells found to have low or no self (Z)
a. Kill target cells by the same mechanisms as CD8+ T cells (A)
b. Express a complex array of activating and inhibitory receptors (e.g. (B), which
recognize MHC Class I molecules).
2. Antibody Dependent Cellular Cytotoxicity
(intertwined with the adaptive immune response)
3. Early (C) production- e.g. before an effector T cell response has been mounted or has been recruited
4. Secretion of a slew of (D)

A 
X = bone marrow
Y = TCR or Ig
Z = MHC I
A = perforin, granzyme, TNFa, FasL, TRAIL
B = KIRs
C = IFN-g
D = cytokines
105
Q

Innate Immunity: B1 B Cells:
Secrete “(X)” in body cavities (pleura, peritoneum). Somewhat restricted set of V regions and very little use of (Y), BCR recognizes (Z)

A 
X = natural antibody
Y = N nt
Z = common foreign epitopes
106
Q

Innate Immunity: γδ T cells

X) specificity than normal (αβ) T cells. Recognize (Y

A 
X = Less
Y = bacterial proteins/lipids
107
Q

Innate Immunity: Intracellular Infections (viral, mycobacterial, rickettsial, listerial…)

Antigens can be on cell surface (like viral proteins in the cell membrane) which can be dealt with by (X) or other tools, but most are dealt with via adaptive immunity (i.e. virally infected cells release cytokines, dead cells release viral particles, (Y) get activated, upregulate MHC II and (Z), travel via lymphatics to draining LN, the APCs activate (A), the CTLs kill the infected cells)

A 
X = natural antibodies
Y = APCs
Z = B7.1/B7.2
A = naïve CD8+ T cells (CTLs)
108
Q

Adaptive Immunity: In the (X), rearrangement of the BCR or TCR occurs (as well as elimination of (Y)), in the periphery, these naïve cells continuously recirculate among the (Z) until they see antigen (which may never happen) and proliferate/activate into (A)

A 
X = central lymphoid organs
Y = self reactive cells
Z = SLO
A = mature lymphocytes

HST.175 Immunology (4 decks)

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