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Immunology > Checkpoint questions (up to midterm material) > Flashcards

Checkpoint questions (up to midterm material) Flashcards

1
Q

what are the 2 major cell types that function in the adaptive immune system and in which arm do they function

A

T cells: cell-mediated immunity
B cells: humoral immunity

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2
Q

how do symbiotic microorganisms protect us from pathogen infection

A

compete with pathogenic microbes
produce antimicrobial substances
strengthen the physical barrier
immune system modulation

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3
Q

what are the different categories of pathogens

A

viruses
bacteria (and protozoa)
fungi
parasites

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4
Q

what are some examples of physical barriers

A

skin
oral mucosa
respiratory epithelium
intestine

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5
Q

what are some examples of chemical barriers

A

histadins
RegIIIy
cathelicidin
defensins
enzymes (lysozyme and pepsin)

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6
Q

how does the enzyme lysozyme act as a chemical barrier

A

creates defects in the peptidoglycan layer and exposes the cell membrane to other antimicrobial agents

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7
Q

what is the mode of action of beta-defensins

A

positively charged defensins interact with the charged surface of the cell membrane and become inserted in the lipid bilayer
this leads to the formation of pores and loss of membrane integrity

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8
Q

what are the two lineages derived from hematopoietic stem cells

A

lymphoid and myeloid

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9
Q

what are the different types of granulocytes in the immune system

A

neutrophils: phagocytosis and bactericidal mechanisms
eosinophils: killing of parasites
basophils: promote allergic response and augmentation of anti-parasitic immunity
mast cells: release histamine

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10
Q

what are the different types of agranulocytes in the immune system

A

monocytes: premature macrophages circulating in blood
macrophages: PHAGOCYTOSIS, APC and cytokine production
dendritic cells: APC AND CYTOKINE PRODUCTION
NK cells: recognize and destroy virus-infected and tumor cells
ILCs: secrete cytokines to activate innate immune cells

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11
Q

what are the different steps in inflammation

A

bacteria trigger macrophages to release cytokines and chemokines
vasodilation and increased permeability cause redness heat and swelling
inflammatory cells migrate to tissue
inflammatory mediators (which cause pain) are released

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12
Q

what are the cardinal signals of inflammation

A

heat, swelling, redness, pain

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13
Q

what are the major classes of PRRs

A

TLRs: bind many different ligands (bacteria, viruses, fungi)
Lectin: bind carbohydrates
Scavenger receptor: bind -ve charged ligands
Cytosolic innate receptor: binds intracellular PAMPs
Opsonin receptor: binds pathogens tagged with opsonins

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14
Q

what types of PAMPs can PRRs bind

A

Lectin = sulphated sugars and polysaccharides
Scavenger receptors = LTA, LPS
Cytosolic innate receptors = DNA, RNA, cyclic dinucleotides
opsonin receptor = opsonized pathogens

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15
Q

what are the major cytokines secreted during an innate immune response

A

interleukins, interferons, IFN, TNF

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16
Q

what structural features are shared within the TLR family of proteins

A

leucine-rich repeats
ITRs
overall C form

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17
Q

what key signalling molecules responsible for aiding the innate immune response are secreted by macrophages

A

TNF-alpha
IL-1
IFN-y
IFN-a
IFN-B
IL-6
IL-8
IL-12

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18
Q

what are the 4 stages of neutrophil migration

A

rolling adhesion (tethering and rolling)
tight binding (activation and firm adhesion)
Diapedesis (transmigration)
Migration (chemotaxis)

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19
Q

describe how NK cells can detect an intracellular pathogen

A

cytokines (such as IL-12) cause NK cells to travel to virus-infected cell and bind their activtaing receptors so that perforin and granzymes can be released

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20
Q

why is the release of TNF in the bloodstream problematic

A

leads to systemic edema which causes decreased blood volume
blood vessels collapse causing multiple organ failure and eventually death

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21
Q

which complement protein is most important in directly targeting the pathogens for destruction

A

C3

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22
Q

what are the cleavage products of C3 and what does each one do to facilitate pathogen elimination

A

C3a: causes inflammation by triggering degranulation of leukocytes
C3b: opsonizes pathogen by covalently attaching to its surface - renders pathogen more susceptible for phagocytosis

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23
Q

what are 3 pathways of complement activation

A
  1. alternative: C3 undergoes spontaneous hydrolysis to initiate deposition of C3 converetase on microbial surfaces
  2. Lectin: MBL and ficolins bind carbohydrates on the pathogen surface
  3. Classical: C1q interacts with pathogen surface or with antibodies bound to surface
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24
Q

during the alternative pathway of complement activation, 2 C3 converses are formed. which proteins make these up?

A

classical + lectin: C4b2a
alternative: C3bBb

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25
Q

which complement protein is responsible for forming pores in pathogen membrane with the MAC

A

C5b initiates MAC formation (pore formation)
C9 completes it

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26
Q

which acute-phase proteins are the 2 initiating opsonins of the lectin and classical pathways?

A

lectin = Mannose-binding lectin (MBL) and ficolins assosciated with MASPs
classical = C-reactive protein (CRP)

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27
Q

which complement cleavage products constitute the classical C3 convertase

A

C4b and C2a

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28
Q

what are some common complications associated with a deficiency in the complement system?

A

abnormal clearance of bacteria
hypersensitivity responses and autoimmune disorders
increased infection (due to malfunction in MAC)

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29
Q

what are the differences between primary and secondary lymphoid tissue?

A

primary: where T and B cells are made and mature
secondary: where T and B cells congregate and interact with pathogens

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30
Q

explain the roll of secondary lymphoid tissue in the adaptive immune response

A

site for antigen capture and presentation, activation of naive lymphocytes, clonal expansion and differentiation

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31
Q

at what locations with lymph nodes are T and B cells activated?

A

T-cell activation: paracortical area
B-cell activation = primary lymphoid follicle and germinal centre

32
Q

how are antigens delivered to Mucosa-Associated Lymphoid Tissues (MALT)?

A

Peyers patches in the gut are covered with M cells which capture and deliver antigens from the lumen to immune cells in MALT through transcytosis.

33
Q

describe the structure and composition of an antibody

A
  • 2 heavy chains
  • 2 light chains
  • antigen binding site at NH2 terminal
  • effector site at COOH terminal
  • disulfide bonds (join chains)
34
Q

what are the functions associated with an antibodies primary components

A

NH2 terminal (variable): antigen binding
COOH terminal (constant): effector function

35
Q

define the Fab region of an antibody

A

each antibody has 2
antigen binding activity

36
Q

define the Fc region of an antibody

A

each antibody has 1
does not interact with antigen
carries out biological activity
differs between H chain isotypes

37
Q

what is the importance of an MHC molecule in the adaptive immune system

A

MHC presents peptides on themselves for recognition - needed for T-cell activation

38
Q

what are the 5 major functions of soluble Igs

A

antigen binding
neutralization
opsonization
complement activation
Antibody-Dependent Cellular Cytotoxicity

39
Q

what type of antigens do MHC class I and II present

A

MHC I: small peptides (8-10aa) from intracellular proteins
MHC II: larger peptides (13-25aa) from extracellular proteins

40
Q

what subunits are required for a properly functioning TCR complex

A

a-subunit and B-subunit
CD4 or 8 coreceptor
MHC
CD3

41
Q

list the 5 major soluble Ig isotypes

A

IgG
IgM
IgA
IgE
IgD

42
Q

what are similarities between TCRs and BCRs/Igs

A
  • have variable and constant regions
  • specificity - recognize one specific antigen
  • go through clonal expansion
  • membrane-bound form
43
Q

what are differences between TCRs and BCRs/Igs

A
  • Igs have a free-floating form, TCRs MUST be membrane bound
  • TCRs need MHC to recognize peptides
  • TCRs only recognize peptides, BCRs recognize peptides, carbohydrates and more
44
Q

why is the CD3 complex required in a functional TRC complex

A

CD3 complex recruits signalling molecules that are activated upon TCR engagement - drives T-cell activation

45
Q

compare and contrast the structures of MCH I and II

A
  • MHC I has 1 soluble and 1 TM domain, MHC II has 2 TM domains
  • MHC I binds shorter peptides, MHC II binds larger peptides
  • Antigen binding site of MHC I is a1a2 and MHC II is a1B1
  • MHC I binds intracellular pathogens, MHC II extracellular pathogens
  • MHC I present to CD8, MHC II present to CD4
  • MHC II has CLIP
46
Q

What are the similarities between somatic recombination in T and B cells

A
  • a-chain (T) and light chain (B) undergo VJ combination
  • B-chain (T) and heavy chain (B) undergo VDJ recombination
  • initiated by RAG-1 and RAG-2 proteins
  • generate junctional diversity
  • guided by flanking DNA sequences
47
Q

what are the differences between somatic recombination in T and B cells

A
  • TCR has a and B chains, BCR has heavy and light chains
  • T cells in thymus, B cells in bone marrow
48
Q

what key component of an immunoglobulin is removed by alternative splicing to produce soluble, secreted immunoglobulins

A

membrane-spanning (transmembrane) domain

49
Q

deficiencies in RAG-1 and RAG-2 cause a form of SCID in which patients lack B and T cells. Why is this the case

A

RAG proteins are essential for V(D)J recombination
deficiency prevents the generation of functional BCRs and TCRs.

50
Q

how is the V domain of the heavy chain and light chain genes broken up

A
  • During V(D)J recombination, RAG-1 and RAG-2 cleave the RSSs, facilitating the rearrangement of gene segments.
  • The resulting joined segments form the variable regions of the heavy and light chains, which are critical for the antigen-binding specificity of antibodies.
51
Q

describe the process of making heavy chains

A
  • somatic recombination combines D and J regions
  • second round of SR combines V and DJ regions
  • transcription creates the primary RNA trasncript
  • splicing creates mRNA
  • translation completes assembly of the heavy chain polypeptide
52
Q

describe the process of making light chains

A
  • somatic recombination combines V and J regions
  • transcription creates the primary RNA trasncript
  • splicing creates mRNA
  • translation completes assembly of the heavy chain polypeptide
53
Q

what are the mechanisms by which B cells generate receptor diveristy

A

combinational diversity: use of different V D and J segments
junctional diversity: different N and P nucleotides in each clone

54
Q

explain the process of antigen presentation by MHC class I

A
  • MHC Ia chain binds calnexin and then B2 binds
  • MHC I complex is released from calnexin and binds chaperon proteins then binds TAP
  • antigenic peptide fragments from the cytosol are delivered to the ER by TAP
  • this peptide binds MHC I and completes its folding
  • MHC I is released from the TAP complex and exported to the cell membrane
55
Q

explain the process of antigen presentation by MHC class II

A
  • invariant chain (li) forms complex with MHC II
  • li is cleaves leaving CLIP bound to the MHC II
  • phagolysosomes with imported antigens fuse with MHC II vesicle
  • HLA-DM binds MHC II, releasing CLIP and allowing the antigen peptide to bind
  • MHC II travels to the cell surface
56
Q

what is the role of cross-presentation in dendritic cells

A

DC’s take up, process and present antigens from exogenous sources with MHC I to CD8 T-cells

57
Q

give an example of non-peptide antigen presentation

A

small lipid containing antigens, small molecules, or metabolites can be presented by CD1 or MR1 proteins for the activation of NK cells or unconventional T-cells

58
Q

what are the 2 primary modes of mast cell degranulation

A

IgE-dependent (immunologic): occurs when an antigen binds to IgE antibodies that are already attached to high-affinity IgE receptors
IgE-independent: (non-immunologic): does not involve IgE receptors but directly stimulates the mast cells to release their granules (e.g. by MPGRX2 receptor)

59
Q

explain the roll of the host-microbiota cross-talk in atopic dermatitis pathogenesis

A

Host-microbiota cross-talk has mechanisms involving dysbiosis, impaired skin barrier function, altered immune responses, and inflammation.

60
Q

how does atopic dermatitis impact overall quality of life

A
  • painful, itchy skin
  • impaired sleeps
  • missed work/school
  • financial burden
  • social isolation
  • depression
61
Q

what classifies mast cells as “sentinels”

A
  1. they are tissue-resident cells found at host-environment junctions
  2. they have diverse receptor expression to detect a variety of molecules
  3. rapid response to stimuli - activation occurs in seconds to minutes
62
Q

what bacterial molecules do MRGPRX2/b2 detect to induce mast cell activation

A

quorum-sensing molecules
neuropeptides
antimicrobial peptides

63
Q

what are some advantages of using therapeutics which enhance the body’s immune response against infection to treat infections over conventional antibiotics with direct antimicrobial effects

A

reduce the risk of antibiotic resistance
broad-spectrum efficacy
preservation of beneficial microbiota
reduce side effects

64
Q

why might a patient be given mupirocin ahead of surgery

A

reduce the risk of post-operative infections decontamination of nasal carriage prevention of surgical site infections effective against MRSA

65
Q

what distinguishes a super antigen and what does it lead to the production of

A

A superantigen is an antigen that can induce a very strong immune response by bypassing the normal antigen-processing pathway
non-specific T-cell activation
cytokine “storm”

66
Q

how does S.aureus evade the host immune system

A

interferes with complement activation
proteins SAK, Sbi, Spa and SSL10 prevent C1q from binding antibody
SCIN stabilizes inactive C3 convertase fibrin sheild
ClfA proteins bind to host structurral proteins to promote adhesion
shield MAMPs by coating the bacterium with host proteins to block the detection of peptidoglycan

67
Q

what costimulatory interaction is required between T cells and APCs

A

CD28 on T cells binds to B7-1 (CD80) and B7-2 (CD86) on APCs

68
Q

what is the importance of activating protein-tyrosine kinases at the initiation of the formation of an immunological synapse between T cells and APCs

A

PTK activation (Lck and ZAP-70) allows for 3 signal transduction pathways from the T cell receptor to become activated

69
Q

clonal expansion of T cells requires the activation of transcription factors to promote gene activation. what 3 transcription factors are activated during T-cell activation

A

NFAT, NFkB and AP-1

70
Q

is binding of a single cell-surface Ig to an antigen sufficient for B cell activation? why or why not

A

it is not sufficient for B cell activation
Full activation requires additional costimulatory signals from T helper cells, along with cytokine support

71
Q

how is B-cell activation through BCR complex different from T-cell activation through the TCR complex

A
  • BCR recognizes native antigens, TCR recognized antigens on MHC
  • have different signalling complexes
  • B cell co-receptor is CR2, CD19 and CD81 while T-cell co-receptor is CD8 and CD4
  • BCRs must cluster together, TCRs don’t
72
Q

how is the transcriptional activation in B cells during their activation similar to that within T cells?

A

initial antigen recognition
requires costimulatory signals activation of shared intracellular signaling pathways
induction of the same transcription factors
changes in gene expression

73
Q

why were Edward Jenner’s observations critical to our understanding of immunology

A

introduced the concept of vaccination, demonstrated the principles of immunity and immunological memory, and laid the groundwork for modern vaccine development

74
Q

what key observations led to the discovery of soluble mediators that protect us from infection

A

discovery of soluble mediators that protect us from infection arose from key observations in the fields of humoral immunity, the complement system, cytokine signaling, and advancements in molecular biology

75
Q

who contributed to important discoveries associated with vaccines

A

Edward Jenner: first live vaccine
Louis Pasteur: first live attenuated vaccine

76
Q

what are the 4 principles of immunology

A

recognition: distinguish self vs foreign
response: elimination of disease
regulate: prevent things from going out of control
recall: memory

Immunology (20 decks)

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