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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
which complement protein is responsible for forming pores in pathogen membrane with the MAC
C5b initiates MAC formation (pore formation) C9 completes it
26
which acute-phase proteins are the 2 initiating opsonins of the lectin and classical pathways?
lectin = Mannose-binding lectin (MBL) and ficolins assosciated with MASPs classical = C-reactive protein (CRP)
27
which complement cleavage products constitute the classical C3 convertase
C4b and C2a
28
what are some common complications associated with a deficiency in the complement system?
abnormal clearance of bacteria hypersensitivity responses and autoimmune disorders increased infection (due to malfunction in MAC)
29
what are the differences between primary and secondary lymphoid tissue?
primary: where T and B cells are made and mature secondary: where T and B cells congregate and interact with pathogens
30
explain the roll of secondary lymphoid tissue in the adaptive immune response
site for antigen capture and presentation, activation of naive lymphocytes, clonal expansion and differentiation
31
at what locations with lymph nodes are T and B cells activated?
T-cell activation: paracortical area B-cell activation = primary lymphoid follicle and germinal centre
32
how are antigens delivered to Mucosa-Associated Lymphoid Tissues (MALT)?
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
describe the structure and composition of an antibody
- 2 heavy chains - 2 light chains - antigen binding site at NH2 terminal - effector site at COOH terminal - disulfide bonds (join chains)
34
what are the functions associated with an antibodies primary components
NH2 terminal (variable): antigen binding COOH terminal (constant): effector function
35
define the Fab region of an antibody
each antibody has 2 antigen binding activity
36
define the Fc region of an antibody
each antibody has 1 does not interact with antigen carries out biological activity differs between H chain isotypes
37
what is the importance of an MHC molecule in the adaptive immune system
MHC presents peptides on themselves for recognition - needed for T-cell activation
38
what are the 5 major functions of soluble Igs
antigen binding neutralization opsonization complement activation Antibody-Dependent Cellular Cytotoxicity
39
what type of antigens do MHC class I and II present
MHC I: small peptides (8-10aa) from intracellular proteins MHC II: larger peptides (13-25aa) from extracellular proteins
40
what subunits are required for a properly functioning TCR complex
a-subunit and B-subunit CD4 or 8 coreceptor MHC CD3
41
list the 5 major soluble Ig isotypes
IgG IgM IgA IgE IgD
42
what are similarities between TCRs and BCRs/Igs
- have variable and constant regions - specificity - recognize one specific antigen - go through clonal expansion - membrane-bound form
43
what are differences between TCRs and BCRs/Igs
- 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
why is the CD3 complex required in a functional TRC complex
CD3 complex recruits signalling molecules that are activated upon TCR engagement - drives T-cell activation
45
compare and contrast the structures of MCH I and II
- 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
What are the similarities between somatic recombination in T and B cells
- 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
what are the differences between somatic recombination in T and B cells
- TCR has a and B chains, BCR has heavy and light chains - T cells in thymus, B cells in bone marrow
48
what key component of an immunoglobulin is removed by alternative splicing to produce soluble, secreted immunoglobulins
membrane-spanning (transmembrane) domain
49
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
RAG proteins are essential for V(D)J recombination deficiency prevents the generation of functional BCRs and TCRs.
50
how is the V domain of the heavy chain and light chain genes broken up
- 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
describe the process of making heavy chains
- 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
describe the process of making light chains
- 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
what are the mechanisms by which B cells generate receptor diveristy
combinational diversity: use of different V D and J segments junctional diversity: different N and P nucleotides in each clone
54
explain the process of antigen presentation by MHC class I
- 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
explain the process of antigen presentation by MHC class II
- 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
what is the role of cross-presentation in dendritic cells
DC's take up, process and present antigens from exogenous sources with MHC I to CD8 T-cells
57
give an example of non-peptide antigen presentation
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
what are the 2 primary modes of mast cell degranulation
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
explain the roll of the host-microbiota cross-talk in atopic dermatitis pathogenesis
Host-microbiota cross-talk has mechanisms involving dysbiosis, impaired skin barrier function, altered immune responses, and inflammation.
60
how does atopic dermatitis impact overall quality of life
- painful, itchy skin - impaired sleeps - missed work/school - financial burden - social isolation - depression
61
what classifies mast cells as "sentinels"
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
what bacterial molecules do MRGPRX2/b2 detect to induce mast cell activation
quorum-sensing molecules neuropeptides antimicrobial peptides
63
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
reduce the risk of antibiotic resistance broad-spectrum efficacy preservation of beneficial microbiota reduce side effects
64
why might a patient be given mupirocin ahead of surgery
reduce the risk of post-operative infections decontamination of nasal carriage prevention of surgical site infections effective against MRSA
65
what distinguishes a super antigen and what does it lead to the production of
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
how does S.aureus evade the host immune system
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
what costimulatory interaction is required between T cells and APCs
CD28 on T cells binds to B7-1 (CD80) and B7-2 (CD86) on APCs
68
what is the importance of activating protein-tyrosine kinases at the initiation of the formation of an immunological synapse between T cells and APCs
PTK activation (Lck and ZAP-70) allows for 3 signal transduction pathways from the T cell receptor to become activated
69
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
NFAT, NFkB and AP-1
70
is binding of a single cell-surface Ig to an antigen sufficient for B cell activation? why or why not
it is not sufficient for B cell activation Full activation requires additional costimulatory signals from T helper cells, along with cytokine support
71
how is B-cell activation through BCR complex different from T-cell activation through the TCR complex
- 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
how is the transcriptional activation in B cells during their activation similar to that within T cells?
initial antigen recognition requires costimulatory signals activation of shared intracellular signaling pathways induction of the same transcription factors changes in gene expression
73
why were Edward Jenner's observations critical to our understanding of immunology
introduced the concept of vaccination, demonstrated the principles of immunity and immunological memory, and laid the groundwork for modern vaccine development
74
what key observations led to the discovery of soluble mediators that protect us from infection
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
who contributed to important discoveries associated with vaccines
Edward Jenner: first live vaccine Louis Pasteur: first live attenuated vaccine
76
what are the 4 principles of immunology
recognition: distinguish self vs foreign response: elimination of disease regulate: prevent things from going out of control recall: memory

Immunology (22 decks)

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