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Immunology > Check point questions - up to final > Flashcards

Check point questions - up to final Flashcards

1
Q

what 3 major cell types found in the thymus play a role in T-cell development

A

Thymic epithelial cells (cTECs and mTECs)
macrophages
dendritic cells

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2
Q

what is the function of thymic epithelial cells in T-cell development

A

cTECs: provide signals for positive selection at DP stage - make sure TCR’s have the affinity for the MHC I or II molecule on APC presenting the antigen
mTECs: role in negative selection at SP stage - SP T-cells in the medulla that bind MHC presenting self-antigens on the surface of mTECs or CDs die by apoptosis

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3
Q

what is the function of thymocytes in T-cell development

A
  • the developing T-cells themselves
  • interact with TECs and other cells
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4
Q

what is the function of dendritic cells in T-cell development

A
  • Found predominantly in the thymic medulla
  • present self-antigens to developing T-cells during the negative selection process
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5
Q

why are individuals who lack the IL-7 receptor unable to produce functioning T cells

A
  • the IL-7 receptor is important for T cell commitment in the double -ve stage
  • IL-7 functions as a signalling protein required for TCR gene rearrangement
    IL-7 provides anti-apoptotic signal (survival)
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6
Q

explain the role of Notch1 in T-cell development and its importance in lymphoid progenitor cell commitment to thymocyte development

A
  • required for T-cell lineage commitment when CLP enters the thymus
  • suppresses alternative fates (B-cell differentiation)
  • turned off during B-selection (at DN4) as a consequence of pre-TCR signalling
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7
Q

what checkpoints can occur as part of the T cell development process

A
  1. TCR-B rearrangement: occurs at DN3 stage, Tests whether the TCRβ chain can pair with a surrogate α-chain to form a functional pre-TCR complex.
  2. TCR-a rearrangement: occurs at DP stage, tests the ability of the complete αβTCR to interact with self-MHC molecules presented by thymic epithelial cells. (positive and negative selection)
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8
Q

why don’t all 3 T cell development checkpoints need to be passed by a developing T cell

A
  • yd T cells do not rearrange the β-chain of the TCR (skip pre BCR checkpoint)
  • some specialized T-cell subsets recognize unconventional antigens or ligands might not strictly require positive selection
  • Some γδ T cells and Treg cells may tolerate self-reactivity because they recognize stressed or altered self-antigens or directly suppressing immune responses
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9
Q

why do developing thymocytes need to use the pre-Ta chain to progress through the B-chain checkpoint?

A
  • the pre-Tα chain serves as a surrogate partner for the newly rearranged TCRβ chain
  • promotes allelic exclusion to ensure each T cell expresses a single, unique TCRβ chain
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10
Q

what are the 3 possible fates of double positive thymocytes continuing their development in the thymus?

A
  1. T-cell has no affinity for MHC on cTEC - leads to death by neglect (apoptosis)
  2. T-cell has moderate affinity for MHC on cTEC - leads to positive selection/maturation so SP thymocyte (what we want!!)
  3. T-cell has high affinity for MHC on cTEC - leads to negative selection (apoptosis)
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11
Q

which signal in differentiating progenitor cells is required to commit differentiation to B-cell development

A

signals from the TFs E2A, FOX01, EBF and PAX5

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12
Q

what are the critical checkpoints of B cell development

A
  1. pre-BCR testing
  2. central tolerance (-ve selection 1)
  3. peripheral tolerance (-ve selection 2)
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13
Q

what is the composition of the surrogate light chain and how does it resemble an immunoglobulin light chain

A

composition = y5 + VpreB
- pairs with a successfully rearranged Ig heavy chain, forming the pre-BCR complex

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14
Q

why is allelic exclusion of an immunoglobulin heavy chain that has not recombined necessary to normal B-cell function

A
  • necessary to ensure that each B cell expresses a single, unique B-cell receptor (BCR) with a specific antigen-binding site
  • maintains specificity and functionality of the adaptive immune system
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15
Q

compare and contrast the 3 possible fates of negative selection of self-reactive immature B cells

A
  1. Clonal Deletion (Apoptosis): Self-reactive B cells that strongly bind to self-antigens undergo apoptosis
  2. Receptor Editing: additional light chain rearrangements give immature B cells in bone marrow additional chances to replace auto reactive BCR with non reactive BCR
  3. Anergy (Functional Inactivation): Anergic B cells are functionally inactivated and cannot respond to their antigen even if they encounter it again
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16
Q

define the process of peripheral tolerance that occurs in B-cell development in the spleen

A

in SLO’s (such as the spleen) peripheral tolerance ensures that self-reactive B cells are either deleted, inactivated, or prevented from responding to self-antigens

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17
Q

what is the role of T cell priming in an adaptive immune response

A
  • priming is the first contact that antigen-specific naive T cells have with an antigen
  • happens in SLO’s by interactions between APCs and naïve T cells
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18
Q

both macrophages and DCs are capable of phagocytosis and processing antigens. why are macrophages not a major contributor to T-cell activation?

A
  • DCs are the primary initiators of T-cell activation due to their role in antigen presentation, high expression of co-stimulatory molecules, and efficient migration to lymph nodes
  • Macrophages are more involved in effector functions such as clearing pathogens and modulating immune responses, rather than in initiating new T-cell responses from naïve T cells
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19
Q

explain the process of T cell migration into SLOs

A
  • binding of L-selectin to GlyCAM-1 and CD34 allows T-cell rolling on endothelium
  • LFA-1 is activated by CCR7 signalling in response to CCL21 or CCL19 on endothelial cell surface
  • activated LFA-1 binds to ICAM-1
    lymphocyte enters lymph node via diapedesis
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20
Q

what costimulatory interaction is required between T cell and APCs

A

CD28 on the T-cell binds B7 on the APC

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21
Q

describe the role of TH1 cells

A
  • release IFN-y
  • amplify host responses to intracellular pathogens through classical activation of macrophages
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22
Q

describe the role of TH2 cells

A
  • release IL4, 5 and 13
  • coordinate type 2 responses by recruiting eosinophils, mast cells and basophils
  • target helminth’s and parasites + repair tissue injury
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23
Q

describe the role of TH17 cells

A
  • release IL 17 and 22 to produce the production of AMPs by epithelial cells
  • coordinate type 3 responses by recruiting neutrophils
  • target extracellular bacteria and fungi
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24
Q

describe the role of CTLs

A

induce apoptosis in infected target cells while sparing neighbouring uninfected cells
kill by releasing perforin, granzymes and granulysin

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25
Q

summarize the extrinsic pathway of apoptosis that CTLs use on target cells

A
  • the Fas ligand binds and trimerizes Fas
  • clustering of death domains allows Fas to recruit FADD
  • FADD recruits and activates pro-caspase 8
  • activated cascade 8 cleaves pro-caspase 3 which cleaves I-CAD
  • CAD enters the nucleus and cleaves DNA
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26
Q

summarize the intrinsic pathway of apoptosis that CTLs use on target cells

A
  • mitochondria release cytochrome C which binds to Apaf-1
  • this assembles into an apoptosome which activates pro-caspase 9 which then activates pro-caspase 3
    -pro-caspase 3 cleaves I-CAD then CAD enters the nucleus and cleaves DNA
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27
Q

explain the role of Tregs in peripheral tolerance

A
  • bind to DC then release TGF-B and IL10
  • inhibit the activation of other T cells
  • target self and microbiome-derived pathogens
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28
Q

explain the interactions that must occur on the surface of a B cell that recognizes a thymus-dependent antigen for activation to take place

A
  • BCR binds and internalizes one epitope on the antigen
  • CD40 on B cell binds CD40L on helper T cell - signal for survival and proliferation
  • MHC II on B cell presens a different epitope of the same antigen and presents it to TCR of helper T cell
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29
Q

how are B cells that recognize TI-1 activated

A
  • multivalent pathogen with repeating epitopes binds dimerized BCR signalling and TLR on B cell surface
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30
Q

how are B cells that recognize TI-2 activated

A
  • multivalent antigen binds to BCR and cause cross-linking
  • CR2 on co receptor on B cell recognizes C3d on pathogen
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31
Q

what signals are provided by TH cells to activate B cells recognizing TD antigens

A
  • CD40:CD40L = signal for survival and proliferation
  • IL-21 = proliferation and differentiation
  • cytokines = isotype switching
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32
Q

characteristics of primary foci in B-cell differentiation

A
  • clusters of proliferating B cells that form early during the B-cell differentiation process
  • no TFH interaction
  • form in the medullary cords of lymph nodes or the red pulp of the spleen (outside the follicle)
  • composed of proliferating plasmoblasts
  • produce low-affinity IgM
  • role in early neutralization
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33
Q

characteristics of secondary foci in B-cell differentiation

A
  • clusters of plasma cells that form later (after the germinal center reaction) in B cell differentiation
  • remain inside the follicle
  • close association with TFH
  • Consist of B cells in germinal centers
  • produce high affinity class-switched antibodies (IgE, IgA, IgG)
  • role in pathogen clearance
34
Q

why is it important that centrocytes undergo a second round of selection within germinal centers

A
  • Ensuring affinity maturation by selecting B cells that produce high-affinity antibodies.
  • Preventing autoimmunity by eliminating self-reactive B cells.
  • Optimizing the immune response by retaining only the most effective B cells.
  • Supporting long-term immunity by generating high-quality memory B cells
35
Q

how does the activity of TH cells drive isotype/class switching

A
  • the cytokine they secrete will determine which isotype is produced
36
Q

what are the properties and functions of IgM

A
  • low affinity
  • not class switched
  • rapid first phase of B cell response to primary infection
  • primarily in blood
  • activate complement
  • form pentamer
37
Q

what are the properties and functions of IgD

A
  • co-expressed with IgM during maturation
  • no known function
38
Q

what are the properties and functions of IgG

A
  • class switching
  • found in blood and extracellular fluid
  • transported across placenta
  • high affinity
  • diffusion into extracellular sites
  • participate in opsonization, neutralization, sensitization and compliment activation
39
Q

what are the properties and functions of IgE

A
  • class switching
  • sensitization of type 2 immune cells (mast cells)
  • high affinity
40
Q

what are the properties and functions of IgA

A
  • class switching
  • diffuse into secretions at mucosal epithelial surfaces
  • high affinity
  • diffuse into extravascular space
  • involved in neutralization
41
Q

what are the different properties of ILC subsets in terms of their immune function

A

cytotoxic ILCs: release IFN-y to target viruses
Group 1 ILCs: release IFN-y to target intracellular bacteria
Group 2 ILCs: release IL-13 and IL-5 to target helminths (parasites)
Group 3 ILCs: release IL-17 and IL-22 to target extracellular bacteria

42
Q

how does immunological memory work to prevent and fight disease

A
  • established after an initial infection or vaccination and involves both humoral immunity
  • the adaptive ability to recognize previously encountered pathogens upon re-exposure
43
Q

migration pattern and function of central memory T cells

A

recirculate between blood, T cell zones of SLO and lymph

44
Q

migration pattern and function of effector memory T cells

A

recirculate between non lymphoid tissues, lymph, lymph nodes and blood
some remain in blood circulation and migrate only through spleen

45
Q

migration pattern and function of resident memory T cells

A

do not recirculate - are confined to a single tissue

46
Q

differentiate between the primary and secondary immune response

A

Primary = naive B cells involved, longer lag time and onset time, IgM with lower affinity
Secondary = memory B cells involved, shorter lag time and onset time, IgG with higher affinity

47
Q

what is the purpose of negative signalling in naive B cells through activation of FcyRIIIB1

A
  • FcyRIIB1 is an inhibitory receptor on the surface of naive B cells
  • interacts with Fc component of IgG
  • regulatory mechanism to prevent overactivation of the immune system and ensure self-tolerance
  • delivers inhibitory signals to B cells when bound to immune complexes
48
Q

why are mucins effective as a defense against infection at mucosal surfaces

A
  • thick and sticky consistency allows it to trap pathogens
  • antimicrobial properties
  • retains sIgA and AMPs to neutralize pathogens
  • neutralize microbial toxins
49
Q

how is antigen capture and delivery to SLO’s different at an open wound than mucosal surfaces

A

Mucosal surface
- capture antigen in M cells found in the epithelium
- mucus provides a physical barrier to trap pathogens
- Antigen-bound sIgA neutralizes pathogens
- priming in MALT
- Mucosal DCs often induce Tregs for tolerance to commensals and dietary antigens
- Local mucosal immunity (sIgA, Th17, Th2 responses)

Open wound
- Exposed to external pathogens and tissue damage; barrier breached
- capture antigen by phagocytosis, opsonization, neutralization and
- delivery to SLO’s by lymphatic drainage, antigen presentation and pro-inflammatory cytokines
- Systemic immunity (IgG, cytotoxic T cells)

50
Q

explain the process of antigen delivery to mucosa-associated lymphoid tissue driven by M cells

A
  • M cells are embedded in the epithelial lining of mucosal tissues, primarily in the follicle-associated epithelium (FAE) overlying MALT
  • they are specialized for transcytosis of microbes into the MALT
  • sub-epithelial dome below M cells is rich in DCs which capture and process antigens delivered by M cells
51
Q

would you predict that an organism that is deficient in the production of NOD2 would be more or less susceptible to infection in mucosal tissue?

A
  • Deficiency in NOD2 impairs mucosal immunity by weakening antimicrobial defenses, disrupting barrier integrity, and compromising immune regulation.
  • the organism would be more susceptible to infections in mucosal tissues, particularly those caused by bacteria exploiting weak epithelial defenses.
52
Q

how do DCs provide oral tolerance for an organism

A
  • Gut DCs promote oral tolerance by inducing Tregs which work to inhibit pro-inflammatory T cells to prevent unnecessary immune responses to harmless pathogens found in food
  • Gut DCs present antigens to CD4 T cells which stimulate B cells to secrete IgA
53
Q

name the innate immune cells that play a role in mucosal immunity and describe their functions

A

Type A IEL’s: function like effector T cells (TCR activation leads to release of perforin granzymes and FasL)
Type B IEL’s: function like NK cells (act independently of TCR activation through NKG2D)
ILC’s: respond to microbes that breach the epithelium - release cytokines
Intestinal macrophages: promote PGE2 repair
Gut DC’s: promote oral tolerance by inducing Tregs and IgA production

54
Q

explain the role of antibodies in mucosal immunity (mostly IgA)

A
  • bind and neutralize pathogens on gut surface or internalized in exosomes
  • export toxins from the lamina propria while being secreted
  • bind to Dectin-1 on M cells to allow transport of antigen to DC’s
55
Q

what is immunodeficiency

A
  • immune system’s ability to respond to infections or other challenges is impaired
  • results in susceptibility to infection
56
Q

how does inherited immunodeficiency differ from acquired?

A

inherited: caused by genetic mutations, present from birth, examples = SCID and XLA
acquired: caused by external factors, develops later in life, examples = HIV/AIDS

57
Q

how does a deficiency in the innate immune system lead to disease

A
  • defects in the complement cascade lead to decreased destruction of diseased cells and decreased opsonization
  • decrease in phagocytes lead to accumulation of pathogens
  • decrease in ROS needed for killing pathogens
58
Q

how does a combined deficiency in lymphocyte development or action lead to disease

A
  • impairs B and T cell functions due to inherited mutation
  • causes susceptibility to recurrent infections
  • can’t maintain self-tolerance
59
Q

how does a deficiency in T-cell action lead to disease

A
  • less helper T-cells impairs B cell function of clearing extracellular pathogens
  • less effector T cells impairs clearance of infected cells
60
Q

how does a deficiency in B-cell action lead to disease

A
  • cannot clear extracellular pathogens due to lack of antibodies being produced
61
Q

how does HIV cause AIDS

A
  • HIV attacks CD4+ T cells - destruction of these cells and the depletion of the immune system leads to immune deficiency
  • gp120 protein on the HIV surface recognizes the proteins CD4 (helper T), CCR5 and CXCR4 receptors
62
Q

what are primary ways that pathogens evade the immune system defenses

A
  • antigenic variation: Pathogens can alter their surface antigens to evade recognition
  • antigenic shift: sudden major change in the viral genome involving the reassortment of genetic material from different virus strains
  • antigenic drift: slowly accumulated mutation that results in minor alterations in the structure of the virus’s surface proteins
  • viral latency: viruses enter a latent or dormant state in the host, evading immune detection for long periods
63
Q

how does genetic variation allow pathogens to evade the immune system

A

memory cells won’t be able to recognize these variations upon a second exposure

64
Q

how do pathogens hide from the immune system

A

latency

65
Q

what are the different types of hypersensitivity reactions

A

type 1: immediate - IgE mediated
type 2: cytotoxic - IgG/IgM mediated
type 3: immune complex - immune complex mediated
type 4: delayed type - T cell mediated (helper and effector)

66
Q

how does type 1 hypersensitivity occur

A
  • 1st exposure to allergen causes sensitization - class switching to produce IgE
  • 2nd exposure to allergen causes effector mechanism - cross-linking of Ig bound to high-affinity receptors on mast cells
67
Q

what factors are responsible for type II hypersensitivity reactions

A
  • occurs when IgG recognize cell surface molecules and bind to them, leading to destruction of cells
68
Q

how does type III hypersensitivity reaction occur

A
  • occurs when immune complexes (antigen-antibody complexes) form in the bloodstream and deposit in tissues
  • activate the complement system (classical pathway)
  • C5a binds to and sensitizes mast cells (anaphylatoxin)
  • FcyRIII on mast cells is activated and their contents are released
  • causes local inflammation and blood vessel occlusion
69
Q

what is delayed-type hypersensitivity

A
  • occurs when T cells recognize an antigen and release cytokines, triggering an inflammatory response
  • takes 24-72 hours to develop
  • inflammation results from the activation of macrophages and other immune cells, leading to tissue damage
70
Q

what is the relationship between self-tolerance and autoimmunity

A
  • lack of self-tolerance leads to autoimmunity because the immune system cannot distinguish self from non-self
71
Q

how do genetic and environmental factors affect the progression of autoimmune diseases

A

genetic: MHC polymorphisms, non-MHC mutations (such as genetic defects in transcription factors)
environmental: infections, chemical exposure, physical trauma

72
Q

explain why many autoimmune diseases are caused by the production and action of autoantibodies

A
  • autoantibodies are self-reactive Igs which react to self-antigens
  • production occurs when the immune system loses its ability to distinguish between self and non-self antigens, a breakdown in self-tolerance
73
Q

when is a normal adaptive immune response to a pathogen capable of inducing an autoimmune response

A
  • molecular mimicry: similarities between foreign and self-antigens favour autoreactive T- or B-cell activation
  • genetic predisposition
74
Q

what are some strategies to treat autoimmune diseases

A
  • corticosteroids: inhibit dendritic cells, monocytes and macrophages from secreting cytokines and prevent phagocytosis
  • NSAIDs: inhibit COX1/2 to inhibit production of prostaglandins (PGE2)
  • Anti-TNF-a: blocks activity of TNF-a which suppresses the immune system
75
Q

compare and contrast the direct and independent pathways of allorecognition

A

Direct: donor cell alloAg recognized by donor DCs and migrate to SLO’s - activate recipient T cells - effector T cells migrate to graft - graft rejection
Indirect: donor cell alloAg recognized by recipient DCs and migrate to SLO’s - activate recipient T cells - effector T cells migrate to graft - graft rejection

76
Q

explain how cyclosporine A functions to block T-cell activation

A
  • inhibits the enzyme calcineurin by blocking Ca2+ release
  • NFAT can no longer function to promote the expression of IL-2 genes
77
Q

how do vaccines prevent disease

A
  • train the immune system to recognize and respond to antigens without causing sickness
  • introduce antigens prompting the immune system to produce specific antibodies and activate memory cells
  • if the body encounters the pathogen in the future, these memory cells enable a faster and stronger immune response
78
Q

what are the different types of viral and bacterial vaccines

A

live attenuated
killed pathogen
inactivated toxoid
subunit/conjugate
RNA/DNA vaccine

79
Q

what are the strategies to make attenuated vaccines

A
  • pathogenic virus is isolated from a patient and grown in cultured human cells
  • cultured virus is used to infect monkey cells
  • the virus acquires many mutations to allow it to grow in monkey cells
  • virus no longer grows well in human cells but is still perceived as antigen, so it can be used as a vaccine
80
Q

what are the criteria for a safe and effective vaccine

A
  • gives sustained protection
  • induces neutralizing antibodies
  • protects against illness resulting from exposure to live pathogen
  • induces protective T cells
  • doesn’t cause illness or death
81
Q

what is the role of an adjuvant vaccine

A

enhance immunogenicity by promoting innate immunity (TLR’s, etc.)

Immunology (22 decks)

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