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Adaptive immune response Flashcards

1
Q

Implications of an adaptive immune system (based on protein antigens)?

A

Proteins are infinitely diverse and a complementary diversity of receptors if therefore required

There is significant likelihood of cross-reactivity between prokaryotic proteins and their eukaryotic homologues

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2
Q

What gives antibody diversity (given there is not sufficient genes to code for each one individually)?

A

Gene rearrangement

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3
Q

How are heavy and light chains split up (genes)?

A

H and L regions each split into a V, D, J and C encoded by distinct gene segment

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4
Q

How is combinational diversity for antibodies generated?

A

Multiple gene segments for each region can be mixed and matched in any combination for significant combinational diversity

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5
Q

What enzyme catalyses somatic gene rearrangement?

A

V(D)J recombinase

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6
Q

What are the 4 levels of antibody variation at the genome level?

A

Multiple copies of V, D, J and C gene segments may be randomly recombined

D region genes may be transcribed in multiple reading frames

Imprecise joining may occur during rearrangement of genes and excision of the intervening DNA

Nucleotides are randomly inserted or deleted from the region flanking the sites where joining occurs

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7
Q

When can further specificity and variation in antibody structure occur?

A

At the antigen binding stage/during the immune response.

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8
Q

What does somatic hypermutation produce

A

Somatic hypermutation introduces mutations - producing closely related B-cell clones that differ subtly in specificity and antigen recognition.

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9
Q

Where does somatic hypermutation occur?

A

Dark zones of germinal centre of lymph node

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10
Q

How are mutations induced in somatic hypermutation?

A

Mutations are induced by Activation induced deaminase (AID) - this enzyme deaminates cytosine to uracil at the hypervariable hotspots.

Error prone DNA repair pathways create double strand breaks and introduce mutations

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11
Q

Most mutations (somatic hypermutations) are … ? What happens to these cells ?

A

Negative on B-cells ability to bind to the original antigen - these cells become apoptotic in the germinal centres and are engulfed by macrophage.

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12
Q

What happens if mutation is positive for antigen binding?

A

Antibody selected for - cells have increased survival rate.

These cells may successfully present a complimentary antibody to ap T follicular helper cells/ dendritic cell in light zone, which then signal them to re-enter the dark zone to accumulate further mutations

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13
Q

What T cells do developing B cells present antigens to?

A

Tfh cells

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14
Q

Where do developing B cells interact with Tfh cells?

A

The light zone

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15
Q

How to Tfh cells keep B cell alive?

A

CD40 ligand, IL-21 secretion

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16
Q

What is class switching, where does it occur?

A

Light zone, this involves the changing of the Fc region (depending on the stage of the immune response).

Initially, all are IgM/D, but later can convert to IgA/E/G.

Occurs after antigen activation

Class switch recombination underpinned by switch regions

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17
Q

Initial antibodies produced

A

IgM, IgD

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18
Q

MHC I structure

A

Heterodimers, with a polymorphic heavy α-subunit (gene within MHC locus) and a β2 microglobulin subunit (gene located outside of it).

In humans, there are 3 class I α genes HLA-A, HLA-B and HLA-C.

This α-unit is composed of three domains (α1, α2, α3), α1 and α2 form the deep peptide-binding groove

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19
Q

MHC II structure

A

Heterodimers have polymorphic α and β subunits (HLA-DR, HLA-DP and HLA-DQ).

The peptide-binding groove of MHC-II molecules is formed by both α1 and β1 subunits of the heterodimer, unlike MHC-I molecules, where only one chain is involved.

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20
Q

MHC restriction

A

MHC restriction implicates that antigen recognition by T-cells depends on the MHC genotype.

T-cell receptor binding prerequisite being for both antigen and MHC – heightening the specificity of the response.

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21
Q

MHC I location (infection speciality)

A

Nearly all somatic cells, except erythrocytes, express MHC I molecules on their surface.

This allows the identification of intracellular infection and damage as HLA acts as a ‘window’ into the cell, by the presentation of epitopes from the internal environment.

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22
Q

MHC II location (infection speciality)

A

MHC II molecules only reside on the cell surface of ‘professional antigen presenting cells’ such as dendritic cells and macrophages

This allows fragments of extracellular pathogens to be presented due to these cells specific abilities to phagocytose or undergo receptor-mediated endocytosis.

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23
Q

MHC I cell activates

A

CD8+

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24
Q

MHC II cell activates

A

CD4+

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25
Q

Endogenous vs exogenous pathways for MHC

A

Endogenous (MHC I, expresses intracellular proteins degraded by the proteasome)

Exogenous (MHC II, expresses extracellular proteins degraded by phagocytosis in professional APCs)

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26
Q

Why can dendritic cells cross present?

A

Cytotoxic T-cells recognise viral peptides bound to MHC I, but target cell lysis requires their prior activation.

Research suggests that dendritic cells are central in this process, and must also express MHC I which binds to the same peptide to activate naïve CD8 cells.

But, not all pathogens will infect dendritic cells, restricting the extent to which these cells can generate peptide fragments and MHC I.

To remedy this, dendritic cells exhibit cross presentation, which suggests that they can present extracellularly sourced peptides on MHC I molecules.

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27
Q

What are CD4/CD8 receptors and what do they do

A

The co-receptors CD8 and CD4 stabilize the interaction between the TCR and either MHC class I or class II

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28
Q

TCR diversity

A

Multiple copies of V, D, J and C gene segments may be randomly recombined

D region genes may be transcribed in multiple reading frames

Imprecise joining may occur during rearrangement of genes and excision of the intervening DNA

Nucleotides may be randomly inserted or deleted from the regions flanking the sites where joining occurs

Any a chain may pair with any possible b chain to generate 10^9 – 10^16 TCRs with different specificity

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29
Q

T cell activation

A

Requires three independent signals.

  1. Peptide-MHC complex presented
  2. Co-stimulatory molecules CD40/CD80: promote survival and expansion of T cells
  3. Pro-inflammatory cytokines (i.e IL-12): direct differentiation of T cell
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30
Q

Primary lymphoid tissues

A

Primary lymphoid organs include the thymus and bone marrow and are the tissue sites where antigenic receptor repertoires of T and B cells respectively, are selected.

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31
Q

Bone marrow site of

A

Creation of T cells and the production and maturation of B cells (from common lymphoid progenitor) - primary site of haematopoiesis.

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32
Q

What is the role of the osteoblastic niche?

A

The osteoblastic niche Protects the HSC (haemopoietic stem cell) pool

Maintains quiescence among HSC to prevent their exhaustion

The endosteal surface offers physical protection from trauma and toxins

Bone absorbs environmental radiation, preventing DNA damage

Significant distance from a blood supply ensures a low O2 tension, reducing exposure to oxidative stress

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33
Q

What happens when blood cells leave the osteoblastic niche?

A

Expansion and differentiation of progenitors

B cells immediately join the circulatory system and travel to secondary lymphoid organs in search of pathogens.

T cells travel from the bone marrow to the thymus, where they develop further and mature

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34
Q

What happens in the thymus?

A

T cells mature from thymocytes, proliferate, and undergo a selection process in the thymic cortex before entering the medulla to interact with epithelial cells.

Thymic stromal cells allow for the selection of a functional and self-tolerant T cell repertoire (central tolerance).

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35
Q

What is the role of the secondary lymphoid tissues?

A

Secondary tissues sample antigens from different body compartments, accumulation of components of the adaptive immune system.

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36
Q

Three types of secondary lymphoid tissue

A

The spleen is highly vascularised

Peyer’s patches serve the gut

Lymph nodes drain tissue fluid from interstitial tissues

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37
Q

Spleen structure

A

Specialised to capture antigens that enter the blood stream (vascular network by branches of central arteriole)

Lymphoid tissue component called white pulp

Separated from red pulp by marginal sinus

T and B cells initially delivered to the marginal sinus (rich in macrophages and marginal zone B cells)

T cells migrate to periarteriolar lymphoid sheath (PALS)

B cells to follicles (some germinal centers where hypermutation occurs)

Follicular dendritic cells present - specialised to present antigens

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38
Q

Lymph node structure

A

Specialised to analyse extracellular fluid for antigens

T and B cell areas

B cell follicles located just under outer capsule, these have germinal centres where B cells mature

T cell zones surround follicles in paracortical areas

Connections to both lymphatic system (afferent, efferent ducts) and the bloodstream (artery and vein/ high endothelial venules HEV)

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39
Q

MALT structure

A

Associated with bodies epithelial surface.

Peyer’s patches are lymph node like structures under the surface of the mucosa

They have B cell follicles and T cell zones

Epithelium overlying contains M cells (adapted to pathogens directly from gut)
B cells become committed to IgA.

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40
Q

High endothelial venules

A

HEV are found within the paracortex of lymph nodes and act as portals for the entry and exit of cell types (naïve T-cells from thymus)

HEV constitutively express the adhesion molecules GlyCAM-1, CD34 and ICAM-1

HEV mimic inflamed endothelium at sites of infection

Binding of L-selectin on naïve T cells to GlyCAM-1 and CD34 induces rolling along the luminal surface

Activation of LFA-1 results in tight binding to ICAM-1 and diapedesis

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41
Q

Dendritic cells at lymph nodes

A

Means presentation of foreign antigen to naïve T cells in the paracortical T cell zones.

The paracortex represents the highest density of naïve T cells

A single DC can simultaneously interact with up to 200 T cells in order to identify rare clones with a complementary TCR

Functional ligation of the TCR leads to T cell activation and clonal expansion

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42
Q

CD4 cells differentiate into

A

Th1, Th2, Th17, Tfh and Treg

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43
Q

Th1

A

IFNγ (intracellular pathogens), activates macrophages, CTLs and b cells

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44
Q

Th2

A

IL-4, IL-13 (extracellular parasites) mainly activates b cells

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45
Q

Th17

A

IL-17a, IL-17f (extracellular bacteria and fungi)

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46
Q

Tfh

A

Help B-cells and humoral immunity to extracellular pathogens by promoting germinal centres

Tfh cells activate antigen-specific B cells through interaction of CD40L with the co-stimulatory molecule CD40

Secretion of IL-21 sustains B cell proliferation and formation of germinal centres

47
Q

What causes Tfh cells to migrate to primary follicles?

A

Expression of CXCR5 confers on Tfh cells the capacity to migrate from the paracortex to the primary follicles

48
Q

Memory B cells vs Naive cells

A

Memory cells are a subset of B-cells, naïve cells are different from memory cells in several ways

Memory cells have already undergone class switching and are, therefore, capable of producing an isotype appropriate for the pathogen

Memory cells show constitutive down-regulation of cell cycle inhibitors enabling them to rapidly undergo clonal expansion

Somatic mutation ensures that the affinity of antibodies is many orders of magnitude higher than that of naïve B cells

49
Q

3 types of B cells?

A

Short lived plasma cells, long lived plasma cells and memory b cells

50
Q

Difference between long lived plasma cells and memory B cells?

A

Long-lived plasma cells (LLPCs) constitutively secrete antibody to neutralize antigen immediately upon reinfection (reside in bone marrow), whereas memory B cells (MBCs) produce antibody only upon restimulation by specific antigen

51
Q

T memory cells

A

CD4+ and CD8+ T cells also develop into memory cells of two types:

Effector memory T cells (TEM):
Generated early in the immune response

Central memory T cells (TCM):
Generated late in the immune response

These can persist for decades in the body but need continuous replication - mechanism not known

52
Q

How are autoreactive B cell clones eliminated?

A

Recognition of self-antigens by naïve B cells in the bone marrow drives clonal deletion to eliminate autoreactive clones. This ensures the B-cell population is tolerant to self antigens.

53
Q

What bone marrow cells express self antigens?

A

Stromal cells in the bone marrow express Fc receptors for ‘natural’ IgM antibodies that bind a spectrum of self-proteins for presentation to emerging B cells.

54
Q

If the BCR can bind strongly to self-antigen, then the B cell undergoes one of which four fates

A

Clonal deletion (cell death by apoptosis)

Receptor (L chain) editing (remove self receptor)

Anergy (migrate to periphery and die as don’t receive survival signals)

Ignorance (binding so weak can’t normally activate cell)

55
Q

Limitations of B Cell Clonal Deletion, what helps this?

A

Although initial self reactive B cells removed in BM, confounded by somatic hypermutation of immunoglobulin genes during the course of the immune response

Another level of tolerance is, therefore, imposed at the level of Th cells since deprivation of T cell help inhibits B cell activation

56
Q

Stromal cell types in the thymus

A

Stromal cell types include macrophages, DC and thymic epithelial cells (TEC), either medullary (mTEC) or cortical (cTEC).

57
Q

T cell development from new thymocytes to CD4+/CD8+ thymocytes

A

Thymocytes (when enter the thymus)

α:β and γ:β are the first two subtypes of T cell.

α:β/ CD4-/8- type differentiates into CD4/8 cells

Interactions with thymic stroma stimulate this development

pre-TCR (newly rearranged B chain)

Ligation of the pre-TCR halts further b chain gene rearrangement - alpha chain locus accessible to the V(D)J recombinase - rearrangement of the alpha chain locus

Up-regulation of CD4 and CD8 leading to the ‘Double Positive’ phenotype

Drives thymocyte proliferation as a prelude to positive selection

58
Q

What are pro/pre T cells called?

A

CD4-8- (absence of CD4/8)

59
Q

What is a pre-T cell receptor composed of?

A

Composed of a newly rearranged b (somatic gene rearrangement) chain with an invariant pTa chain

60
Q

Positive T cell selection benefit and important cells

A

Positive selection rescues thymocytes from cell death and produces a lineage commitment.

Cortical Thymic Epithelial Cells (cTEC) are very important in this process

61
Q

How are cTEC adapted to interacting with thymocytes?

A

cTEC form a 3-dimensional network with no basement membrane

The stellate morphology of cTEC ensures maximum interaction with developing thymocytes

cTEC constitutively expresses both SELF MHC class I and class II allowing thymocytes to assess the restriction specificity of their newly rearranged TCRs

62
Q

What happens if double positive thymocytes cannot recognise a self antigen?

A

Small double positive thymocytes express small amounts of TCR, most of these cannot recognise a self peptide: self MHC complex, they will fail positive selection and die.

63
Q

What happens to the cells that can recognise self peptide: self MHC complexes?

A

Positively selected, mature and express more TCR.

Those that are MHC I restricted stop expressing CD8 co-receptor - CD4+ formed

Those that are MHCII restricted stop expressing the CD4 co-receptor - CD8+ formed

64
Q

Where is the site of T cell negative selection?

A

Medulla of thymus

65
Q

What underpins self antigen expression in the thymus?

A

Dendritic cells are migratory and patrol the body acquiring self antigens which are then transported to the thymus

mTEC exhibit patterns of ‘promiscuous gene expression’ permitting expression of diverse self proteins (not required by them for their own function).

Promiscuous gene expression is mediated by the transcription factor AIRE and casts an immunological self shadow within the thymus

66
Q

When self peptide MHC binds strongly to TCR in thymus…

A

T-cell undergoes apoptosis.

67
Q

How can recognition of the same ligand by the same TCR lead to the opposite outcomes of survival and maturation versus death by apoptosis?

A

Avidity of antigen recognition is a key factor in determining positive versus negative selection

Thresholds of avidity define a narrow window of avidity for the emergence of mature T cells from the thymus and their colonization of secondary lymphoid organs

68
Q

What are the limitations of negative T cell selection?

A

Inadequate provision of self-antigens - in the thymus may makes negative selection incomplete (AIRE does not code for everything)

Developmental antigens - Ectopic re-expression of developmental antigens in later life may activate self-reactive T cells that were never subject to negative selection

Molecular mimicry - among T cell epitopes may stimulate self-reactive T cells, (i.e self peptide may be very similar to microbial peptide)

69
Q

As well as negative selection what other mechanisms are useful for preventing autoimmunity?

A

Anergy: T cell anergy helps restrict the impact of autoreactive T cells that evade negative selection

Immune privilege: Some tissues and organs display immune privilege in order to limit collateral damage

Treg cells: A repertoire of Treg cells polices the immune system to reinstate self-tolerance

70
Q

What induces T cell anergy?

A

T cell anergy can be induced by self-antigen recognition due to AIRE expression in the periphery.

Recognition of antigen by CD4+ Th cells presented to them by AIRE+ APC, induces profound anergy and lack of subsequent responsiveness to conventional stimuli

The anergic state is highly stable and resistant to perturbation

71
Q

Immune privilege

A

The capacity to repel an autoimmune response.

72
Q

Immune privileged tissues include

A

The central nervous system

The anterior chamber of the eye

The testis

Foetus in pregancy

73
Q

Mechanisms of immune privilege

A

Physical barriers to sequester tissue-specific antigens from the immune system

Lack of lymphatic drainage isolating the tissue from the adaptive immune system

Expression of inhibitory receptors such as FasL that induce apoptosis of leukocytes (i.e NK cells)

Induction of a local anti-inflammatory environment due to secretion of TGF-b

Depletion of essential amino acids to deprive T cells of the nutrients they require (e.g. tryptophan)

74
Q

Acquired Immune Privilege of Tissues

A

Established tumours may actively exploit the principles of immune privilege in order to avoid immune surveillance

Recruitment of M2 macrophages and secretion of anti-inflammatory cytokines such as IL-10 and TGF-b may counteract the local inflammatory response

Down-regulation of MHC class I renders tumour cells invisible to CTL

75
Q

Treg cell main role

A

The role of Treg cells is conferring immune privilege on any tissue

76
Q

Key transcription factor that defines Treg lineage?

A

FoxP3 -defines commitment to Treg lineage

77
Q

Natural Treg cells (nTreg)

A

Become committed to the lineage during repertoire selection in the thymus

78
Q

Induced Treg cells (iTreg)

A

Naïve CD4+ T cells recognizing antigen under specific circumstances in the periphery may become polarised towards induced Treg cells (iTreg).

Incomplete chronic stimulation of naïve CD4+ T cells is the main stimulus for induction of induced Treg

79
Q

nTreg vs iTreg

A

Both require expression of FoxP3 as a master transcription factor

iTreg modulate responses to harmless foreign antigens

nTreg are more phenotypically stable and inhibit responses to self antigens

80
Q

How do Treg cells compare in avidity to effector T cells?

A

Treg cells have even higher avidity for self antigens than effector T-cells.

81
Q

Mechanisms of action of Treg

A

Direct inhibition of the activation of neighbouring T cells through cytokine release

Inhibition of DC maturation through secretion of IL-10

Since immature DC lack the costimulatory molecules required for full T cell activation, they induce further Treg cells, perpetuating the tolerant state

82
Q

All B lymphocytes are derived from haematopoietic stem cells - T/F

A

True

83
Q

In a humoral immune response to a previously unencountered antigen IgM expression always precedes IgG expression T/F

A

True

84
Q

Memory B cells never leave secondary lymphoid organs- T/F

A

False

85
Q

Pre-B cells do not secrete immunoglobulin - T/F

A

True

86
Q

The increased affinity of IgG antibodies in a recall antigen response is due to somatic hypermutation and
clonal selection - T/F

A

True

87
Q

Are primary lymphoid organs are also sites of haematopoiesis?

A

No (only bone marrow)

88
Q

Are primary lymphoid organs are sites of lymphocyte production and activation?

A

No, only production, not activation (secondary lymphoid organs)

89
Q

Within which part of a mesenteric lymph node do B cells undergo isotype switching and affinity maturation?

A

Germinal centre

90
Q

Dendritic cells carrying recently acquired antigen enter the mesenteric lymph node via which structure?

A

Afferent lymphatic

91
Q

Rheumatic fever is caused by what?

A

Cross reactive antibodies to Streptococcus pyogenes

92
Q

Increased susceptibility to pyogenic infection is most likely to be caused by which one of the following?

A

Deficiency of all B cells

93
Q

A Th1 T cell response is characterised by which of the following?

A

Secretion of cytokines that activate macrophages

94
Q

These proteins, which are secreted by CD4+ Th2 type T helper cells, have important effects on B lymphocyte growth and Ig class switching.

A

Interleukin-4 (IL-4) and Interleukin-5 (IL-5)

95
Q

What happens in the nine days post infection that accounts for the dramatic improvement a patient’s condition to Streptococcus pneumoniae?

A

Generation of high titre capsule specific IgM antibodies

96
Q

Which class of secretory cells of the immune system are principally responsible for regulating the functions of other leukocytes?

A

CD4+ T helper cells

97
Q

What surface glycoprotein is a “marker” for these cells?

A

CD4

98
Q

Which cytokine, produced by CD4 cells is a growth factor for T lymphocytes?

A

IL-2

99
Q

Which cytokine, produced by these cells, promotes Th2 differentiation and proliferation?

A

IL-4/ IL-2

100
Q

Which cytokine, produced by CD4 cells, activates macrophages?

A

IFN gamma

101
Q

List three surface molecules that characterize T-cells.

A

CD4/CD8

MHC I/II

TCR-CD3

102
Q

Give three mechanisms by which T-cells avoid responding to self-antigens.

A

Positive selection: T cells failing to respond to MHC will undergo apoptosis

Negative selection: AIRE expressed by mTEC cells, if T cells are autoreactive they are induced to anergy/apoptosis

Treg cells

103
Q

If B cell encounter cognate antigen before reaching primary follicle,

A

They are activated to become short lived plasma cells which migrate to medullary cords of lymph node where they secrete IgM

104
Q

What do short lived plasma cells secrete?

A

IgM

105
Q

If cognate antigen encounters B cell in primary follicle

A

Proliferation and clonal expansion forms germinal centre

106
Q

What is the germinal centre site of?

A

Somatic hypermutation and affinity maturation

Ig class switching

107
Q

What do cells in the germinal centre develop into?

A

Plasma cells (migrate to bone marrow, secondary lymphoid organs) and memory B cells in germinal centre remain quiescent and respond to same infection

108
Q

Immune responses to blood-borne antigens occur primarily

A

In the spleen

109
Q

Naive T lymphocytes enter the spleen via high-endothelial venules

A

False

110
Q

Germinal centres are conspicuous in non-antigen-stimulated lymph nodes

A

True

111
Q

The medulla of an antigen-stimulated lymph node contains numerous plasma cells

A

True

112
Q

Afferent lymphatics carry antigens from the intestinal lumen to Peyer’s patches

A

False

113
Q

What do medullary cords contain?

A

Antibody-secreting plasma cells

Pathology (21 decks)

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