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Immunology (Parham) > Chapter 9 > Flashcards

Chapter 9 Flashcards

1
Q

How are B cell receptors cross-linked and what is the result?

A
  • binding to multiple identical carbohydrate epitopes
  • clustering sends signal to B cell
  • Igα and Igβ each have 2 ITAMs
    • association with tyrosine kinases
    • start phosphorylation cascade by activating Syk
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2
Q

What 2 signals are needed to activate naive B cell?

A
  • signal from cross-linked receptors
  • signal from BCR associated with B-cell co-receptor (on B cell surface)
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3
Q

What is the role of B-cell co-receptor?

A
  • built of 3 proteins
    • CR2 or CD21 recognises iC3b and C3d
    • CD21 consists of 16 modules = CCP
      • 2 outermost bind C3d
      • the rest forms flexible stalk to catch C3d tagged proteins
    • CD19 is a signalling chain
    • CD81 binds to CD19 -> brings to surface (otherwise absence of co-receptor in B cells)
  • once CR2 binds B cell receptor and co-receptor are brought closer
  • CD19 can be phosphorylated -> signal sent
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4
Q

What is CR1?

A
  • complement receptor
  • binds to C3b which becomes susceptible to cleavage
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5
Q

What are thymus-independent antigens?

A
  • bound by IgM from B1 cells
  • extensive cross-linking + clustering of B cell co-receptors -> no T cells needed for activation
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6
Q

How are antigens presented to B cells?

A
  • lymph with antigens enters subcapsular sinus
    - subcapsular sinus macrophage have CR2 -> bind complement-tagged antigens
  • rest captured by follicular dendritic cells (FDCs)
  • B cell area of lymph node (primary follicle) contains FDCs
  • FDCs store antigens to present to BCR
    • no phagocytic activity (antigens intact)
    • large surface area -> dendrites
    • CR2 receptors catch C3d (complement-tagged antigens)
  • in sinuses of medulla -> medullary sinus macrophages (have pahgocytic activity -> destroy pathogens)
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7
Q

What happens once naive B cell binds to antigen?

A
  • CD69 expressed
    • stopped expression of S1P receptor -> remain in lymph node
  • endocytosis of BCR with antigen -> presentation of MHC class II
  • CCR7 (chemokine) is produced -> binds to CCL21 and CCL19 -> B cell to B cell-Tcell area boundary
  • B cells interact with T_FH cells
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7
Q

How do naive B cells from blood (via HEV) know where to enter?

A
  • attracted to T cell area by chemokines (CCL21 and CCL19)
  • then into B cell follicle by CXCL13
  • in subcapsular sinus screen antigens held by macrophages
    • if bind, enter primary follicle for activation
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8
Q

What happens to T_FH cell before meeting B cell?

A
  • reduction of CCR7
  • expression of CXCR5 (receptor for CXCL13) -> moves to boundary of primary folilcle
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9
Q

What happens after B cell and T_FH cell bind?

A
  • cognate pair
  • T_FH expresses CD40 ligand (binds to CD40 on B cell)
  • further activation (described in chapter 8)
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10
Q

What is primary focus of clonal expansion?

A
  • pair of proliferating T cell and B cell
  • moved to secondary lymphoid tissue (medullary cords)
  • creates B lymphoblasts = plasmablasts secreting IgM
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11
Q

What happens later during primary focus?

A
  • B lymphoblasts stay in medullary cords, stimulated by IL-5 and IL-6 (secreted by T_fh cell)
    • form plasma cells
    • transcription of genes for IgM production instead of cell proliferation
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12
Q

What happens to B lymphoblasts that did not become IgM plasma cells?

A
  • move to primary follicle with T_fh cell
  • form germinal centre
    • proliferation stimulated by IL-6, IL-15, 8D6, BAFF from FDCs
    • become centroblasts
  • T cells make cytokines, CD40 ligands used to bind B cells
  • B cells produce enzymes for somatic hyper mutation and isotype switching
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13
Q

What happens after somatic hypermutation and isotype switching are activated?

A
  • proliferation of antigen-specific B cell
  • primary follicle (where it’s happening) -> secondary follicle
    • germinal centre with proliferating B and T cells
    • naive B cells pushed (look for antigen) -> form mantle zone
  • overall called germinal center reaction
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14
Q

How are B cells in germinal center selected for maturation?

A
  • new centrocytes move to outside of the germinal center
  • antigens on FDCs scarce -> competition
  • highest affinity receptor binds (affinity maturation)
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15
Q

What happens after a B cell from germinal center has been selected?

A
  • FDCs and B cell attached form a synapse
    • antigen + survival signals to B cell
  • outer region has helper T cells
    • bind to antigen on MHC class II
  • expression of Bcl-x_L -> protection from apoptosis
  • become plasma cells
    • staying in lymph node -> fight infection (short-lived)
    • move to bone marrow -> systemic source of ab
16
Q

What are tingible body macrophages?

A
  • centrocyte fails to bind antigen -> apoptosis
  • phagocytosed by macrophage
  • if centrocyte binds self-antigen -> anergic (helper T cells and other cells in germinal center)
17
Q

How does isotype switching occur?

A
  • T_FH cells produce cytokines which stimulate B cells
  • dependent on infection, different cytokine produced
18
Q

What determines whether a cell is converted to a plasma or memory cell?

A
  • IL-21 and IL-10 stimulate differentiation into
    • plasma cells at the beginning of the immune response
    • later, memory cells
      • quiescent -> reactivation by pathogen
19
Q

Why are IgG not degraded like other plasma proteins taken up by cells from extracellular fluid?

A
  • protected by receptor FcRn (from Fc receptors)
  • these receptors protect IgG by binding them (to prevent degradation)
  • releasing in sites where antibodies are needed
20
Q

What is the function of both dimeric IgA and pentameric IgM?

A
  • mucosal epithelia exposed to external factors
  • IgA and IgM transported by poly-Ig receptor to site of infection
    • lymphoid tissue under mucosal epithelium
  • dim IgA and pen IgM -> same J chain
    • receptor binds
    • transport from one side of cell to another = transcytosis
    • protease cleaves when at the right side, leaving a small part (secretory component) still attached
      • Igs retained on mucosal surface
21
Q

What is different about IgE compared to rest of antibodies?

A
  • cell-surface receptor for antigen
  • not soluble antibody
  • short-lived, small amounts
  • secreted IgE extracted from circulation by FcεRI receptor (on mast cells, basophils)
    • high affinity -> constant binding (especially when no antigen is present)
    • cells are kept in waiting state (ready to act)
22
Q

How does IgE protect the body from parasites/toxic substances?

A
  • antigen binds to IgE on mast cell surface
  • cross-linking of FcεRI receptor
  • activation of smooth muscle -> sneezing, coughing, diarrhea etc.
  • mast cells are most often found in connective tissue under mucosa of GI tract, around blood vessels
  • mast cells: histamines in cytoplasm -> induce inflammation
    • prepared granules released immediately after cross-linking of IgE
23
Q

How is allergy and asthma caused?

A
  • by IgE responding to regular antigen
  • mast-cell degranulation -> inflammatory response (anaphylaxis)
23
Q

How can IgG contribute to protection from parasites?

A
  • binds to Fcγ receptor on eosophil
  • when antigen bound -> degranulation (release of toxins onto parasite surface)
24
Q

Which antibodies and how are passed from mother to offspring?

A
  • IgG is transfered by FcRn across placenta into fetal bloodstream
  • dimeric IgA is obtained from mothers’ milk
    • transfered to baby’s gut
25
Q

Which antibody is responsible for neutralisation of viruses and bacteria?

A
  • high affinity dimeric IgA
  • mucosal surfaces affected first
  • bacteria have adhesins -> surface proteins that allow binding to epithelial cells
  • IgA coats the pathogen -> no binding
26
Q

Which antibodies are used for toxin neutralisation?

A
  • high affinity IgG and dimeric IgA
  • toxins bind to receptors on cells -> endocytosis
  • ab bind to toxin -> prevent binding to receptors
27
Q

Which antibodies activate complement effectively?

A
  • IgM and IgG3
  • IgM binds to antigen
    • Fc region has a binding site for C1q
    • several attachements made between 1 mol of IgM and 1 mol of C1q
  • classical pathway: C1r activated -> C1s binds and cleaves C4 and C2 -> C4bC2a -> C3 into C3b and C3a
28
Q

Do IgG activate complement by classical pathway?

A
  • yes
  • however, only one C1q site
    • multiple IgGs needed for activation
29
Q

What are immune complexes?

A
  • formed by IgG (due to high affinity binding)
  • IgG + soluble multivalent antigens
  • immune complexes activate complement classical pathway
30
Q

How are immune complexes disposed?

A
  • by erythrocytes
  • high number of CR1 receptors (for C3b)
  • go through liver and spleen -> removed by macrophages
  • if not removed, bind to podocytes in kidneys during ultrafiltration
31
Q

How are immune cells activated by IgG?

A
  • effector cells bind through FcγRI receptor
  • small structural difference determine which subclass of IgG is bound best
  • once a cluster of IgG is bound by myeloid cell -> cascade -> phagocytosis + antigen presentation
32
Q

Which Fc receptors bind with lower affinity to IgG?

A
  • FcγRII and FcγRIII
  • only bind to IgG when it’s already bound to antigen -> higher sensitivity to antigen
  • IgG not related to the current infection doesn’t occupy the space
  • FcγRII types
    • 1 activating (FcγRIIA): uptaek and destruction of pathogens by many myeolid cells
    • IgA binds to FcγRIIA
    • 2 inhibitory
      • FcγRIIB2: macro, neutro, eosino controls inflammatory response (by inhibiting Fc receptors)
      • FcγRIIB1: mast, B cells
      • ITIMs in cytoplasmic tails -> inhibitory signal
33
Q

What is the role of FcγRIII in NK cells?

A
  • low affinity for Fc
  • signal from FcγRIII activates NK cells (ADCC)
  • apoptosis
34
Q

What is the receptor for monomeric IgA?

A
  • FcαRI

Immunology (Parham) (13 decks)

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