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inf & imm > (FE) Week 9 Innate and Adaptive Immunity > Flashcards

(FE) Week 9 Innate and Adaptive Immunity Flashcards

1
Q

What is the timeline of infection and immunity?

A

First 12 hours: Epithelial barriers + innate immunity

> 12 hours - 5 days: Lymphocytes -> Antibodies, Effector T cells

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2
Q

What is innate immunity?

A
  • Responses that start acting immediately upon encounter
  • Without history of previous encounter
  • Generic response against invading pathogens
  • Recognises broad classes of microbes
  • No long-lasting immunity
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3
Q

How do physical and chemical barriers help in immunity?

A
  • In the absence of wounds, pathogens normally cross epithelial barriers by binding to molecules on internal epithelial surfaces
    ~ Avoids dislodgement by air or fluid across the epithelial surface
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4
Q

What are some examples of the exterior defense barriers?

A
  • Lysozyme in secretions
  • Cilia in nasopharynx
  • Skin
  • Mucus in trachea
  • Rapid pH change in stomach
  • Flushing of urinary tract
  • Normal flora
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5
Q

How do antimicrobial peptides work in innate immunity?

A
  • Defensins
    ~ Secreted by epithelial cells, macrophages, neutrophils and dendritic cells
    ~ Direct bactericidal properties (insertion into membranes leading to cell lysis)
  • Lysozymes
    ~ High concentrations in macrophages, neutrophils and dendritic cells
    ~ Hydrolyses polysaccharide component of bacterial and yeast cell walls
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6
Q

How do commensal bacteria aid in innate immunity?

A
  • Prevents pathogen colonization and attachment by producing bacteriocins
    ~ Antimicrobial peptides which inhibit growth of similar bacteria
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7
Q

How does innate immune receptor binding work?

A
  • Pathogens have Pathogen Associated Molecular Patterns (PAMPs) which are recognized by Pattern Recognition Receptors (PRRs) on innate cells
    ~ PAMPs are invariant molecular patterns shared by broad classes of related pathogens
    ~ PRRs recognize patterns of repeating structural motifs on pathogens
    ~ PRRs can be secreted, located on the cell surface or intracellular on the innate immune cells
  • Eg of PRR: Toll-like receptor (TLR)
    ~ On cell surface: To identify bacteria components
    ~ Intracellular: Sense viral RNA and bacterial DNA, and tumor-derived nucleic acids
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8
Q

What are the effects of innate immune receptor binding?

A

1) Phagocytosis
2) Complement activation
3) Production of inflammatory cytokines and chemokines
4) Killing of infected cells by NK cells
5) Induce immune cell recruitment to infected sites
6) Induce T cell activation by APC

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9
Q

What is phagocytosis?

A
  • Engulfing and digestion of a microbe by neutrophils, monocytes, macrophages and dendritic cells
  • Induced by ligation of cell-surface receptors that recognize pathogens
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10
Q

What are the mechanisms of phagocytosis?

A

1) By membrane receptors (direct)
- Mannose receptor: Directly binds to polysaccharides on microbes
- Scavenger receptor: Directly recognizes charged molecules on targets

2) Opsonin directors (indirect)
- Fc receptors: Only binds to Ab-opsonized targets
- Complement receptors: Only recognizes complement-reacted targets (including Ab)

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11
Q

IFN in innate vs adaptive immunity?

A

Type 1 IFN: IFN-alpha (innate)
- Anti-viral cytokines
- Can be produced by almost all nucleated cells in response to viral infx
- Interferes with viral replication in neighbouring cells (paracrine activity)

Type 2 IFN: IFN-gamma (adaptive)
- Activates macrophages
- Aids in differentiation of Th1 cells
- Mostly produced by activated T cells and NK cells

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12
Q

What is the complement system?

A
  • A family of defense proteins that act in a cascade to produce different effector responses/functions
    ~ Opsonisation (to enhance phagocytosis)
    ~ Inflammation
    ~ Complement-mediated cytotoxicity + cytolysis through membrane-attack complex (MAC)
  • Defends against extracellular bacteria and fungi
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13
Q

What is an example of how the cascade in complement system works?

A
  • Activated C3 -> C3a and C3b
    ~ C3b binds to microbe to initiate opsonisation
  • C3b spits C5 -> C5a and C5b
    ~ C5b binds to C6 to form MAC
  • C3a + C5a cause mast cells to release histamine
    ~ Inflammation
    ~ C5a attracts phagocytes
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14
Q

What are the stages of inflammatory response?

A
  • Release of chemical signals (eg histamine) upon tissue injury
  • Dilation of capillaries to increase blood flow
  • Increased leakiness/ escape of plasma proteins (eg Ab, complement) from bloodstream
  • Phagocytes consume bacteria and cell debris
  • Leucocyte transmigration through the endothelium and accumulates at the injury site
  • Tissue heals
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15
Q

What proteins are elevated in plasma in acute phase response of inflammation?

A
  • CRP (synthesized by liver in response to IL-6, TNF and IFN)
  • Procalcitonin
  • ESR
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16
Q

How do NK cells aid in innate immunity?

A
  • Defense against intracellular viruses, bacteria and parasites
  • Exerts function in early phase of infection to contain it
    ~ Compared to T cells, which clear the infection when viral titer has decreased
  • Activated by IFN, TNF and IL-12 cytokines
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17
Q

How do dendritic cells aid in bridging innate and adaptive immunity?

A
  • Small numbers of DC activate large numbers of T cells
  • Recognition of PAMPs by TLR/PRRs on immature DC is followed by ingestion of antigens in tissues -> becomes mature
    ~ Mature DC migrate to lymph nodes
  • DC presents fragments of the antigen to T cells to stimulate the adaptive immune response
18
Q

What is adaptive immunity?

A
  • Immunity that occurs after recognition of an antigen by specific receptors on T/B lymphocytes
  • Takes over when innate response is insufficient to control an infection
    ~ Adaptive response is stronger and more focused but takes a few days to be initiated
  • Provides host with long-term protection from reinfection through memory cells
    ~ Quicker and more efficient response
  • 2 types of responses
    ~ Humoral (B cells and Ab)
    ~ Cell-mediated (T cells)
19
Q

Where are antigen receptors found on T and B cells?

A
  • Cell surface on T/B cells
  • Secreted by B cells
    ~ Known as antibodies
20
Q

How do T cells recognize antigens?

A
  • TCR binds to peptides from foreign particle that is expressed on MHC (formed by complement in innate immunity)
  • APC (bearing MHC) go to lymph nodes and spleen to find naive T cells

Note: Must always have MHC; no direct binding b/w T cell and bacteria antigen

21
Q

What are the functions of APCs?

A

1) Dendritic cells
- Transport antigens to lymphoid organs to present to naive T cells
- Results in T cell activation, clonal expansion and differentiation into effector T cells

2) Macrophages
- Presents antigens to T cells in tissues but does not migrate to LN
- Results in T cell activation and macrophage activation to kill microbes

3) B lymphocytes
- BCR recognizes and uptakes antigen to present to T cells using MHC
- Results in T cell and B cell activation, and antibody production

4) Provides “second signals” for T cell activation
- First comes from costimulatory molecules and cytokines
- Ensures that T cells respond best to microbial agents

22
Q

What happens in TCR-MHC interaction?

A
  • TCR recognizes part of MHC (found on APC) as “self”
    ~ So that it is only activated by the correct MHC
  • TCR are also specific for peptide antigen of foreign body
23
Q

What are the signals needed for T cell activation?

A
  • Both signals are provided by activated APCs
  • Signal 1: (ensures that T cells are Ag- specific)
    ~ MHC + Peptide
  • Signal 2: (prevents excessive immune responses to self-antigens)
    ~ Costimulatory molecules and cytokines
24
Q

What is antigen processing?

A
  • Conversion of native antigen into peptides capable of binding to MHC molecules
  • Source of pathogen determines class of MHC:
    ~ MHC I (intracellular antigens) expressed by CD8+ T cells
    ~ MHC II (extracellular antigens) expressed by CD4+ T cells
25
Q

What is the exogenous pathway for APCs?

A
  • Extracellular pathogen is engulfed by phagocytosis and degraded in the phagosome (eg in macrophage or APC)
  • Antigen is presented on MHC II to CD4+ T cells
  • CD4+ T cell activates macrophages to kill phagocytosed microbes (eg in macrophage at start)
26
Q

What is the endogenous pathway for APCs?

A
  • Intracellular virus is degraded into viral proteins, which are processed in the ER
  • Antigen is expressed on MHC I to CD8+ T cells
  • CD8+ T cell signals infected cell to kill itself
27
Q

What is the difference in effector function in CD4+ and CD8+ T cells?

A

CD4+ (effector and memory cells):
- (E) Releases cytokines which
~ Activates macrophages to
~ Initiates inflammation and recruits more neutrophils
~ Stimulates B lymphocytes
~ Type of cytokine ditermines function
- (M) For quicker response upon re-exposure to pathogen

CD8+:
- Recognition causes CD8 cell to kill infected cell

28
Q

How do T and B cells activate each other?

A

1) B cells -> T cells
- Before becoming plasma cells, B cells function as APC
~ Displays antigens to activate T cells, for proliferation into CD4+ or CD8+ cells

2) T cells -> B cells
- T cells release cytokines which stimulate B cells to proliferate and become plasma cells -> produce Ab
- B cells + Ag can secrete IgM only but
- B cell + CD40L (on T cell) + cytokines can cause isotype switching

29
Q

How are B cells activated?

A
  • Naive B cells enter LN and spleen and respond to antigen encounter with T cell help (by cytokines)
  • Activated B cells differentiate into plasma cells (produces Ab) or memory B cells
30
Q

What are the immunoglobulin structure and functional parts?

A

Fab (fragment antigen binding):
- Binds to and recognises Ag and toxins
- Interferes w ability to interact w cells

Fc (fragment crystallisable):
- Part that interacts with other cells
- Activates effector functions and complement

31
Q

How are plasma cells formed?

A
  • After B cells displays antigen on MHC II to CD4+ T cell, CD40 ligand on T cell interacts with B cells and activates it, with help of cytokines

(TCR triggering upregulates costimulatory molecule of CD40L)

32
Q

B cell specificity?

A
  • Each B cell expresses a single type of immunoglobulin with unique specificity
    ~ When activated, it secretes Ab of that same specificity
33
Q

Why does isotype switching occur?

A
  • After activation, B cells initially only secrete IgM
  • Immunoglobulins with the same variable region (specific for the same Ag) but different constant regions are isotypes
    ~ Upon isotype switching, Ab retain the same Ag specificity but have different effector functions
  • Switching diversifies the functional properties of the Ab bc different isotypes perform different functions
    ~ Should switch for different variable regions too so more Ag can be detected
34
Q

What are the different effector functions of antibodies?

A
  • Arises from the ability of the Fc region to interact with other components of the immune system

1) IgM
- Activates complement (recap functions of complement)

2) IgG
- Neutralise microbes and toxins
- ^ Opsonisation for phagocytosis
- Activate complement system
- Activates NK cells
- Neonatal immunity

3) IgA
- Mucosal immunity in GIT and RT
- Neutralise microbes and toxins

4) IgE
- Defense against helminths
- Inflammation

35
Q

How does isotype switching occur?

A
  • Dependent on CD40L on T cells (signal to switch isotype) + type of cytokine released (to which kind of Ab)
    ~ Original: IgM
    ~ IgM + CD40L + IFN = IgG
    ~ IgM + CD40L + TGF = IgA
    ~ IgM + CD40L + IL-4 = IgE
36
Q

What are memory B cells?

A
  • Generated during primary response (when naive cell comes into contact w microbe to become APC OR when helper T cells activate B cells)
  • Typically isotype switched to IgG or IgA
  • Longer-lived than naive B cells
37
Q

Naive vs mature vs effector cells?

A

Naive cell: Not encountered Ag yet

Mature cell: After development in bone marrow and thymus

Effector cell: Been activated by Ag, tasked to eliminate microbes

38
Q

How are microbes and toxins neutralised?

A
  • Presence of Ab block binding of microbe or toxin to epithelial or tissue cells
    (think of competition for enzyme substrates)
    ~ Mainly IgG and IgA
39
Q

How does antibody-dependent opsonisation occur?

A

1) Microbe gets opsonised by Ab
2) Opsonised microbes bind to Fc receptors on phagocytes
3) Fc receptors activate phagocytosis
4) Killing of ingested microbe

40
Q

What is Type 1 Hypersensitivity Rxn by IgE?

A
  • Defence against helminths
  • Resting mast cells have IgE Ab linked to Fc receptors
  • Multivalent antigen cross-links bound IgE antibody to release granules
    ~ Contains histamine and other inflammatory mediators

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