adaptive immune system Flashcards

1
Q

MHC class 1

A

CD8

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2
Q

MHC class 2

A

CD4

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3
Q

MHC peptide

A

only can present a limited repertoire

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4
Q

MHC 1 antigen processing

A
  • Proteins degraded by proteasome into peptides in cytoplasm
    • Peptides pumped into endoplasmic reticulum (ER) by TAP, binding to MHC 1
      MHC 1/peptide transported to cell surface
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5
Q

MHC 2 antigen processing

A
  • Extracellular proteins are phagocytosed, degraded by lysosome
    • MHC II generated in ER, invariant chain puts MHC II into MIIC vesicle
    • MIIC fuse with lysosomes, peptides loaded onto class II in MIIC vesicles
      MHCII/peptide is exported to cell surface
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6
Q

how many major classes of MHC are there

A
3 class 1
3 class2 
= polygenic
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7
Q

CD4 cycle

A
  1. a naïve t-cell receives antigen recognition
    1. Release cytokines (e.g. IL-2)
    2. Cloning
      Differentiation
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8
Q

Th1 summary

A

cytokine release - IFN-gamma
target cell - macrophages
host defence - intracellular pathogens

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9
Q

Th2 summary

A

cytokine release - IL-4, IL-5, IL-13
target cell - eosinophils
host defence - parasite

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10
Q

Th17 summary

A

cytokine release - IL-17, IL-22
target cell - neutrophil
host defence - extracellular pathogens

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11
Q

Th0

A
  • drives clonal expansion
    • Have a choice for differentiation
      Determined by signal 3 (cytokine secreted by dendritic cells)
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12
Q

Th1 process

A
  • IL-12 and IFN-gamma drive Th1 differentiation
    • Dendritic cells and natural killer cells = good source of IFN-gamma
    • Macrophages have receptors for IFN-gamma
    • IFN-gamma activate macrophages into M1 macrophages (good killers of intracellular organisms)
      Th1 cytokine promote IgG isotype switching
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13
Q

Macrophages affected by th1

A
  • Th1 secrete IFN-gamma, macrophages have IFN-gamma receptor
    • Th1 express CD40L (macrophages have CD40)
    • Causes release of cytokines (TFN-a, IL-1, IL-12)
      ○ Induces production of antimicrobial agents (NO and O2-)
      Increase expression of MHC
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14
Q

th17 process

A
  • IL-1, IL-6, IL-23 and TGF-B drive Th17 differentiation
    • Dendritic cells and macrophages = good source of these cytokines
    • Mobilise neutrophils
      ○ Acts on epithelial and endothelial cells to secrete chemokines - hey attract neutrophils - killing extracellular bacteria
      IL-22 acts on epithelial cell layers to increase integrity
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15
Q

CTL

A
- Contain:
		○ Perforin
		○ Granzymes
	- Perforin allows Granzymes to enter cells
Granzymes activate apoptotic pathway
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16
Q

Th1 on dendritic cells

A

Th1 cells activate dendritic cells to become better activators of CTL differentiation
CTL secrete IFN-gamma - promoting Th1

17
Q

Intracellular bacteria

A
  • Th1 activate macrophages to kill microbes in phagolysosomes
    • CTL kill infected macrophage
      Both important
18
Q

virus prevent MHC1 processing and presentation

A
Natural killer cells kill downgraded MHC1 viruses
	- NK cells activated by type 1 interferon
	- NK cells have two types of receptors
		○ Activating receptors recognise stress ligands on infected cells
		○ Inhibitory receptors recognise class 1 MHC
If NO MHC class 1 - inhibitory receptor not engaged = killing cell
19
Q

B Cells

A
  • Recognise free antigen
    • Differentiate into effector B cells (plasma cells)
      Plasma cells secrete antibody
20
Q

what region of the antibody determines if the isotype can interact with Fc receptors or complement

A

the constant region

21
Q

IgM

A
  • Pentamer
    • Receptor for naïve b cells
    • First antibody response
    • Low affinity
    • High avidity
    • GOOD for complement - only one IgM is needed to bind to complement
      ○ Opsonisation
      ○ Inflammation
      Lysis
22
Q

IgG

A
  • Activated complement
    • High affinity - good for neutralisation
      Neonatal immunity - can cross placenta
23
Q

IgA

A
  • High affinity - good for neutralisation
    • Found in milk
    • NO complement
    • 2 types:
      ○ IgA1
      § 15%
      § Pro-inflammatory
      ○ IgA2
      § Mucosal secretions
      non-inflammatory
24
Q

IgE

A
  • Good for fighting helminths
    • Causes allergy
    • Found on surface of eosinophils and basophils
    • No complement
      No neutralising
25
Q

IgD

A
  • Receptor for naïve B cells

Function obscure

26
Q

Evasion strategies against antibodies

A
  • Cleave antibodies

Bind antibodies

27
Q

how do antibodies neutralise viruses

A

by binding to them, preventing them from bind to host cell - REQUIRES HIGH AFFINITY (IgG, IgA)

28
Q

Antibodies can fight infections in 3 ways

A
  • Neutralisation - high affinity (IgG, IgA) - blocks binding
    • Opsonisation (IgG and IgA, IgM with complement)
      Lysis (complement IgG, IgM)
29
Q

opsonisation

A
  • Classical complement pathway deposits C3b on cell surface
    ○ Phagocyte recognises C3b - phagocytosis
    • Phagocytes express Fc receptors specific for heavy chain constant region
      ○ Antibody binds to pathogen
      ○ Phagocyte recognises Fc receptor on antibody
      Phagocytosis
30
Q

lysis

A
  • Binding of C3b to microbe
    • Membrane attack complex creates pores in microbial membrane
      Induces osmotic shock - lysis
31
Q

what antibody is initially produced

A

IgM produced with no T cell help

32
Q

IgM + T cell help

A

IgG, IgA, IgE produced

33
Q

time of antibody production

A
  • First antibody produced is IgM (low affinity), peaks at around day 7
    • IgM diminishes as B cells switch to other isotypes (IgG) - affinity increases
    • Primary response peaks at day 14
      If re-exposure secondary response is greater and quicker (memory cells)
34
Q

b cell stimulation

A

B cells present antigen to t cells on MHC II

T cells stimulate b cells with CD40L and cytokines

35
Q

antibody differentiation

A

IgM is default
IgG driven by IFN-gamma
IgE driven by IL-4
IgA driven by TGF-B