Innate, Adaptive, Humoral and Cell-mediated Immunity Flashcards

1
Q

Describe how humoral immunity works

A
  1. Antigen binds to antibody on B lymphocyte
  2. Plasma cells
  3. Antibodies produced
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2
Q

Define Humeral Immunity

A

Defence against extracellular bacteria and secondary viral infections

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3
Q

What are the ‘fab’ regions of the antibody

A

The variable region that bind to antigen on pathogen

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4
Q

What are the ‘fc’ regions of the antigen

A

The ‘constant’ regions which bind to receptors of phagocytes and NK cells - eliminate antigen)

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5
Q

Why are the chains in an antibody called heavy and light

A

Light - 25kD

Heavy - 50kD

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6
Q

Are the variable and constant regions encoded by the same exon

A

Nope

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7
Q

How does the genome give rise to specific antibody shapes

A

Multiple V regions in the genome can recombine and mutate during B cell differentiation

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8
Q

What antibody is IgG similar to

A

IgD

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9
Q

What antibody has a similar shape to IgG and IgD but can be found as a dimer instead

A

IgA

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10
Q

Structure of IgD

A

The two polypeptide chains that make the constant (Fc) region have three amino acids each

The two polypeptide chains that make the fab region have two amino acids each

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11
Q

Structure of IgG, IgA and IgD

A

The two polypeptide chains that make the constant (Fc) region have two amino acids each

The two polypeptide chains that make the fab region have two amino acids each

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12
Q

Structure of IgM

A

Pentamer of ‘Y-shaped’ antibodies joined together by J chain in the centre

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13
Q

Role of IgG

A

Secondary and Memory responses

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14
Q

How is IgG inherited

A

Cross the placenta

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15
Q

Role of IgM

A

Primary responses

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16
Q

Role of IgA

A

Protects mucosal surfaces

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17
Q

Role of IgE

A

Allergy and response to parasitic infections

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18
Q

How does the level of IgM and IgG vary from primary to secondary response

A
  1. IgM increases rapidly during primary and there’s a delayed increase of IgG as specific antibodies are made. Both reach the same conc peak before declining
  2. Upon secondary infection, IgG levels increase earlier and more rapidly than IgM and reach almost triple the conc. IgM reaches the same peak as the primary infection conc. wise.
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19
Q

How do antibodies protect against infections

A
  1. Neutralise toxins (IgG and IgA)
  2. Immobilise microbes (IgM)
  3. Prevents binding to host cells
  4. Form complexes
  5. Enhance innate mechanisms (complement system activation)
  6. Bind Fc receptors
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20
Q

Result of binding to phagocytic Fc receptors (IgG and IgA)

A

Enhances phagocytosis

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21
Q

Result of binding to Mast Cell Fc receptors (IgE)

A

Release of inflammatory mediators

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22
Q

Result of binding to NK cells (IgG) Fc receptors

A

Enhanced killing

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23
Q

4 steps involved in therapeutic research involving pathogens

A
  1. Identify and label molecules in complex mixtures
  2. Serotype pathogens
  3. Identifying cell types
  4. Humanised antibodies used in therapy
24
Q

What product found in the body can indicate transplant rejection

A

OKT3 which binds to CD3

25
Q

What do B cells recognise

A

Soluble native antigens

26
Q

What do T cells recognised

A

Cell-associated processed antigens

27
Q

What chromosome encodes Major Histocompatibility proteins

A

Chromosome 6

28
Q

What are MHPs important in

A

Graft rejection

29
Q

What are Major Histocompatibility proteins also known as

A

HLA molecules

30
Q

What property do all MHPs have

A

Very polymorphic

31
Q

What is the role of MHP

A

Initiate T cell responses

32
Q

Role of MHC I

A

Display antigen to CD8 (cytotoxic T cells)

33
Q

Role of MHC II

A

Display antigen to CD4 (helper cells)

34
Q

What three cells express MHC II

A
  1. Macrophages
  2. Dendritic Cells
  3. B cells
35
Q

What happens to a viral-infected cells so that the CD8 recognises peptide bound to MHC I

A

Viral proteins broken down in cytosol

Peptides transported to ER and bind to MHC I

36
Q

What happens to T helper cells physiologically when they interact with MHC II

A
  1. Macrophage/Dendritic cell/B cell internalises and breaks down foreign material
  2. Peptides bind to MHC II in endosome which are displayed on cell surface
  3. Antibody production
37
Q

How do cytokines act

A

Locally

38
Q

Role of IL-1

A

Induces Inflammation, fever and activates leukocytes

39
Q

Role OF IL-2

A

Stimulates T, B and NK cell growth

40
Q

Role of IL-4

A

Induces IgE production and TH2 differentiation

41
Q

Role of IL-8

A

Induces neutrophil chemotaxis

42
Q

Role of IL-10

A

Down-regulates TH1 cytokines and MHCII expression

43
Q

Where are IL-1 made

A

Macrophages, endothelial and epithelial cells

44
Q

Where are IL2 made

A

T cells

45
Q

Where are IL-4 made

A

Mast cells and TH2 cells

46
Q

Where are IL-8 made

A

Macrophages, endothelium, fibroblasts, keratinocytes

47
Q

Where are IL-10 made

A

Monocytes and TH2 cells

48
Q

Role of INF gamma

A

Activates macrophages and NK cells

Increases MHC II expression

49
Q

Where are INF made

A

TH1 and NK cells

50
Q

Where are TNF alpha made

A

T, macrophages and NK cells

51
Q

Role of TNF alpha

A

Activates neutrophils and endothelial cells

Wasting

52
Q

What do TH1 cells produce (cytokines)

A

IL2, INF-gamma, TNF-beta

53
Q

What do TH2 produce (cytokines)

A

IL4,5,6,10,13

54
Q

What do TREG cells produce and why

A

IL-10 and TGF-beta - to down-regulate or act against the other cytokines

55
Q

How does infection protect against allergy

A

Promotes IL-10 and TGF-beta production to reduce number of TH1 and TH2 (increase in TREG)