Principles Immunology Flashcards

1
Q

What does our immune system do?

A

Identify and eliminate micro-organisms and other harmful substances as well as abnormal cancer cells

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2
Q

How is the skin a constitutive barrier of infection?

A

Tightly packed and waterproof
Low pH: 5.5
Sebaceous glands secrete hydrophobic oils lysosymes, ammonia, antimicrobial peptide

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3
Q

How are mucous membranes a constitutive barrier to infection?

A
Mucous traps the bacteria
Ciliates cells moves the mucus out
Secretory IgA stops invasion
Enzymes that kill pathogens
10^14 commensal bacteria
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4
Q

Ways healthcare provision can breach constitutive barriers

A

Insertion of hardware
Antibiotics - break down commensals and damage mucous membranes
Other therapeutics - anti-acids, nasal decongestants, inflammatory response

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5
Q

Natural killer cells

A

Release performing protein into membrane of target cell
Cell rupture - apoptosis
NK cells will not kill healthy cells as these express specific proteins

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6
Q

What is innate immunity?

A

A defence mechanism that is presence that is present from birth

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7
Q

What is adaptive/acquired immunity?

A

Induced by the presence of foreign material
Can take 5-7 days to kick in
Better than innate immune system

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8
Q

A defective innate immune system results in

A

No initial killing of pathogen, adaptive takes time to kick in

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9
Q

Defective adaptive immune system

A

Innate immune system OK at first but can’t keep up with it

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10
Q

Macrophages develop from

A

Circulating monocytes

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11
Q

Dendritic cells are

A

Phagocytic

Abundant in tissues in contact with the external environment

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12
Q

Mast cells

A
Single nucleus, highly granular
In tissues and soft mucosal membranes
Step in for large parasites
Activated by danger signals and pathogen
1. Degranulation
2. Gene expression
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13
Q

Recognition of pathogens

A

Pathogens express signature molecules not found in humans (PAMPs)
Innate immune cells express partner receptor on the cell surface and cytoplasm (PRRs)

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14
Q

Phagocytosis

A
  1. Macrophages express PRRs
  2. Receptor binding to PAMPs signals the formation of the phagocytic cup
  3. Cup extends around the target and pinches off, forming a phagosome
  4. Fusion with lysosome to form a phagolysosome
  5. Debris is released into extracellular fluid
  6. Pathogen-derived peptides are expressed on special cell surface receptors
  7. Pro-inflammatory mediators are released
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15
Q

Define opsonisation

A

The coating of pathogens by soluble factors to enhance phagocytosis

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16
Q

What are interferons?

A

Matter released by infected cells as danger signals

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17
Q

Define chemokinase

A

Any substance that induces a directed movement of a cell

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18
Q

What can cause neutrophilia

A

TNF alpha

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19
Q

What is the role of neutrophils in inflammation?

A

Involved in the initiation and maintenance of inflammation

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20
Q

What is the mechanism by which neutrophils are transported out of the blood stream?

A

Transendothelial migration

Pro-inflammatory mediators cause leaky vessels and vasodilation allowing neutrophils to move to the sides

21
Q

By what mechanisms do neutrophils kill pathogens?

A

Phagocytosis
Degranulation
Neutrophil extracellular traps (NETs)

22
Q

Name two other systemic responses

A

Fevers

Acute phase response of the liver

23
Q

The acute phase response

A

Changes in plasma concentration of specific proteins in response to inflammation
Mediated by liver hepatocytes which produce acute phase proteins for example CRP

24
Q

The complement system

A

Approx. 30 proteins

When they’re triggered complement proteins can enzymatically activate other complement proteins in a cascade reaction

25
Q

Mannose binding lectin pathway

A

Human cells don’t express mannose
Mannose binding lectin binds to the bacterium to form a complex that cleaves C3
C3 —> C3b and C3a

26
Q

Alternative activation pathway

A

C3b is unstable and rapidly degrades unless it binds to cell surfaces and can cause an amplification loop.
Human cells have inhibitory processes that stop this, pathogens do not
Downstream reaction will occur on the pathogen

27
Q

The membrane attack complex

A

The last 5 proteins in the complement cascade self associate to form a membrane attack complex (MAC)
MACs insert themselves into pathogen membranes and allow extracellular salts and water to enter causing the pathogen to swell and burst

28
Q

C3b causes

A

An amplification loop, opsonisation and conversion to C5

29
Q

C3a and C5a causes

A

Acute inflammation

Anaphylotoxins

30
Q

C5b causes

A

MACs to cause pathogen killing

31
Q

B-cells

A

Mature in bone marrow
Responsible for humoral immune response
Produce antibodies that attack pathogens circulating in the lymph

32
Q

T cells

A

Mature in the thymus
Responsible for cellular immune response
Key role in Defense against intracellular pathogens
CD4+ T cells are regulators of the entire immune system
CD8+ T cells kill virally infected cells

33
Q

Define antibody

A

Protein that binds to one specific antigen

IgM, IgG, IgA, IgE, IgD

34
Q

Adaptive immune responses in secondary lymphoid tissues

A
  1. Lymph flows into lymph nodes through the afferents lymphatic vessels bringing pathogens
  2. B cells and T cells enter lymph nodes through high endothelial venues (HEV)
  3. Once B cells come through HEV they go into the lymphoid follicle
  4. Once T cells enter they form the T cell zone in the centre of the lymph node
35
Q

B cells need to receive to signals before they become fully active and proliferate

A
  1. Antigen

2. ‘Helper’ signals from T cells

36
Q

The germinal centre forms with…

A

Proliferation if enough B cells are in the germinal centre they differentiate to plasma cells

37
Q

Later in the germinal centre reaction, T cells help produce and secrete what…

A
‘Better’ antibodies
High affinity
Other Ig classes
Long lived plasma cells -> migrate to bone marrow
Also stimulate memory cells production
38
Q

IgM

A

First Ig type produced and secreted during the humoral immune response

39
Q

Agglutination (immune complex formation)

A

The action of an antibody when it cross links multiple antigens creating clumps of antigens
Mediated to IgM and IgG antibodies

40
Q

IgG

A

Second class produced in immune response
Functions: agglutination, complement system activation, foetal immune protection, neutralisation, opsonisation, natural killer cell activation
Transient low IgG levels at 6 months

41
Q

IgA

A

Second most abundant Ig type
Monomeric form - present in serum
Dimeric form - present in secretory fluids
Neonatal defense, neutralisation

42
Q

Unlike B cells, T cells can only recognise what?

A

Peptide antigens

43
Q

Major Histocompatibility Complex (MHC) molecules

A

Displayed peptide antigen to T cells
Also referred to as human leukocyte antigens (HLA)
Able to present many different peptides

44
Q

Two classes of MHC molecules

A

Class I - expressed on all uncleared cells, will be located with all peptides in the cells allowing for T cells to scan it, present antigens to TD8+ T cells

Class II - expressed only on antigen presenting cells, present peptide antigen to TD4+ T cells

45
Q

TH0

A

Result from cell proliferation, produce IL-2 to promote proliferation

46
Q

TH1

A

TH0 can differentiate into TH1 enter blood to get to the site of infection and produce IFN gamma if cell presenting antigen is found

IFN gamma forms cell death

47
Q

TFH

A

Migrates into B cell zone
Can help B cells become fully activated by producing co-stimulators molecules
Tell B cells to differentiate into memory cells

48
Q

Antigen activated CD8+ cells differentiate into killing cells

A

Cytotoxic T lymphocytes

  1. Recognises and binds virus-infected cell
  2. Programmes for death
  3. Moves on to new target
  4. Target cell dies by apoptosis