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Medicine Year 1 - Semester 2 - Part 1 > Innate Immunity > Flashcards

Innate Immunity Flashcards

1
Q

Function of the immune system

A

Protective responses against external pathogens

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2
Q

What is the innate immune system ?

A

The first line of defence against external pathogens.

It is not specific.

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3
Q

What is adaptive immunity ?

A

Specific response
Can involve memory

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4
Q

State the 3 phases of response to initial infection

A

Innate Immunity
Early induced response
Adaptive Immune response

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5
Q

Innate immunity response time

A

Immediate : 0-4 hours

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6
Q

Early induced response time

A

Early : 4-96 hours

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7
Q

Adaptive Immune Response time

A

Late >96 hours

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8
Q

Describe innate immunity

A

Infection

Recognition of preformed non-specific effectors

Removal of infectious agent

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9
Q

Describe early induced response

A

Infection

Recruitment of effector cells

Recognition and activation of effector cells

Removal of infectious agent

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10
Q

Describe adaptive immune response

A

Infection

Transport of antigen to lymphoid organs

Recognition by native B and T cells

Clonal expansion of effector cells

Removal of infectious agent

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11
Q

How do pathogens get access ?

A

Mucosal surfaces

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12
Q

Describe the pathogen : influenza virus, neisseria meningiditis

A

Route of entry : Airway

Mode of transmission : Inhaled droplets

Disease : Influenza, Meningococcal disease

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13
Q

Describe the pathogen : salmonella typhi, rotavirus

A

Route of entry : GI tract

Mode of transmission : Contaminated food/ water

Disease : Typhoid fever, diarrhoea

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14
Q

Describe the pathogen : treponoma pallidum

A

Route of entry : GU

Mode of transmission : Physical contact

Disease : Syphilis

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15
Q

Describe the pathogen : flavivirus, plasmodium, borrelia burgdorferi

A

Route of entry : Insect bites

Mode of transmission : Mosquito, Ticks

Disease :Yellow fever, Malaria, Lyme disease

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16
Q

Describe the pathogen : tinea pedis

A

Route of entry : External surface

Mode of transmission : physical contact

Disease : Athletes foot

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17
Q

Describe the pathogen : bacillus anthracis, clostridium tetani

A

Route of entry : Wounds and abrasions

Mode of transmission : Minor skin abrasions, punctures

Disease : Anthrax, Tetus

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18
Q

State the 3 types of barriers to infection

A

Mechanical
Chemical
Microbiological

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19
Q

Mechanical Barrier

A

Tight Junctions between cells

Air and fluid flow across epithelium

Movement of mucus by cilia

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20
Q

Chemical Barrier

A

Fatty acids on skin

Enzymes : lysosome in saliva, sweat and tears

Low stomach pH

Antibacterial peptides

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21
Q

Name some antibacterial peptides

A

Defensins (skin and gut)
Cryptidins (gut)

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22
Q

Microbiological Barrier

A

Normal flora compete for nutrients and attachment, also produce antibacterial substances

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23
Q

Describe Innate Immunity

A

Recognition by phagocytic cells in the bloodstream/body : neutrophil/macrophage.

Phagocytosis - Engulfing and Destroying pathogen

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24
Q

State the anti-bacterial effects and agents produced by phagocytes

A

Acidification - pH 3-4, (low pH environment)

Toxic oxygen derived products
Toxic nitric oxides

Peptides
Enzymes

Competitors - depriving pathogen of nutrients

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25
Q

Where do all immune cells derive from ?

A

Haematopoietic stem cells

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26
Q

State the polymorphonuclear leukocytes

A

Neutrophils
Basophils
Eosinophils

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27
Q

Describe monocytes

A

Circulate in bloodstream, differentiate into macrophages in tissues.

(macrophage precursor)

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28
Q

Describe the action of macrophages

A

Phagocytosis and killing of microorganisms

Activation of T cells and initiation of immune reponse

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29
Q

Describe neutrophils

A

Most numerous & important granulocyte of innate immunity.

Phagocytosis and killing of microorganisms

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30
Q

What does neutrophil deficiency lead to ?

A

Overwhelming bacterial infections

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31
Q

Describe eosinophils

A

Evolutionarily important in parasite defence.

Killing of antibody-coated parasites through release of granule contents.

32
Q

State the following about neutrophils :

Duration of Action :
Percentage of WBCs :

A

DOA : short : 12 hours, once in tissue 2 days

% WBCs = 70%

33
Q

Neutropenia

A

Low numbers, may be genetic or the result of mediation including chemotherapy.

34
Q

State some facts about eosinophils :

  • Duration of action
  • What the granules contain
A

DOA : short 12 hours, survive in tissues for 3 days

Granules : histamine, major basic protein

35
Q

Describe basophils

A

Granulocyte

Function similar to eosinophils and mast cells

36
Q

Describe mast cells

A

When activated release a number of substances that effect vascular systems.

IgE mediated triggering in allergies

37
Q

Describe lymphocytes

A

Either B or T cells

Within these populations lie adaptive immune response

38
Q

Describe B cells

A

Produce antibodies

39
Q

Describe T cells

A

Become cytotoxic T cells or helper T cells

40
Q

Plasma cells

A

Fully differentiated form of B cell that secretes antibodies.

41
Q

Describe natural killer cells

A

Large granular lymphocytes
Recognise virus infected cells non-specifically

42
Q

Describe dendritic cells

A

Most important immune cell

Bridges the innate and adaptive immune responses.
Specialised in antigen uptake and presentation.

43
Q

State the 3 functions of natural killer cells

(IMP EXAM Q)

A

Induce resistance to viral replication in all cells

Increases MHC class 1 expression and antigen presentation in all cells.

Activate NK cells to kill virus-infected cells.

44
Q

What do Natural Killer cells secrete ?

(IMP EXAM Q)

A

Interferon alpha
INterferon beta

45
Q

State the difference between NK cells and CD8 T cells

A

NK cells are not antigen specific

They do not require to undergo the lengthly expansion of T cells in lymph nodes when the virus is detected.

46
Q

Describe the green curve of NK cells

A

Production of interferon alpha and beta, tumour necrosis factor.

Peak of chemical signals which indicate infection, help cells become resistant to viral infection.

47
Q

Describe the blue curve of NK cells

A

NK-cell killing of infected cells.

Helps get rid of and control virally infected cells during the initial stages of an infection.

48
Q

Role of NK cells in immune reponse

A

Provide initial coverage to allow the adaptive immune response to get going over a period of time.

Keeps things under control until you start making your highly effective antibody response.

49
Q

Describe the red curve of NK cells

A

Antibody response
T-cell killing of infected cells.

(secondary immune response)

50
Q

Describe the yellow curve of NK cells

A

Amount of virus you could detect in the bloodstream of a person.

51
Q

Interaction of NK cell with uninfected healthy cell

A

No killing of healthy cell

52
Q

Interaction of NK cell with target cell in which MHC class 1 expression is lost

A

Killing of virus infected cell in which MHC class 1 expression is inhibited

53
Q

Interaction of NK cell with healthy cell in the presence of anti-MHC class 1 antibodies

A

Anti-MHC class 1 antibody prevents interaction between the inhibitory receptor and the MHC class 1.

54
Q

What is the complement pathway ?

A

A cascade of activated proteins that are pre-formed floating in your bloodstream and are available for immediate activation to fight off pathogens

55
Q

What are the 3 main ways to trigger the complement cascade ?

A

Classical Pathway
Lectin Pathway
Alternative Pathway

56
Q

Describe the Classical Pathway

A

Antibody binds to specific antigen on pathogen surface

57
Q

Describe the lectin pathway

A

Mannose-binding protein binds to pathogen surface.

58
Q

Describe the alternative pathway

A

Pathogen surface creates local environment conductive to complement activation.

59
Q

Describe complement

A

Comprises a large number of distinct plasma proteins

60
Q

Describe the outcomes of complement activation

A

Recruitment of inflammatory cells

Opsonisation of pathogens, facilitating uptake and killing by phagocytic cells

Lysis and death of pathogens

61
Q

C3b

A

Membrane binding protein and OPSONIN

62
Q

Opsonin

A

Coats bacteria and enhances phagocytic effects

63
Q

C3a

A

Direct peptide MEDIATORS of INFLAMMATION

64
Q

What is the classical pathway initiated by ?

A

Activation of the C1 complex

65
Q

Describe C3a and C3b in the classical pathway

A

C3a - floats away and helps other phagocytic cells come to the site of infection

C3b - sticks on the surface of the pathogen, helps it be opsonised and phagocytosed

66
Q

Difference between classical and alternative pathways

A

Alternative pathway : activation of C3b directly on the surface, you don’t need C1 component to start with (no pre-existing antibody response)

67
Q

Trigger of the alternative pathway

A

Bacteria

68
Q

Describe the assembly of the membrane attack complex (MAC)

A

Activation of C8 and C9 leads to formation of a pore which punctures through the membrane of the bacterial cell wall.

These pores are big enough to allow internal components of the bacteria to escape and kills the bacteria.

69
Q

Activation of C8 and C9

A

Great way of directly killing bacteria

70
Q

Function of regulation of the complement activation

A

Protects host cells from damage

Series of inhibitory molecules floating around in the bloodstream.

71
Q

DAF

A

Decay accelerating factor

72
Q

MCP

A

Membrane cofactor protein

73
Q

CR1

A

complement receptor 1

74
Q

How do you stop the membrane attack complex (MAC) from punching holes in your own cells ?

Exam Q

A

CD59 stops the membrane attack complex from forming on your own cells.

75
Q

Complement deficiencies

A

Repeated bacterial infections
C2 - inflammatory disease
C3 - recurrent bacterial infections

Medicine Year 1 - Semester 2 - Part 1 (51 decks)

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