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

Innate Immunity Flashcards

(75 cards)

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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
Where do all immune cells derive from ?
Haematopoietic stem cells
26
State the polymorphonuclear leukocytes
Neutrophils Basophils Eosinophils
27
Describe monocytes
Circulate in bloodstream, differentiate into macrophages in tissues. (macrophage precursor)
28
Describe the action of macrophages
Phagocytosis and killing of microorganisms Activation of T cells and initiation of immune reponse
29
Describe neutrophils
Most numerous & important granulocyte of innate immunity. Phagocytosis and killing of microorganisms
30
What does neutrophil deficiency lead to ?
Overwhelming bacterial infections
31
Describe eosinophils
Evolutionarily important in parasite defence. Killing of antibody-coated parasites through release of granule contents.
32
State the following about neutrophils : Duration of Action : Percentage of WBCs :
DOA : short : 12 hours, once in tissue 2 days % WBCs = 70%
33
Neutropenia
Low numbers, may be genetic or the result of mediation including chemotherapy.
34
State some facts about eosinophils : - Duration of action - What the granules contain
DOA : short 12 hours, survive in tissues for 3 days Granules : histamine, major basic protein
35
Describe basophils
Granulocyte Function similar to eosinophils and mast cells
36
Describe mast cells
When activated release a number of substances that effect vascular systems. IgE mediated triggering in allergies
37
Describe lymphocytes
Either B or T cells Within these populations lie adaptive immune response
38
Describe B cells
Produce antibodies
39
Describe T cells
Become cytotoxic T cells or helper T cells
40
Plasma cells
Fully differentiated form of B cell that secretes antibodies.
41
Describe natural killer cells
Large granular lymphocytes Recognise virus infected cells non-specifically
42
Describe dendritic cells
Most important immune cell Bridges the innate and adaptive immune responses. Specialised in antigen uptake and presentation.
43
State the 3 functions of natural killer cells (IMP EXAM Q)
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
What do Natural Killer cells secrete ? (IMP EXAM Q)
Interferon alpha INterferon beta
45
State the difference between NK cells and CD8 T cells
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
Describe the green curve of NK cells
Production of interferon alpha and beta, tumour necrosis factor. Peak of chemical signals which indicate infection, help cells become resistant to viral infection.
47
Describe the blue curve of NK cells
NK-cell killing of infected cells. Helps get rid of and control virally infected cells during the initial stages of an infection.
48
Role of NK cells in immune reponse
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
Describe the red curve of NK cells
Antibody response T-cell killing of infected cells. (secondary immune response)
50
Describe the yellow curve of NK cells
Amount of virus you could detect in the bloodstream of a person.
51
Interaction of NK cell with uninfected healthy cell
No killing of healthy cell
52
Interaction of NK cell with target cell in which MHC class 1 expression is lost
Killing of virus infected cell in which MHC class 1 expression is inhibited
53
Interaction of NK cell with healthy cell in the presence of anti-MHC class 1 antibodies
Anti-MHC class 1 antibody prevents interaction between the inhibitory receptor and the MHC class 1.
54
What is the complement pathway ?
A cascade of activated proteins that are pre-formed floating in your bloodstream and are available for immediate activation to fight off pathogens
55
What are the 3 main ways to trigger the complement cascade ?
Classical Pathway Lectin Pathway Alternative Pathway
56
Describe the Classical Pathway
Antibody binds to specific antigen on pathogen surface
57
Describe the lectin pathway
Mannose-binding protein binds to pathogen surface.
58
Describe the alternative pathway
Pathogen surface creates local environment conductive to complement activation.
59
Describe complement
Comprises a large number of distinct plasma proteins
60
Describe the outcomes of complement activation
Recruitment of inflammatory cells Opsonisation of pathogens, facilitating uptake and killing by phagocytic cells Lysis and death of pathogens
61
C3b
Membrane binding protein and OPSONIN
62
Opsonin
Coats bacteria and enhances phagocytic effects
63
C3a
Direct peptide MEDIATORS of INFLAMMATION
64
What is the classical pathway initiated by ?
Activation of the C1 complex
65
Describe C3a and C3b in the classical pathway
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
Difference between classical and alternative pathways
Alternative pathway : activation of C3b directly on the surface, you don't need C1 component to start with (no pre-existing antibody response)
67
Trigger of the alternative pathway
Bacteria
68
Describe the assembly of the membrane attack complex (MAC)
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
Activation of C8 and C9
Great way of directly killing bacteria
70
Function of regulation of the complement activation
Protects host cells from damage Series of inhibitory molecules floating around in the bloodstream.
71
DAF
Decay accelerating factor
72
MCP
Membrane cofactor protein
73
CR1
complement receptor 1
74
How do you stop the membrane attack complex (MAC) from punching holes in your own cells ? Exam Q
CD59 stops the membrane attack complex from forming on your own cells.
75
Complement deficiencies
Repeated bacterial infections C2 - inflammatory disease C3 - recurrent bacterial infections

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

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