5.1 Barrier Defence and Innate Immunity Flashcards

1
Q

What lies above epihtelia to offer immune protection?

A

mucous

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2
Q

What lies underneath epithelia to offer immune protection?

A

Paneth Cells (secrete anti-microbial peptides like defensins)

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3
Q

What are the 3 features of the innate immune defence system?

A

ready to activate
no memory
low specificity

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4
Q

What cells of the innate immune system recognise threats?

A

Professional Antigen Presenting Cells (APCs)
Such as:
dendritic cells
macrophage / monocytes

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5
Q

What cells of the innate immune system engulf and destroy threats?

A

phagocytes (macrophage, neutrophils)

granulocytes (neutrophils, eosinophils, mast cells, basophils)

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6
Q

Name 4 examples of macrophage found around the body

A
Alveolar macrophage (phagocytose pathogens)
Kupffer cellls (blood borne infection + liver remodelling)
Microglial cells (eliminate old or dead neurones)
Splenic macrophage in red pulp of spleen eliminate old red cells and blood pathogens
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7
Q

What do dendritic cells do?

A

capture antigens, turning proteins into peptides which are then presented on their surface on MHC

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8
Q

What is MHC?

A

major histocompatibility complex

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9
Q

What is the basic functinon of neutrophils?

A

phagocytic granulocytes

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10
Q

What is the basic function of mast cells?

A

important for acute phase response and allergic responses

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11
Q

What is the basic function of basophils?

A

important for acute phase response and allergic responses

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12
Q

What is the basic function of eosinophils?

A

important for parasite killing

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13
Q

How are pathogens recognised?

A

pattern recognition receptors (PRRs) recognising Pattern-associated molecule patterns (PAMPs)

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14
Q

What are the 4 families of PRRs?

A

Toll like receptors (TLR)
Nucleotide Oligomerisation Receptors (NLR)
C-type lectin receptors (CLR)
RIG-1 like receptors (RLR)

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15
Q

What PRR families are intracellular and which are extracellular?

A

intracellular - NLR, RLR, TLR

extracellular CLR, TLR

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16
Q

What does PRR recognition stimulate?

A

cytokine production

17
Q

How can monoclonal antibodies be used therapeutically?

A

may be cytokine agonists or antagonists

so could bind to cytokine or block a receptors

18
Q

What are the key families of cytokines?

A
interferon
chemokines
TNF
Inteleukins
Haematopietins
Transforming growth factors beta family
19
Q

What are interferons?

A

Anti-viral proteins

20
Q

What do chemokines do?

A

direct cell migration, adhesion and activation

21
Q

What does TNF do?

A

regulates inflammatory and immune responses

22
Q

What do interleukins do?

A

this varies massively

23
Q

What do Haematopoietins do?

A

promote cell proliferation and differentiation

24
Q

What does the transforming growth factor beta family do?

A

regulates immune cells

25
Q

What is opsonisation?

A

coating a pathogen to make it more visible to the immune system

26
Q

What 3 ways might microbes and antigens be opsonised?

A

Complement
CRP and other acute phase protiens
Immunoglobulin

27
Q

What is immunoglobulin produced by?

A

B cells

28
Q

What are the 3 mechanisms to the complement pathway?

A

classical pathway, initiated by antibody / antigen binding

lectin pathway, initiated by carbohydrate sugars (C2 and C4 actviate C3)

Alternate pathway (C3b) constantly activating in water by only when it makes direct contact with microbial polysaccharides

29
Q

What is the overall effect of the different compliment mechanisms?

A

we always end up with C3b activating C5 and the terminal complex and compliment components (C5,6,7,8)

30
Q

What events does C3 trigger?

A
inflammation
Cytolysis
Opsonisation
Chemotaxis
Inactivation of Complement
31
Q

What happens in inflammation?

A

C3 triggers the release of histamine from Mast Cells

32
Q

What happens in Cytolyis?

A

formation of a membrane attack complex (MAC) which punches a hole in microbial membranes

33
Q

What happens in chemotaxis?

A

C5a acts as a neutrophil chemoattractant

34
Q

Where can the compliment system go wrong?

A
hereditary andiodema (C1 esterase inhibitor deficiency)
this causes uncontrolled bradykinin activation leading to oedema