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Year 1 > Innate immunity and inflammatory process > Flashcards

Innate immunity and inflammatory process Flashcards

1
Q

What is innate immunity?

A

Immunological response 0-4 hours after infection.

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2
Q

What are the advantages of innate immunity?

A

Instructs the nature of the acquired immune response, prevents pathogen expansion and limits multiplication to prevent early death.

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3
Q

What are the non-immunological barriers to infection?

A

Mechanical: Tight junctions with epithelia, longitudinal flow of air in the skin and gut and cilia mucus movement in the lungs
Chemical: Low ph, salivary enzymes, fatty acids in the skin such as sebum
Microbiological: Flora

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4
Q

What is the complement system?

A

It is a cascade which enhances the function of phagocytic cells and antibodies to clear foreign microbes.

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5
Q

What are the 3 pathways of the complement system?

A

Classical pathway, MB-lectin pathway and alternative pathway. The pathways each aim to activate C3 convertase enzyme.

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6
Q

What is the classical pathway?

A

C1q is the first component which binds to the antigen-antibody complex. This activates C1r and C1s which associates with serine proteases to form the C1 complex. C1 complex triggers the cleavage of C2 and C4 into a larger and smaller fragment. The larger fragments of each polymerise to form C4bC2a which cleaves C3 to form C3 convertase.

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7
Q

What is the Mannose Binding- Lennin pathway pathway?

A

Lennin protein binds to Mannose residue on pathogen surfaces. This triggers formation of serine proteases MASP-1 and MASP-2 along with Mannose-binded Lenin on the pathogen surface. These molecules cleave C4 and C2 into fragments and the larger fragments polymerise to form C4bC2a which cleaves C3 to form C3 convertase.

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8
Q

What is the alternative pathway?

A

C3 undergoes spontaneous hydrolysis to form C3(H20) which binds to factor B and forms C3 (H20)B. This is cleaved by Factor D to form C3 convertase.

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9
Q

What is the function of C3 convertase?

A

Cleaves C3 into C3a and C3b.

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10
Q

What is the function of C3a?

A

C3a works with C5a for inducing inflammation to recruit phagocytes.

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11
Q

What is the function of C3b?

A

Binds to complement receptors on phagocytes for opsonisation to trigger phagocytosis. It activates the terminal component of the complement cascade MAC complex which forms cytotoxic pores on microbial surface for pathogen lysis.

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12
Q

What is the MAC complex composed of?

A

C5b binds to C6 and C7 to form C5bC6C7 complex, inserted into membrane by attachment of C8 and polymerisation of C9 attachment creates a cytotoxic pore on the membrane for pathogen lysis.

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13
Q

What is the acute inflammatory response?

A

Bacteria initiates cleavage of C3Bb into C3b which opsonises the bacterium via recognition of the surface receptor on phagocytic cell and C3a which works with C5a to release inflammatory mediators and vascular permeability mediators to cause redness and swelling and recruit immune cells.

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14
Q

Difference between adaptive and innate immune response?

A

Innate immunity is faster, fixed, limited specificity and constant. Adaptive is slower, variable, high specificity and improves during response. Both are required to destroy pathogens.

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15
Q

What are the characteristics of innate immunity?

A

Specificity is inherited, recognises broad classes of pathogens and interacts with a range of pathogens. It is expressed by all cells of a type.

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16
Q

What are the characteristics of adaptive immunity?

A

Requires gene rearrangement to achieve specificity and can differentiate between closely related molecular structures.

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17
Q

How are phagocytic receptors coupled to function?

A

Binding of pathogens to macrophages triggers release of cytokines and inflammatory mediators.

18
Q

What is the LPS receptor?

A

Lipidpolysaccharide receptor which is a type of pattern recognition receptor for identification of gram-negative bacteria by immune cells. Activation via binding triggers release of lipid inflammatory mediators.

19
Q

What is the role of epithelial cells in immunity?

A

Secretes cytokines to recruit phagocytes.

20
Q

Which protein is present on gram negative bacteria?

A

Flagellin and lipoteichoic acid.

21
Q

What are Toll-like receptors?

A

TLR receptors recognise pathogen-associated patterns to differentiate the type of pathogen, and can discriminate between gram-positive and gram-negative bacteria. It initiates inflammation and adaptive immune response by releasing IFN-gamma and IL-17.

22
Q

What is the process of phagocytosis?

A

Pathogen binds to pathogen associated receptor and triggers endocytosis and fusion to form phagolysosome degrades the pathogen.

23
Q

What is respiratory burst?

A

Neutrophils rapidly release toxic oxygen radicals via activation of NADPH oxidase which kills microbes via membrane lysis.

24
Q

What are the microbicidal mechanisms of phagocytes?

A

They release lactoferrin which damages gram-negative bacteria, low ph, toxic oxygen radicals, lysozymes and defensin which disrupt membranes.

25
Q

What is the order of composition of phagocyte types?

A

Neutrophils, lymphocytes, monocytes, eosinophils. Basophils and dendritic cells are both lowest.

26
Q

What are neutrophils?

A

It is polymorphonuclear which means multi-lobed nucleus. It is responsible for respiratory burst and is the most abundant WBC type. It is highly phagocytic and found in tissue depots.

27
Q

What happens following neutrophil activation?

A

Creates NETs (Neutrophil extracellular traps) formed of chromatin, granule proteins and enzymes to degrade virulence factors and catch bacteria.

28
Q

What is a virulence factor?

A

Molecules released by pathogens which cause damage to an organism.

29
Q

Where do macrophages arise form?

A

Mainly non-haematopoietic stem cells. Arise from haematopoietic stem cells via monocyte formation from GM-CSF which moves to infected tissue and forms macrophages. They are host cells for many pathogens and are long lived.

30
Q

What are Kuppfer cells?

A

Macrophages of the liver derived from the embryonic yolk sac.

31
Q

What are dendritic cells?

A

Antigen presenting cells involved in the adaptive immune response and can be sedentary or migratory.

32
Q

What is cellular egress from macrophages?

A

Release of cytokines and chemokines from neutrophils to cause localised vasodilation and recruit leukocytes.

33
Q

How does a monocyte become a macrophage?

A

Monocyte binds to adhesion molecules on the vascular endothelium. Receives signals and migrates to surrounding infected tissue and differentiates to a macrophage.

34
Q

What are cytokines and chemokines?

A

Signalling hormones of the immune system which have a specificity to receptors. The receptors are highly regulated to control the duration and target of response

35
Q

What are chemoctactic cytokines?

A

Signalling hormones which stimulate cell migration.

36
Q

How do steroids affect cytokine release?

A

Steroids cross the cell membrane and bind to the steroid receptor. This causes the release of the associated protein Hap90. The steroid receptor complex crosses the membrane and binds to regulatory sequences to activate transcription.

37
Q

What is an interferon?

A

A cytokine released by virally-infected host cells.

38
Q

What is TNF?

A

Tumour necrosis factor for cell proliferation, differentiation or death. It is the principal cytokine of the cascade responsible for rheumatoid arthritis.

39
Q

What are the implications of TNF blockade?

A

TB reactivation and increased risk of secondary infection.

40
Q

What is Type 1 immunity?

A

Response to microbial killing and tissue damage

41
Q

What is type 2 immunity?

A

Response to helminth responses, fibrosis and repair.

Year 1 (191 decks)

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