Innate Response Flashcards

1
Q

Ways complement system can be activated

A

Classical pathway, Mannose-binding lectin pathway, alternative pathway

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2
Q

Classical pathway

A

Only occurs when there are antibodies specific to a foreign antigen

Antibody complexes bound by component C19 detects bound antibodies to pathogens

Activates subsequent complement components

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3
Q

Mannose-binding lectin

A

Mannose is a carbohydrate not present on self cells but often on bacteria cells

Activation through mannose-binding lectin binding to mannose on bacteria

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4
Q

Alternative pathway

A

Involves complement component C3 - which spontaneously activates and binds to nearby membranes

Host cells have control proteins on their surface to prevent further complement activation by degrading C3

Bacterial cells do not have control proteins so the complement is activated via further activation of C3 proteins

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5
Q

Result of complement activation

A

Complement lysis

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6
Q

Complement lysis

A

Membrane attack complex MAC forms in membrane of bacteria

Barrel like structure is formed from multiple late complement components (C6-C9)

This disrupts osmotic balance as the semi-permeable membrane is destroyed —> water rushes in, ions rush out, bacteria swells and bursts

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7
Q

Complement components

A

Soluble complement proteins are released on complement activation —> their release helps trigger immune response and amplify inflammation by causing blood vessels to become leaky -> resulting in recruitment of immune cells and activation of mast cells

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8
Q

Opsonisation

A

Activated by membrane bound complement components

Complement component binds to bacteria -> phagocytes have complement receptor which bind membrane bound component -> encourages phagocytosis by switching on killing mechanisms

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9
Q

Phagocytes

A

Neutrophils, macrophages, dendritic cells

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10
Q

Neutrophils

A

Good at killing - kill as much as possible, use so much energy that they then die very quickly

Recruited rapidly to site of infection

Very short lived

Constituent of pus

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11
Q

Macrophages

A

Reside in tissue

Good at killing if activated

Also involved in tissue healing, clearance of dead cells and metabolism

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12
Q

Dendritic cells

A

Initiate adaptive immune responses

Reside in tissues

Poor at killing

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13
Q

Extravasion

A

How neutrophils get to the site of inflammation from the circulation

Endothelium of blood vessel altered by inflammatory cytokines so neutrophil can loosely associate, ROLLING ADHESION —> neutrophil tightly adheres to endothelium TIGHT BINDING —> neutrophil overs through epithelium, only occurs where there is inflammation as creates leaky epithelium DIAPEDESIS ->MIGRATION of neutrophils up the chemokine gradient to the site of infection

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14
Q

Phagocytosis

A

Phagocyte detects pathogen and engulfs it —> forms phagocyte —> Lysosome (contains toxic products) fuses with phagosome to form PHAGOLYSOSOME —> phagolysosome matures as more lysosomes fuse with it —> hydrogen ions are pumped in —> protease, oxygen radicals, nitric oxide degrade pathogen

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15
Q

Macrophage Activation

A

Macrophages can uptake bacteria before activation - but require activation in order to engage in phagocytosis

Macrophages are activated via danger signalling or via cytokines —> especially interferon gamma

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16
Q

Neutrophil Extracellular Traps

A

Neutrophils can extrude their DNA, acting like a net - to stop pathogens spreading through he body by trapping them

17
Q

Antigen presentation

A

Dendritic cells sense danger —> they mature and upregulate different chemokine receptors —> resulting in migration to the lymphatics and draining lymph node —> Present antigen to T-cells

18
Q

Dendritic cells migrate

A

Into T-cell area to find the random specific antigen receptor

19
Q

B-cell receptor

A

Can recognise soluble antigen in its normal form

20
Q

T-cell receptor

A

Has to have antigen ‘presented to it on Major Histocompatibility Complex (MHC) on another cell

Antigen must be chopped up into peptides as T cells can’t recognise full protein

21
Q

Antigen presentation with no danger signal

A

Results in no response prevents autoimmunity

22
Q

Antigen presentation with danger stimuli

A

Needs to have danger stimuli (co-stimulation), cytokine storm and antigen presentation in order to trigger an immune response