Acute Immunology Flashcards

1
Q

Describe the phases of wound healing

A
  1. Inflam. phase: wound sterilisation + clearance
    - phagocytosis
    - removal of infection + damaged tissue
  2. Prolif. phase: wound closure
    - angiogenesis
    - granulation tissue
    - fibroblast prolif
    - collagen synthesis
    - ECM reorganisation
    - early epithelialisation
  3. Remodelling phase: returns tissue to normal function
    - full epithelialisation
    - ECM remodelling
    - increase in tensile strength
    - apoptosis + removal prolif cells
    - scar maturation
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2
Q

Name the cardinal signs of inflammation

A
  1. Redness
  2. Heat
  3. Swelling
  4. Pain
  5. Loss of function
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3
Q

Name the cells of innate immunity

A
  • macrophage
  • neutrophil
  • complement
  • basophil
  • mast cell
  • eosinophil
  • NKC
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4
Q

Name the cells of adaptive immunity

A
  • T cell
  • CTC
  • HTC
  • B cell
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5
Q

What is the function of dendritic cells?

A

Switch on adaptive immunity

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6
Q

What is non-self and how is it recognised?

A
  • microbes
  • triggers inflam response
  • IS recognises PAMPs
  • adaptive immune response to eliminate infection
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7
Q

What is altered self and how is it recognised?

A
  • damaged/necrotic tissue
  • inflam response to remove necrotic cells + debris
  • IS recognises DAMPs = released by damaged/necrotic tissue
  • does not typically lead to adaptive immune response
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8
Q

Describe how the complement system is activated and initiates inflammatory responses

A

Detection - classical, lectin and alternative pathway

Detection/disposal - opsonisation

Disposal - lysis

Communication - inflammation

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9
Q

How does pathogen recognition by macrophages initiate inflammatory responses?

A
  • Bacteria trigger macrophage to release cytokines + chemokines (TNF alpha + CXL8) + lipid mediators of inflam
  • Vasodilation + increased vasc. perm = redness, heat + swelling
  • Inflam. cells migrate into tissue releasing inflam. mediators that cause pain
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10
Q

Describe local inflammatory responses

A
  • Inactive WBC’s recruited + activated
  • WBC production from bone marrow progenitors increases
  • Specific B+T cells activated + expand in LN’s - travel to site
  • Increased production of complement molecules by liver hepatocytes
  • Cytokines co-ordinate these responses + turn off system once infection cleared
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11
Q

What are cytokines?

A

Umbrella term - describes

  • Interleukins (-IL)
  • Interferons (-IFN)
  • Tumour necrosis factor family (-TNF)
  • Chemokines
  • Colony stimulating factors (-CSF)

Majority = soluble

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12
Q

Name the function of cytokines

A
  • Cellular diff
  • Cellular prolif
  • Leukocyte mobilisation
  • Cellular activation
  • Cell death
  • Cell survival
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13
Q

How do cytokines achieve specificity and regulate activity?

A
  1. Bind to specific receptors
  2. Expression of cytokine receptors can be regulated by altering responsiveness of cells to cytokines
  3. Cytokine secretion = brief + self-limited
  4. Limited range of activity - typically local cellular enviro
  5. Cytokines influence synthesis + action of other cytokines - effects can be propagated + amplified
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14
Q

Name to 2 main inflammatory processes regulated by cytokines

A
  1. Inflammation e.g. TNF alpha- proinflam cytokine

2. Movement of cells e.g. CXL8 - chemokine

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15
Q

Describe the role of TNF alpha

A
  1. Mobilises body pathogen defence
    - activates endothelial cells to allow leukocytes to enter tissue
  2. Induces acute phase response
    - diffuses via blood stream to liver + upregulates expression of proteins (inc. complement)
    - increases body temp
    - mobilises energy stores from fat + muscle
  3. Encourages clotting of small damaged BV’s to prevent systemic spread

Overall: increased inflam, cell recruitment, angiogenesis + complement expression

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16
Q

What is the effect of TNF-alpha expression in sepsis?

A
  • Increases system wide vasc. permeability
  • Reduces BP
    = SHOCK
17
Q

What is the effect of TNF-alpha expression in arthritis?

A
  • Increased inflam in joints drives TNF expression
  • Increased metalloproteinase synthesis
    = loss of CT in joints
18
Q

What is the role of CLX8?

A
  • 1st chemokine to be cloned + characterised
  • Recruits neutrophils to site of infection
  • Directs neutrophils along chemotactic gradient
  • Induced by PAMPs, TNF + other pro-inflam cytokines
19
Q

Describe the process of neutrophil migration during inflammation

A
  • Local TNF alpha = increases selection expression of BV to slow down passing neutrophils + make BV’s more permeable
  • Secreted IL-8 tethers to cell surfaces + ECM
  • Interaction of IL-8 with IL-8 receptors on neutrophils activates adhesion molecules = tight binding of cells to BV ready for migration
  • Sub-endothelial space - neutrophils follow gradient of IL-8 tethered to ECM towards infected site
20
Q

How is CLX-8 receptor expression in neutrophils induced?

A

By other cytokines or recognition of PAMPs by TLR’s or other PRR’s