Lecture 15 Flashcards

(45 cards)

1
Q

Innate System: Second Line of Defence

Soluble Components

A
  • Plasma proteins
  • cytokines
  • Interferons
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2
Q

How does the body respond to invasion

A

▪ Recognition

▪ Attack

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3
Q

How does the body recognize an invasion

A
  • PAMPs
  • DAMPs
  • Sometimes Opsonization
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4
Q

PAMPs

A

Essential to microbial survival and metabolism
which makes them relatively invariant and
evolutionary stable

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5
Q

Give me examples of PAMPs

A

-Peptidoglycan
-LPS
-Mannose
-Nucleic acids
Flagellin
Non-methylated CpG repeats

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6
Q

TOLL-LIKE RECEPTORS: PATHWAY

A

-Recognize the PAMPS
-Cascade occurs
Activation of transcription factors
-Increased expression of cytokines

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7
Q

What are ways the innate immune system attacks

A
  • Phagocytosis
  • Opsonization
  • Secretions
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8
Q

What is the general activity of phagocytes

A
  • To suvey
    -To ingest
    -To o extract immunogenic
    information from foreign
    matter
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9
Q

Professional Phagocytes

A
  • Neutrophils

- Macrophages

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10
Q

Non-Professional phagocytes

A

Lymphocytes, NK cells, Epithelial cells, Endothelial cells,

Fibroblast

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11
Q

What is Opsonization

A

to ensure
cell is readily identified, and
more efficiently taken by
phagocytes

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12
Q

What receptors are used for opsonization

A
✓CR1 – complement receptor
for C3b fragment
(complement cascade)
✓Fc receptors for Fc region of
immunoglobulins
(antibodies)
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13
Q

Main opsonin for the antibodies

A

IgG

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14
Q

What’s special about IgM

A

-There are no Fc receptors for IgM but IgM activates the complement system for opsonization

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15
Q

What are the main complement opsonin’s

A

C3b, C4b, and C1q

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16
Q

How do the complement molecules opsonize

A
  • Opsonize the antigen

- Opsonized antigen binds to CR1 receptor on the phagocyte

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17
Q

Name three opsonin’s

A
  • antibodies
  • complement molecules
  • circulating proteins
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18
Q

Microbial degradation within the phagolysosome occurs

along two pathways:

A
  • Oxygen dependent

- Oxygen independent

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19
Q

Describe Oxygen-dependent degradation: (Oxidative Burst)

A

NADPH oxidase produces superoxide which
recombines with other molecules to produce reactive
free radicals
✓ Superoxide anions are then used by superoxide
dismutase to produce hydrogen peroxide
✓ Myeloperoxidase uses the derived hydrogen peroxide
to produce hypochlorite or bleach (second most
important enzyme)

20
Q

What happens when there is a defeciency in NADPH oxidase

A
Absence of NADPH
oxidase will prevent
the formation of
reactive oxygen species
and will result in
chronic granulomatous
disease (CGD)
21
Q

What type of infections are associated with NADPH defeciencies

A

catalase
positive infections
(Candida, Serratia, H. pylori,
Actinomyces, Pseudomonas, E. coli, S. aureus)

22
Q

Common symptoms of CGD

A
  • Mouth ulcers
  • Neutrophil function impaired
  • Pneumonia
  • Menningitis
  • Abcess
  • Cellucitis
23
Q

nitroblue tetrazolium test

A

Blue -Normal

Yellow -abnormal

24
Q

▪ Dihydrorhodamine 123

A

Two peaks - normal

One peak -abnormal

25
Chediak-Higashi Syndrome
autosomal recessive disorder that arises from a mutation of a lysosomal trafficking regulator protein (Microtubule dysfunction) leading to lack of phagolysosome formation. -Large lysosomes in the phagocytes
26
Chediak-Higashi Syndrome presentation
- Albinism - Neutropenia - Peridontal disease - reccurent infections - Hepatomagly - Anemias
27
Principal cells involved in inflammation
- Macrophages | - Neutrophils
28
Role of cytokines in inflammation
Secreted to attract leukocytes to the site
29
Role of histamine in inflammation
causes vasodilation, increased vessel | permeability (redness and heat)
30
What does swelling during an immune response do
Contains the infection
31
What stimulates pain receptors
Bradykinin
32
Resolution/Scar formation
macrophages clean the area; fibroblasts form granulation tissue – lymphocytes mediate long-term immunity
33
Diapedesis
migration of cells out of blood vessels into the tissues
34
Chemotaxis
migration in response to specific chemicals at the site of injury or infection
35
Name 4 cell adhesion molecules
- Selectins - Mucins - Integrins - ICAMS
36
Leukocyte Extravasation
- Rolling - Activation - Arrest/Adhesion - Transendothelial migration
37
Leukocyte Adhesion Defect (LAD)
``` Deficiency of the β-2 integrin subunit (CD18) -neutrophils cannot extravasate and fight against bacteria in tissues ```
38
Hallmarks of LAD
Recurrent skin infections, delayed umbilical separation, absence of pus
39
Extravasation - Rolling
Mediated by binding of selectins (endothelium) to | mucin-like CAMs (leukocyte)
40
Extravasation-Activation
Chemokine binding induces conformational change in | integrins (leukocyte)
41
Extravasation- Arrest/Adhesion
Integrins now capable of binding Ig-superfamily CAMS | endothelium
42
Transendothelial migration
Migration through tight junctions of inflamed | endothelium
43
``` what is β-2 integrin subunit (CD18) involved in ```
formation of the β-2 integrins by dimerization | with different CD11 subunits
44
Inflammatory Process: | Systemic Acute Phase Response
``` Mediated by IL-1, IL-6, TNFα • Act on hypothalamus: fever • Act on liver: ↑ Acute phase proteins (C reactive protein) • Act on bone marrow: ↑ Leukocytosis(left shift and increase in immature cells ) ```
45
Chronic Inflammatory response
- 2 weeks or longer - successful acute inflammatory response - IFNy and TNFα play a major role