(LE3) Innate Immunology Flashcards

1
Q

What are the body’s 3 lines of defense?

A
  1. mechanical and chemical barriers
  2. Innate immune response
  3. adaptive immune response
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2
Q

What are your non-specific defenses?

A

Mechanical & chemical barriers

Innate immune response
- not pathogen-specific, always present, can activate adaptive immune response

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3
Q

What are your specific defenses?

A

Adaptive immune response
- pathogen-specific, builds up slowly in response to pathogen, can enhance innate defenses

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4
Q

How does skin act as a mechanical barrier?

A
  • prevents pathogens from entering
  • some bacteria gain entry through sebaceous glands, hair follicles, etc.
  • Hookworm can burrow through intact skin
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5
Q

What are “flushing” mechanisms?

A
  • tears, saliva, urination, diarrhea, ciliary escalator
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6
Q

How is lysozyme a chemical barrier?

A

Degrades peptidoglycan
- Tears, saliva, sweat

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7
Q

How is sebum a chemical barrier?

A

Low pH due to fatty acids
- skin oil glands

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8
Q

How does salt work as a chemical barrier?

A

Causes plasmolysis in prokaryotes
- sweat, tears

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9
Q

How does the stomach work as a chemical barrier?

A

Has a low gastric pH

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10
Q

What chemical barriers are in your blood?

A

Transferrin- bind to free Fe+

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11
Q

What do neutrophils do?

A

Phagocytosis
- first responders to infection
- 60-70% of all leukocytes
- aka “polymorphonuclear neutrophils”

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12
Q

What do Basophils do?

A

release histamine
- involved in inflammation and allergy response

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13
Q

What do Eosinophils do?

A

Anti-parasitic
- also involved in allergy response

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14
Q

What do monocytes do?

A

Found in blood. Mature into macrophages when they enter tissue -> phagocytosis
- macrophages involved in both innate and adaptive immune response

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15
Q

What do dendritic cells do?

A

Phagocytosis
- non-circulating cells (not in blood)
- important to activate adaptive immune response

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16
Q

What are natural killer cells?

A
  • recognize foreign glycoproteins on surfaces of virus-infected cells
  • Secrete perforin and granzyme -> destroy infected cells and pathogen (collateral damage)
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17
Q

What is GALT system and Peyer’s patches?

A

lymph nodules in the intestinal lining
- B & T cells

18
Q

What are your main phagocytes?

A

Neutrophils, macrophages, dendritic cells
- innate cells
- some activate adaptive response

19
Q

What are the steps of phagocytosis?

A
  1. Chemotaxis - phagocyte finds way to infection. e.g. inflammation via cytokines
  2. Adherence - cells stick to pathogen via toll like receptors (TLR) -> peptidoglycan and LPS
  3. Ingestion - endocytosis into a phagosome
  4. Digestion - phagosomes fuses with lysosome to form phagolysosome. Digestive enzymes destroy pathogen.
  5. Release & sometimes presentation on an MHC molecule
20
Q

How do bacteria resist adherence during phagocytosis?

A

virulence factors like capsules

21
Q

What virulence factor can pathogens have to resist digestion?

A

Leukocidins

22
Q

What is the purpose of an MHC molecule?

A

activates the adaptive immune response

23
Q

What is inflammation?

A

An innate (non-specific) response to tissue damage

24
Q

What is the function of inflammation?

A
  1. destroy/remove injurious agent
  2. send signal to body that damage has occurred (via cytokines)
  3. limit effects of damage by walling off area (granuloma)
  4. repair/replace damaged tissue
25
Acute inflammation vs chronic inflammation
acute: response to infection chronic: wall-off pathogen, can't clear infection, form granuloma
26
What are disease examples of chronic inflammation?
Leprosy, 3rd stage syphilis, TB
27
What is histamine's role in acute inflammation?
Vasodilation - red, warm, skin - bring more RBCs, WBCs, and platelets
28
What cytokines cause pain during inflammation?
Bradykinin and prostaglandin
29
How does the body know where to send WBCs in response to pathogen invasion? What are the steps?
Phagocyte Migration 1. Attracted to chemical signals via chemotaxis 2. Margination - WBCs stick to site of blood vessel 3. Diapedesis - WBCs crawl out of blood vessel
30
What is pus composed of? Is pus a good thing?
Dead phagocytic cells Good sign in short term. Bad long term. Means body is unable to clear out pathogen due to it being an overwhelming amount
31
What are your noncellular innate defenses?
1. Fever 2. Interferons 3. Complement system
32
How is a fever initiated?
- when macrophage ingests exogenous pyrogen (endotoxin) - macrophage secretes Interleukin 1 -> binds receptors in hypothalmus - hypothalamus resets body temperature
33
Why do fever and chills usually go together?
Hypothalamus tricks brain into thinking you're cold to raise body temperature
34
What is the result of a fever?
Increase hematopoiesis, increase phagocytosis, and some organisms are heat sensitive
35
What is considered a high fever? Why is that not ideal?
102.9 Fahrenheit Proteins denature
36
What are interferons' function?
INF-alpha and INF-beta - stimulated by viral infections to cause neighboring cells to die to prevent further spread of viral infection
37
What is the complement system?
series of 20 plasma proteins (C1, C2, etc.) that work as a cascade
38
How do you activate the complement system?
1. Classical pathway: Antibody binds antigen on pathogen. - more efficient, but slower (adaptive response) 2. alternative pathway: C proteins bind cell wall polysaccharides common to most bacteria and fungi - less efficient, but faster
39
What are the three results of complement system activation?
1. Inflammation (mast cells release histamine) 2. Opsonization 3. Membrane attack complex (MAC)
40
What is opsonization's function? How does it work?
Facilitates phagocytosis - coats surface of pathogen with immune proteins (e.g. complement proteins)
41
What is the function of the membrane attack complex?
C5-C9 proteins form in pathogen cell membrane - create holes -> cell lysis