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MICR 262 > (LE3) Innate Immunology > Flashcards

(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
Q

Acute inflammation vs chronic inflammation

A

acute: response to infection
chronic: wall-off pathogen, can’t clear infection, form granuloma

26
Q

What are disease examples of chronic inflammation?

A

Leprosy, 3rd stage syphilis, TB

27
Q

What is histamine’s role in acute inflammation?

A

Vasodilation
- red, warm, skin
- bring more RBCs, WBCs, and platelets

28
Q

What cytokines cause pain during inflammation?

A

Bradykinin and prostaglandin

29
Q

How does the body know where to send WBCs in response to pathogen invasion? What are the steps?

A

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
Q

What is pus composed of? Is pus a good thing?

A

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
Q

What are your noncellular innate defenses?

A
  1. Fever
  2. Interferons
  3. Complement system
32
Q

How is a fever initiated?

A
  • when macrophage ingests exogenous pyrogen (endotoxin)
  • macrophage secretes Interleukin 1 -> binds receptors in hypothalmus
  • hypothalamus resets body temperature
33
Q

Why do fever and chills usually go together?

A

Hypothalamus tricks brain into thinking you’re cold to raise body temperature

34
Q

What is the result of a fever?

A

Increase hematopoiesis, increase phagocytosis, and some organisms are heat sensitive

35
Q

What is considered a high fever? Why is that not ideal?

A

102.9 Fahrenheit
Proteins denature

36
Q

What are interferons’ function?

A

INF-alpha and INF-beta
- stimulated by viral infections to cause neighboring cells to die to prevent further spread of viral infection

37
Q

What is the complement system?

A

series of 20 plasma proteins (C1, C2, etc.) that work as a cascade

38
Q

How do you activate the complement system?

A
  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
Q

What are the three results of complement system activation?

A
  1. Inflammation (mast cells release histamine)
  2. Opsonization
  3. Membrane attack complex (MAC)
40
Q

What is opsonization’s function? How does it work?

A

Facilitates phagocytosis
- coats surface of pathogen with immune proteins (e.g. complement proteins)

41
Q

What is the function of the membrane attack complex?

A

C5-C9 proteins form in pathogen cell membrane
- create holes -> cell lysis

MICR 262 (30 decks)

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