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Immunology -- Jones > Exam 1 --Ch 1 (intro), Ch 2 (Innate system) > Flashcards

Exam 1 --Ch 1 (intro), Ch 2 (Innate system) Flashcards

Ch.1 : What is Immunity? Ch. 2: The Innate System

1
Q

What is hematopoiesis? What does it start with? And what can that become?

A

the formation of new blood cells; starts with Hematopoietic stem cells that can become either a Myeloid Progenerator or a Lymphoid Progenerator

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2
Q

What can a Lymphoid Progenerator become?

A

B cells, T cells, and NK cells, and dendritic cells

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3
Q

What can a Myeloid Progenerator become?

A

Dendritic cells (macrophages, monocytes), Neutrophil, eosinophil, basophil, mast cell, platelets, erythrocyte

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4
Q

What are the three “levels” of protection?

A

physical barrier, innate immunity, adaptive (specific) immunity

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5
Q

What are some physical barriers?

A
  • skin (low pH, high salt)
  • Mucosa and mucus
  • urine and feces
  • saliva
  • tears
  • ciliary escalator
  • normal microbia
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6
Q

What are the Innate System components?

A
  • stuff you are born with!
  • some WBCs (macrophages, neutrophils)
  • Complement System
  • inflammation
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7
Q

What are the two primary cells that are major components of Adaptive Immunity? And what do they do and where do they mature?

A

B cells– when activated produce antibodies (mature in bone marrow)

T cells–helper, killer, regulatory (mature in thymus)

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8
Q

Compare the Innate vs Adaptive Responses:

  1. Response Time
  2. Specificity
  3. Response to repeat infection
  4. Major components
A
  1. Innate: minutes to hours; Adaptive: days
  2. Innate: limited and fixed; Adaptive: highly diverse, adapts to improve during course of response
  3. Innate: same each time; Adaptive: more rapid and effective with each subsequent exposure
  4. Innate: barriers (skin), phagocytes; Adaptive: T and B lymphocytes, antigen-specific receptors, antibodies
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9
Q

What are the key steps of Phagocytosis? (4)

A

Phagocytes migrate to a site of infection and can destroy the infecting bacteria:

  1. chematoxis
  2. adherence
  3. ingestion
  4. digestion
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10
Q

What are the 7 specific steps to Phagocytosis?

A
  1. chemotaxis and adherence of microbe to pahgocyte
  2. ingestion of microbe by phagocyte
  3. formation of a phagosome
  4. fusion of phagosome with a lysosome to form a phagolysosome
  5. digestion of ingested microbe by enzymes
  6. formation of residual body containing indigestible material
  7. discharge of waste materials
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11
Q

Compare antigen vs immunogen

A

Antigen (Ag) = anything that is foreign to the body

Immunogen = something that causes immune response

**all antigens are immunogens, but NOT all immunogens are antigens)

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12
Q

What are the actions of:

  1. T helper cells
  2. T killer cells
  3. T regulatory cells?
A
  1. quarterback–doesn’t kill anything, but regulates system
  2. intracellular pathogens
  3. maintain homeostasis
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13
Q

What is the antigen binding region of the antibody called?

A

Fab

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14
Q

What is the stem region of the antibody called?

A

Fc

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15
Q

What can occur when the immune system doesn’t function correctly?

A
  • overly active or misdirected immune responses
  • immunodeficiency
  • transplantation
  • cancer
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16
Q

What are the primary lymphoid organs?

A

thymus and bone marrow

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17
Q

What are the secondary lymphoid organs?

What occurs there?

A
  • lymph nodes
  • spleen
  • muscosa (ass. lymphoid tissue)
  • other diffuse and loosely organized areas

Areas where lymphocytes encounter antigen

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18
Q

How are secondary lymphoid organs connected?

A

via the blood and lymphatic circulatory systems

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19
Q

What part of the body does the right lymphatic duct drain? What drains the other part of the body then?

A

right side of head, chest, and arm

Thoracic duct drains rest of body

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20
Q

Where are Pattern recognition receptors? What about Pathogen associated molecular patterns?

A

PRR – on WBC

PAMP– on pathogen

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21
Q

What is included in the innate system? (5)

A
  • Existing from birth
  • Complement Proteins
  • Professional Phagocytes
  • Natural Killer Cells
  • Antimicrobial Molecules
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22
Q

What is the complement system?

A

a group of serum proteins made by liver

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23
Q

Once the complement system is activated what are the possible outcomes? (4)

A
  1. membrane lysis
  2. chemotaxis
  3. inflammation
  4. opsonization
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24
Q

What are the 3 activation pathways of the complement system?

A
  1. Classical pathway
  2. Lectin pathway
  3. Alternative pathway
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25
Q

What initiates the classical pathway of the complement system? Then what occurs first?

A

the antibody binding; IgM or IgG binds to a multivalent antigen –> this alllows binding of C1q, C1r, C1s complex

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26
Q

What are the steps of the classical pathway of the complement system?

A
  1. C1 binds antigen-bound antibody
  2. C1 then cleaves C4 into C4a and C4b, followed by C2 into C2a and C2b
  3. C4b2a binds to cell surface C3 convertase is created
  4. C4a and C2b are liberated
  5. C3 convertase cleaves C3 into C3b and C3a, C3a liberated
  6. Some C3b combines with C3 convertase to form C5 convertase (C4b2a3b)
  7. Some C3b opsonizes bacterial cells
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27
Q

What initiates the lectin pathway of the complement system?

A

when soluble proteins recognize microbial antigens

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28
Q

What are the steps of the lectin pathway of the complement system?

A
  1. Lectins bind to microbial surface carbs
  2. Lectins serve as docking site for MBL-ass. serine proteases (MASPs)
  3. MASPs cleave C4 and C2 to form C3 convertase (C4b2a)
  4. some C3b combines with C3 convertase to form C5 convertase (C4b2a3b)
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29
Q

What initiates the alternative pathway of the complement system?

A

several ways; small amounts of C3 are always being cleaved and activated C3b binds to membrane of target cell

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30
Q

What are the steps of the alternative pathway for the complement system?

A
  1. Factor B binds and is cleaved by Factor D
  2. On the membrane is C3 convertase (C3bBb)
  3. C3 convertase is stabilized by Properdin and it cleaves more C3 proteins
  4. Newly activated C3b binds to C3bBb to form C5 convertase (C3bBbC3b)
  5. C5 convertase cleaves many more C5 proteins
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31
Q

When do the three complement pathways converge?

A

at formation of C5 convertase

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32
Q

What does C5 of the complement system initiate? What occurs?

A

generation of Big MAC attack

  • deposition of C5b, C6,C7,C8, and C9 on target cell membrane
  • = a pore structure that disrupts osmotic integrity and cause cell death
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33
Q

What are the C3 convertase combinations for all three pathways of the complement system?

A
  1. Classical – C4b2a
  2. Lectin – C4b2a
  3. Alternative – C3bBb
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34
Q

What are the C5 convertase combinations for all three pathways of the complement system?

A
  1. Classical – C4b2a3b
  2. Lectin – C4b2a3b
  3. C3BbC3b
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35
Q

What type of receptors are on leukocytes and erythrocytes that allow for opsonization?

A

C3b receptors (CR1)

36
Q

What do the C3a and C5a what were released from the complement system do?

A

bind with C3aR/C5aR on granulocytes

37
Q

What occurs when C3a and C5a bind to C3aR and C5aR (receptors) on granulocytes?

A

stimulates release of proinflammatory mediators from basophils, eosinophils, and neutrophils

38
Q

How is the complement system regulated at the C3 convertase level?

A

Decay-accelerating factors promote decay of C3 convertase (so don’t kill host cell)

39
Q

What are two ways we regulate the complement system?

A
  1. Decay-accelerating factors to decay C3 convertase

2. Protectin to inhibit the MAC attack

40
Q

How is the complement system regulated at the MAC attack level? What inhibits it? By binding what?

A

Protectin inhibits the MAC attack

  • binds C5b678 complexes deposited on host cell
  • prevents insertion into plasma membrane
  • blocks C9 recruitment, preventing MAC formation
41
Q

What will antibody depletion by a bacteria do to the complement system?

A

inferfer with antibody-compliment interaction —> therefore inhibit Classical pathway

42
Q

What occurs if a bacteria binds and inactivate the C3bBb C3 convertase?

A

it inhibits the Alternative pathway and C3 convertase cannot cleave any C3 proteins, therefore not forming any C5 proteins

43
Q

What occurs if C4a is degraded by a bacteria?

A

decreases proinflammatory response b/c C5a cannot bind to C5aR on granulocytes and stimulate this

44
Q

What occurs if a bacteria accelerates the decay of C3 convertase bound to bacterial surfaces?

A

it is using our inhibitory system against us

45
Q

What are professional phagocytes?

A

part of innate immune system

  • Fxn = eat stuff
  • Most important = macrophages and neutrophils
46
Q

Where are macrophages found?

A

all over the place (skin, lungs, GI, spleen, etc.), in tissues

47
Q

What are the three stage of readiness of macrophages?

A
  1. Resting
  2. Activated or Primed
  3. Hyperactive
48
Q

What does a resting macrophage do? How fast divide? What do they express? How long do they live?

A
  • basic clean up of dead cells
  • slowly proliferating
  • express few Class II MCHs
  • live for months in tissue
49
Q

When does a macrophage become Primed/activated?

A

after receiving a signal from other cells that pathogens are present
- such as interferon gamma (IFN-gama)

50
Q

What occurs when a macrophage is Primed?

A
  • phagocytosis enhanced
  • Express more Class II MHCs
  • –fxn much more as an antigen presenting cell
  • –work much more with Helper T cells
51
Q

How does a macrophage become hyperactive?

A

after receiving a DIRECT signal from pathogens

52
Q

What does a hyperactive macrophage do?

A
  • stop proliferating
  • excellent Ag presentation (increase levels of MHC II)
  • enhanced phagocytosis
  • releases cytokines (TNF)
  • increase production of ROS
53
Q

What does a macrophage have on its surface that allows recognition of a pathogen?

A

PRRs = Pathogen Recognition Receptors; which bind to antigen on pathogen called a PAMP

54
Q

What are examples of what a PRR (pathogen recognition receptors) may recognize?

A
  • LPS from bacterial cell wall

- Mannose from a bacterial cell wall

55
Q

T/F. When a macrophage is hyperactive it decreases the amount of lysosomes.

A

False, it increases the amount of lysosomes to “digest” the bacteria

56
Q

Simply, what do macrophages do in these stages:

  1. Resting
  2. Primed/Activated
  3. Hyperactive
A
  1. garbage collector
  2. antigen presenting cell and killer
  3. vicious killer
57
Q

Where are neutrophils located? About how many are there?

A

blood; but can exit when activated; ~20 billion

58
Q

T/F. Neutorphils, just like macrophages, present with MHC II.

A

False. Neutrophils DO NOT present antigens like MHC II

59
Q

How long to neutrophils live?

A

short lives (5 days)

60
Q

What are three things neutorphils are?

A
  1. very phagocytic
  2. release harsh chemistry
  3. send out powerful signaling molecules including cytokines
61
Q

What is a neutrophils strategy for leaving the blood?

A

must receive a signal; Roll, stop, exit

62
Q

What adhesion molecules are always found on neutrophils?

A

SLIG (selectin ligand)

63
Q

What is SLIG (selectin ligand)?

A

expressed on surface of neutrophils

64
Q

What is SEL (selectin)? What does it bind to?

A

expressed by endothelial cells thatht line blood vessels AFTER receiving alarm signal
- bind to selectin ligand (SLIG) on neutrophil

65
Q

What is ICAM? What does it bind to?

A

= intercellular adhesion molecule

  • expressed on lumen surface of capillary endothelial cells all the time
  • bind to INT (integrin) on neutrophils
66
Q

What is INT (integrin)? What does it bind?

A
  • pre-made and rapidly transported to surface of neutrophil AFTER being signaled
  • strongly binds to ICAM on epithelial cells
67
Q

What are the ligand pairs important for a neutrophil to exit the endothelium lining of capillary beds?

A

SEL (selectin) binds to selectin ligand (SLIG) on neutrophil

INT (integrin) binds to ICAM (intercellular adhesion molecule) on endothelial cells

68
Q

How do macorphages help the process of neutrophils leaving the lumen?

A

-when macrophages are Primed, they express signal molecules (IL-1 and TNF)

69
Q

What does the signal molecules IL-1 and TNF expressed from macrophages cause?

A

lets neutrophils know pathogen is present

- cause sequence of events to allow neutrophil to exit blood

70
Q

What do IL-1 and TNF expressed by macrophages activate on the endothelial cells?

A

causes endothelial cells to express selectin (SEL) that will bind SLIG on neutrophil = Rolling

71
Q

What is transported to a neutrophils surface that will bind to ICAM on endothelial cell? And what does this cause?

A

neutorphil presents integrin (INT) to surface and binds to ICAM and STOPS/Arrests

72
Q

The rolling of the neutrophil is caused by what?

A

endothelial cells expresses selectin (SEL) and bind SLIG (selectin ligand) that is always on neutrophil

73
Q

The arrest/stop of the neutrophil is caused by what?

A

neutorphil expresses integrin (INT) to surface and binds to ICAM (intercellular adhesion molecule) that is always on endothelial cells

74
Q

What causes neutrophils to exit the blood and enter the tissue?

A

due to chemoattractants being released; like C5a and bacterial fragments (f-met)

75
Q

What amino acid do all bacterial proteins begin with? why is this important?

A

f-met; when macrophages ingest bacteria they release f-met peptides and attract other (like neutorophils)

76
Q

Explain how the Neutrophil leaving the blood into tissue is “Failsafe”.

A

multiple steps are involved

  • endothelial cells express ICAM all the time
  • neutrophils express SLIG all the time
  • must have SEL expressed on endothelials cells before neurtophils invade
  • must have INT expressed on neutrophils before neutrophils invade
77
Q

Where are Natural Killer cells found? How long do they live? Rate of proliferation?

A

blood, liver, spleen; short-lived (1 week); proliferate rapidly

78
Q

T/F. Natural Killer cells have the same strategy as neutrophils for leaving blood, roll, stop, exit.

A

True

79
Q

What are the two roles of Natural Killer cells?

A
  1. give off cytokines

2. force cells to commit suicide (apoptosis)

80
Q

What are two ways that NK cells kill?

A
  1. Perforin

2. Fas ligand

81
Q

How does a NK cell use Perforin to kill?

A
  • pokes a hole in membrane

- inject enzymes that cause cell to die (apoptosis)

82
Q

How does a NK cell use its Fas ligand to kill?

A

Fas Ligand on NK cell binds to Fas protein (transmembrane protien of TNF family) on target cell
–this interaction triggers suicide (apoptosis)

83
Q

How do NK cells know who to kill?

A
  • if target host cell has MHC I receptors = DON’T KILL signal
  • unusal carbs or protein on cell = KILL signal
  • also KILL cells not expressing MHC molecules
84
Q

What are some things that activate a NK cell?

A
  • lack of MHC
  • Unusual surface molecule on cells
  • LPS (in bacterial cell walls)
  • interferon alpha (INF-alpha)
  • interferon beta (INF-beta)
85
Q

What do we have at epithelial surfaces that are apart of our innate immune system?

A

antimicrobial molecules (proteins and peptides)

86
Q

What are the four main aspects of our innate immune system?

A
  • complement proteins
  • professional phagocytes (macrophages and neutrophils)
  • natural killer cells
  • antimicrobial molecules

Immunology -- Jones (14 decks)

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