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Immunology Exam One > Innate Immune System > Flashcards

Innate Immune System Flashcards

1
Q

What is the first phase of the immune response?

A

Innate immune system

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2
Q

What are pattern recognition receptors (PRRs)?

A

Receptors of the innate immune system that recognize common molecular patterns on pathogen surface (PAMPs)

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3
Q

What are pathogen associated molecular patterns (PAMPs)?

A

Molecules specifically associated with groups of pathogens (not shared by host cells) that are recognized by cells of the innate immune system

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4
Q

What are the components of the innate immune system?

A

Complement proteins
Professional phagocytes (macrophages, neutrophils)
Natural killer cells
Dendritic cells

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5
Q

What are the major functions of the complement system?

A

Opsonization
Enhances bactericidal actions of phagocytes (complements activities of antibodies)
Kills pathogens (unlike antibodies)-makes MACs

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6
Q

What is the primary source that makes complement proteins?

A

Liver

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7
Q

Where are complement proteins highly concentrated?

A

Blood, tissues

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8
Q

What are the 3 ways to activate the complement system?

A

Alternative pathway
Lectin pathway
Classical pathway (antibody dependent)

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9
Q

What are facts about the alternate pathway?

A
  • Liver is showering the body with the production of complement proteins
  • Certain complement proteins spontaneously activate and attach to surfaces
  • Antibodies are not needed
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10
Q

What is the general order of steps in the alternate pathway?

A

-C3 spontaneously splits into C3a and C3b
-C3b: neutralized or bind to bad guy’s surface (amino or hydroxyl group)
-Complement protein B attaches to C3b
-C3b becomes C3Bb
-Complement protein D changes C3Bb to C3bBb
-C3bBb can split more C3 and C5 = more complement proteins to coat invader
-C3bBb interacts with C5, convertase splits C5 into C5a and C5b
C5b can combine with other complement proteins
-End result = Membrane Attack Complex (MAC), which drills hole in bacteria’s membrane

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11
Q

What are the chemoattractants and what do they do?

A

C3a and C5a

  • Attract macrophages and neutrophils
  • Activate macrophages and neutrophils
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12
Q

What are the three protection proteins?

A
  • MCP
  • DAF (delay accelerating factor)
  • Protectin
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13
Q

What does the protection protein MCP do?

A

Cleaves both C3b and C4b into inactive form

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14
Q

What does DAF (delay accelerating factor) do?

A

accelerates the destruction of convertase (C3bBb)

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15
Q

What does protectin do?

A

Removes MACs before they drill holes

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16
Q

What protein is involved in the Lectin Activation Pathway and what does it do?

A

Mannose-binding lectin protein (MBL)

  • Produced in liver
  • In blood and tissues
  • Activates the complement system by binding MASP (MBL associated serine protein) which clips C3 to make C3b
  • Lectin is a protein that attaches to a carb
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17
Q

What is the classical pathway?

A
  • Antibody dependent
  • Antibody binds to a bacterial surface, its tail (Fc region) provides a platform to activate C1
  • Once antibodies are produced, compliment activation is increased
  • Both compliment and antibodies coate pathogen and enables phagocytes to engulf and destroy
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18
Q

What are the professional phagocytes and what are their 2 main functions?

A
  • Macrophages and Neutrophils
    • Engulf and digest invading microorganisms
    • Induction of inflammatory response
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19
Q

Where are macrophages found?

A

Roam around in tissue

-Under skin, lungs, intestines

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20
Q

Where are neutrophils found?

A

Roam around in blood

21
Q

What are the 3 stages of macrophage readiness?

A

Resting
Activated or primed
Hyperactive

22
Q

What occurs with a resting macrophage?

A
  • Casually eating or snacking
  • Slowly proliferating
  • Express few Class II MHCs
  • Live for months in tissue
  • Circulate in blood, exit and differentiate in tissues to macrophages
23
Q

What occurs with a primed macrophage?

A
  • Eat much more
  • Express more Class II MHCs (function more as an antigen presenting cell)
  • Primed by any chemical signal ex. interferon gamma (IFN y)
  • Can produce complement proteins (C3, factor B, factor D)
24
Q

What occurs in a hyperactive macrophage?

A
  • Recieves a direct signal from a bad guy (LPS, mannose)
  • Stops proliferating
  • Focus all attention on killing
  • Grows larger
  • Increases rate of eating
  • Emits cytokines (TNF)
  • Increased number of lysosomes
  • Increased production of ROS
25
Q

What are the main functions of macrophages?

A

Garbage collector while resting
Antigen presenting cell and killer when activated
Vicious killer when hyperactivated

26
Q

What are the functions of neutrophils?

A

Incredible eaters
Emit harsh chemistry
Send out powerful signal molecules (TNF)

27
Q

What are some facts about neutrophils?

A
  • 20 million in blood
  • Short lived–5 days
  • Can exit blood and become activated in 30 min
  • Travel rapidly in blood
  • Must receive signal that bad guys are present
  • Roll, stop, exit for leaving blood
28
Q

What are the 4 adhesion molecules?

A

SEL (selectin)
SLIG (selectin ligand)
ICAM (intracellular adhesion molecule)
INT (integrin)

29
Q

What is SEL (selectin)?

A
  • Expressed by endothelial cells that line blood vessels after receiving alarm signals
  • Binds to selectin ligan (SLIG)
30
Q

What is SLIG (selectin ligand)?

A

Expressed on surface of neutrophils (at all times)

31
Q

What is ICAM (intracellular adhesion molecule)?

A

-Always expressed on lumen surface of capillary endothelial cells

32
Q

What is INT (integrin)?

A
  • Pre-made and rapidly transported to the surface of the neutrophil after being signaled
  • Strongly binds to ICAM
33
Q

What is the order of events for rolling, stopping, and exiting neutrophils?

A

When macrophages are primed or hyperactivated they express signal molecules
IL-1, TNF
= let neutrophil know bad guy is present
= cause sequence of events to allow neutrophil to exit blood
-Capillary endothelial cells express selectin (SEL), which is stimulated by IL-1 and TNF
-Neutrophil slows to sense this inflammation
-SEL binds to SLIG
-Neutrophil transports integrin (INT) to surface
-Integrin binds to ICAM
-Neutrophil stops
-Neutrophil exits blood and enters tissue (attracted by C5a)

34
Q

Why is the neutrophil cascade failsafe?

A

To safeguard against damage of selectin floods

  • Must have selectin before neutrophils invade
  • Must have integrin released before neutrophils invade
35
Q

Where are most natural killer cells found?

A

blood, liver, spleen

36
Q

What activates natural killer cells?

A

interferon, IL-12, IL-18

37
Q

What are the 2 roles of natural killer cells?

A
  1. Produce cytokines (like T helper cells do)

2. FOrce infected or cancerous cells to commit suicide (can kill like CTLs)

38
Q

What are the 2 ways natural killer cells can induce cell suicide?

A

Perforin/granzyme B

Fas ligand

39
Q

What does perforin/granzyme B do?

A 
Pokes a hold in the membrane like the complement system
Inject enzymes (granzyme B) that cause cell to die (apoptosis)
40
Q

What does the Fas ligand do?

A

Fas ligand on natural killer cell binds to Fas protein on invader
Interaction triggers suicide (apoptosis)
Fas is a transmembrane protein in the TNF family

41
Q

What produces the “Don’t Kill” signal to natural killer cells?

A

Natural killer cell receptors recognizing normal MHC I on target

42
Q

What produces the “Kill” signal to natural killer cells?

A

Activating receptors (Pattern recognition receptors PRRs)

  • Bind to unusual carb or protein on cell’s surface
  • Recognize molecule being produced by virus or cancerous cell
  • Also kills cells not expressing MHC molecules
43
Q

What do IgG3 receptors do?

A
  • Bind Fc region of IgG
  • Ab forms a bridge between target and NK cell
  • Causes NK cell to kill target (antibody-dependent cellular cytotoxicity)
44
Q

Do natural killer cells have T cell receptors?

A

NO

45
Q

What do natural killer cells do at rest?

A

Make some cytokines and can kill

46
Q

What do activated natural killer cells do?

A

Make many more cytokines and are more effective killers

47
Q

What are signals that activate natural killer cells?

A
  • Lack of MHCs
  • LPS
  • Interferon alpha
  • Interferon beta
  • TNF from hyperactivated macrophages upregulates NK cell IL-2 receptors
  • IL-12 from primed or hyperactivated macrophages
48
Q

When are interferons usually given off by cells?

A

When under a viral attack

Immunology Exam One (4 decks)

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