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Anatomy and Physiology 2 > Week 2: The Immune System > Flashcards

Week 2: The Immune System Flashcards

To learn all the concepts and facts from the lectures, learning materials and textbook chapter for this unit

1
Q

What is the innate (nonspecific) defense system?

A
  • Always prepared
  • Responds within minutes to protect the body from foreign substances
  • Two barricades: the first line of defense = intact skin and mucosae, the second line of defense = called into action when first line has been penetrated, relies on internal defenses such as antimicrobial proteins, phagocytes and other cells to inihibit the invaders’ spread throughout the body. The hallmark of this system is inflammation.
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2
Q

What is the adaptive (specific) defense system?

A

Functions to attack identified substances.

Provides the body’s third line of defense, takes considerably longer to mount than the innate defense response.

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3
Q

Do the innate and adaptive defense systems always work hand in hand?

A

Yes.

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4
Q

Is the immune system a functional system rather than an organ system in the anatomical sense?

A

Yes.

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5
Q

What are the structures of the immune system?

A

A diverse array of of molecules plus trillions of immune cells (especially lymphocytes), that inhabit lymphoid tissues and circulate in body fluids

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6
Q

How are the innate and adaptive defense systems intertwined?

A
  • The innate and adaptive systems release and recognise (bind to) many of the same defensive molecules.
  • The innate responses are not as nonspecific as once thought, they have specific pathways to target foreign substances.
  • Proteins released during innate responses alert cells of the adaptive system to the presence of specific foreign molecules in the body.
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7
Q

When is the immune system operating effectively?

A

When it protects the body from most infectious microorganisms, cancer cells, and unfortunately transplanted organs and grafts. It does this both directly, by cell attack. and indirectly, by releasing mobilizing chemicals and protective antibody molecules.

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8
Q

Innate defenses

A

We become fully equipped with innate defenses such as the mechanical barriers that cover body surfaces and cells and chemicals that act on the initial internal battlefronts, that are ready to ward of pathogens.

Many times our innate defenses ward off infection, and in other cases adaptive immune system is called into action to reinforce and enhance the innate defenses. Either way the innate defenses reduce the workload of the adaptive system by preventing the entry and spread of microorganisms in the body.

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9
Q

Is the body’s first line of defense highly effective? Why?

A

Yes. A formidable physical barrier, and keratin in resistant to most weak acids and bases and to bacterial enzymes and toxins. Intact mucosae provide similar mechanical barriers within the body.

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10
Q

What do mucous membranes line?

A

The digestive, respiratory, urinary and reproductive tracts.

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11
Q

What does the acid mantle of the skin do?

A

Skin secretions (sweat and sebum) that make epidermal surface acidic, which inhibits bacterial growth; also contain various bactericidal chemicals.

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12
Q

What does keratin do?

A

Provides resistance against acids, alkalis, and bacterial enzymes.

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13
Q

What does mucus do?

A

Traps microorganisms in respiratory and digestive tracts.

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14
Q

What do nasal hairs do?

A

Filter and trap microorganisms in nasal passages.

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15
Q

What do cilia do?

A

Propel debris-laden mucus away from the nasal cavity and lower respiratory passages.

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16
Q

What does gastric juice do?

A

Contains concentrated hydrochloric acid and protein-digesting enzymes that destroy pathogens in stomach.

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17
Q

What does the acid mantle of the vagina do?

A

Inhibits growth of the most bacteria and fungi in the female reproductive tract.

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18
Q

What does lacrimal secretion (tears) and saliva do?

A

Continuously lubricate and cleanse eyes (tears) and oral cavity (saliva); contain lysozome, an enzyme that destroy microorganisms.

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19
Q

What does urine do?

A

Normally acid pH inhibits bacterial growth; cleanse the lower urinary tract as if flushes from the body.

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20
Q

What does acid do?

A

The acidity of skin, vaginal and stomach secretion - the acid mantle - inhibit bacterial growth.

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21
Q

What do enzymes do?

A

Lysozome - found in saliva, respiratory mucus and lacrimal fluid of the eye, destroys bacteria. Protein-digesting enzymes in the stomach kill many different microorganisms.

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22
Q

What does mucin do?

A

Dissolved in water forms thick, sticky mucus that lines the digestive and respiratory passageways. This mucus traps many microorganisms. Likewise the music in watery saliva traps microorganisms and washes them out of the mouth into the stomach where they are digested.

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23
Q

What do defensins do?

A

Mucous membranes and skin secrete small amounts of broad spectrum antimicrobial peptides called defensins. Defensin output increases dramatically in response to inflammation when surface barriers are breached. Using various mechanisms, such as disruption of microbial membranes, defensins help to control bacterial and fungal colonisation of exposed areas.

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24
Q

What are other chemicals that keep invaders out of the body, besides, acids, enzymes, mucin and defensins?

A

In skin, some lipids in sebum and dermcidin in eccrine sweat are toxic to bacteria.

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25
Q

What happens when every day knicks and cuts happen (e.g. from brushing teeth and shaving)?

A

The internal innate defenses (the second line of defense) come into play.

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26
Q

What do pattern recognition receptors do?

A

Identify potentially harmful substances by recognising (binding to) molecules with specific shapes that are part of infections organisms (bacteria, viruses, fungi, and various parasites), but not normal human cells.

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27
Q

What do toll-like receptors, a class of pattern recognition censors, do? Give two examples.

A
  • They play a central role in triggering immune responses
  • There are 11 types of human TLRs, each recognising a particular class of attacking microbe.
  • One type responds to a glycolipid in cell walls of the tuberculosis bacterium, and another to a component of gram-negative bacteria such as Salmonella.
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28
Q

Do macrophages have TLRs?

A

Yes.

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29
Q

Do epithelial cells lining the respiratory and gastrointestinal tract have TLRs?

A

Yes.

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30
Q

What do pattern recognition receptors allow cells to do?

A

They allow cells to recognise invaders and sound a chemical “alarm” that initiates inflammation.

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31
Q

What do phagocytes do?

A

Confront pathogens that get through the skin or mucosae into the underlying connective tissue.

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32
Q

When do neutrophils, the most abundant type of white blood cell, become phagocytic?

A

On encountering infectious material in the tissues.

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33
Q

Are macrophages the most voracious phagocytes?

A

Yes.

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34
Q

Where do macrophages derive from?

A

White blood cells called monocytes, that leave the blood stream, enter the tissues and develop into macrophages.

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35
Q

What do free macrophages do?

A

Wander throughout the tissue spaces in search of cellular debris or “foreign” invaders.

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36
Q

What do fixed macrophages do?

A

Stellate macrophages in the liver, are permanent residents of particular organs.

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37
Q

How do phagocytes engulf particle matter?

A

The receptors on its flowing cytoplasmic extensions bind to the particle. The particle is then pulled inside, enclosed within a membrane-lined vesicle. The resulting phagosome then fuses with a lysosome to form a phagolysosome.

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38
Q

What are the five events/steps of phagocytosis?

A
  1. phagocyte adheres to pathogens or debris using receptors.
  2. phagocyte forms pseudopods that eventually engulf the particles, forming a phagosome.
  3. Lysosome fuses with the phagocytic vesicle, forming a phagolysosome
  4. Toxic compounds and lysosomal enzymes destroy pathogens
  5. Sometimes exocytosis of the vesicle removes indigestible residual material.
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39
Q

How do neutrophils and macrophages generally kill ingested prey?

A

By acidifying the phagolysosome and digesting its contents with lysosomal enzymes.

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40
Q

Some pathogens such as tuberculosis bacillus and certain parasites resistant to lysosomal enzymes and even multiply within the phagolysosome. What happens then?

A

Helped T cells release chemicals that stimulate the macrophage, this activates additional enzymes that produce a lethal respiratory burst.

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41
Q

How does the respiratory burst promote killing of pathogens?

A
  • Liberates a deluge of highly destructive free radicals.
  • Produces oxidizing chemicals (hydrogen peroxide and a substance identical to household bleach)
  • Increases the phagolysosome’s pH and osmolarity, which activates other protein-digesting enzymes that digest the invader.
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42
Q

Do neutrophils also pierce the pathogen’s membrane by using defensins?

A

Yes.

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43
Q

In order to ingest a pathogen, must a phagocyte first adhere to that pathogen, a feat made possible by recognizing the pathogen’s carbohydrate “signature”?

A

Yes.

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44
Q

Do some bacteria have external capsules that conceal their carbohydrate signature, allowing them to evade capture because phagocytes can’t bind to them?

A

Yes.

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45
Q

How do out immune systems get around disguised carbohydrate signatures?

A

They coat pathogens with opsonins.

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46
Q

What are opsonins?

A

Opsonins are complement proteins or antibodies. Both provide handles to which phagocyte receptors can bind. Any pathogen can be coated with opsonins, a process called opsonisation, which greatly accelerates phagocytosis of that pathogen.

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47
Q

When phagocytes are unable to digest their targets (e.g. because of size), what can they do?

A

They can release toxic chemicals into the extracellular fluid. Whether killing ingested or extracellular targets, neutrophils rapidly kill themselves in the process. In contrast, macrophages are more robust and can survive to kill another day.

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48
Q

What do Natural Killer (NK) Cells do?

A

Police the body in blood and lymph, are a unique group of defensive cells that can kill cancer cells and virus-infected body cells before the adaptive immune system is activated.

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49
Q

What group are NK cells a part of?

A

A small group of large granular lymphocytes.

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50
Q

Can NK cells eliminate a variety of infected of cancerous cells by detecting general abnormalities such as the lack of “self” cell-surface proteins called MHC?

A

Yes.

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51
Q

Does the name “natural” killer cells reflect the nonspecificity of natural killer cells?

A

Yes.

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52
Q

Are NK cells phagocytic?

A

No.

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53
Q

How do NK cells kill?

A

By directly contacting the target cell, inducing it to undergo apoptosis (programmed cell death).

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54
Q

How do cytotoxic T cells kill?

A

By directly contacting the target cell, inducing it to undergo apoptosis (programmed cell death).

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55
Q

Do NK cells secrete potent chemicals that enhance the inflammatory response?

A

Yes.

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56
Q

What is inflammation?

A

A nonspecific response to any tissue injury.

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57
Q

What are causes of inflammation?

A

Physical trauma, intense heat, irritating chemicals or infection.

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58
Q

What are the several beneficial effects of inflammation?

A
  • Prevents the spread of damaging agents to nearby tissues.
  • It disposes of cell debris and pathogens.
  • It alerts the adaptive immune system.
  • It sets the stage for repair.
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59
Q

What are the for cardinal signs (distinguishing indicators) of acute (short term) inflammation?

A

Redness, heat, swelling and pain.

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60
Q

Do some authorities consider impaired function to be a fifth cardinal sign of inflammation?

A

Yes.

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61
Q

Does the inflammatory process begin with a chemical alarm - a flood of inflammatory chemicals released into the extracellular fluid?

A

Yes.

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62
Q

Are inflammatory chemicals released by injured or stressed tissue cells, and immune cells?

A

Yes.

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63
Q

What do mast cells do?

A

Release the potent inflammatory chemical histamine.

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64
Q

Can inflammatory chemicals also be formed by chemicals circulating in the blood?

A

Yes.

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65
Q

What do other inflammatory chemicals include?

A

Kinins, prostaglandins and cytokines.

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66
Q

If pathogens provoked the inflammation, o a group of plasma proteins known as complement activate to form potent inflammatory chemicals?

A

Yes.

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67
Q

Do all inflammatory chemicals dilate local arterioles and make local capillaries leakier?

A

Yes.

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68
Q

Do inflammatory chemicals attract phagocytes to the injured area?

A

Yes.

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69
Q

Do some inflammatory chemicals have individual inflammatory roles, such as mobilising lymphocytes and other elements of adaptive immunity?

A

Yes.

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70
Q

Histamine: Source

A

Granules of mast cells and basophils.

Released in response to mechanical injury, presence of certain microorganisms, and chemicals released by neutrophils.

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71
Q

Histamine: Physiological effects.

A

Promotes vasodilation of local arterioles, increasing blood flow to injured area. Increases permeability of local capillaries, promoting formation of exudate.

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72
Q

Kinins (bradykinin and others): Source

A

A plasma protein, kininogen, is split by the enzyme kallikrein found in plasma, urine, saliva and in lysosomes of neutrophils and other types of cells. Splitting releases active kinin peptides.

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73
Q

Kinins (bradykinin and others): Physiological effects

A

Same as for histamine. Also induce chemotaxis of leukocytes and prompts neutrophils to release lysosomal enzymes, thereby enhancing generation of more kinins. Induce pain.

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74
Q

Prostaglandins: Source

A

Fatty acid molecules produced from arachidonic acid found in all cell membranes; generated by enzymes of neutrophils, basophils, mast cells, and others.

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75
Q

Prostaglandins: Physiological effects

A

Same as for histamine. Also induce neutrophil chemotaxis. Induce pain. (Some prostaglandins are inflammatory).

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76
Q

What does vasodilation of local arterioles cause?

A

Hyperemia (increased blood flow)

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77
Q

Does hyperemia bring bring more cells and chemicals of the immune system to the injured area?

A

Yes.

78
Q

What does hyperemia account for?

A

Two of the cardinal signs of inflammation: the redness and heat of an inflamed region.

79
Q

Do inflammatory chemicals also increase the permeability of local capillaries and vessels? Does exudate - fluid containing clotting factors and antibodies - seep from the blood into the tissue spaces?

A

Yes.

80
Q

Does the influx of protein-rich fluids into the tissue spaces sweep foreign material into the lymphatic vessels so it can
be processed by the lymph nodes?

A

Yes.

81
Q

Does the influx of protein-rich fluids into the tissue spaces also deliver important proteins such as complement and clotting fluid to the interstitial fluid?

A

Yes.

82
Q

Do the clotting factors, as a result of the influx of protein-rich fluids into the tissue spaces, form a gel-like fibrin mesh that acts as a scaffold for permanent repair?

A

Yes.

83
Q

“Do the clotting factors, as a result of the influx of protein-rich fluids into the tissue spaces, form a gel-like fibrin mesh that acts as a scaffold for permanent repair?” Does this mesh also isolate the injured area by preventing bacteria and other harmful agents from spreading?

A

Yes.

84
Q

Is walling of the injured area such an important defense strategy that some bacteria (such as Streptococcus) have evolved enzymes that break down the clot, allowing them to invade surrounding tissues?

A

Yes.

85
Q

Does the increased tissue fluid cause local swelling (edema) that presses on adjacent nerve endings contributing to the sensation of pain?

A

Yes.

86
Q

Does pain also result from the release of bacterial toxins, and sensitizing effects of released prostaglandins and kinin?

A

Yes.

87
Q

How do aspirin and some other anti-inflammatory drugs reduce pain?

A

They inhibit prostaglandin synthesis.

88
Q

What are the four steps in which phagocytes are mobilized to infiltrate the injured site?

A
  1. Leukocytosis
  2. Margination
  3. Diapedesis
  4. Chemotaxis
89
Q

Describe Leukocytosis.

A

Injured cells release chemicals called leukocytosis-inducing factors. In response, neutrophils enter blood from red bone marrow and within a few hours, the number of neutrophils in blood increases four to five-fold. This leukocytosis, the increase in white blood cells, is characteristic of inflammation.

90
Q

Describe margination.

A

Refers to the phenomenon of phagocytes clinging to the inner walls (margins) of capillaries and post capillary venules. Inflamed endothelial cells spout cell adhesion molecules that signal “this is the place”. As neutrophils encounter CAMs, they bind briefly. This causes them to close and roll along the inner surface of the blood vessel so they can be activated by inflammatory chemicals. Once activated, neutrophils spout additional CAMs on their own plasma membranes. This allows the neutrophils to bind to endothelial cells tightly, creating an initial foothold.

91
Q

Describe diapedesis.

A

Continued chemical signalling prompts the neutrophils to flatten and squeeze between the endothelial cells tightly, creating an initial foothold.

92
Q

Describe chemotaxis.

A

Inflammatory chemicals act as homing devices, or more precisely, chemotactic agents. Neutrophils and other WBCs migrate up the gradient of chemotactic agents to the site of injury. Within an hour after the inflammatory response has begun, neutrophils have collected at the site are devouring any foreign materials present.

93
Q

As the body’s counterattack continues, do monocytes follow neutrophils into the injured area?

A

Yes.

94
Q

Are monocytes fairly poor phagocytes, but within 12 hours of leaving the blood and entering the tissues, do they swell and develop large numbers of lysosomes, becoming macrophages with insatiable appetites? Do these late arriving macrophages replace the neutrophils on the battlefield?

A

Yes. Yes.

95
Q

Are macrophages central actors in the final disposal of cell debris as acute inflammation subsides, and do they predominate all sites of chronic inflammation?

A

Yes.

96
Q

Is the ultimate goal of the inflammatory response to clear the injured area of pathogens? Once this is accomplished does healing usually occur quickly?

A

Yes. Yes.

97
Q

Do a variety of antimicrobial proteins enhance our innate defenses by attacking microorganisms directly or by hindering their ability to reproduce?

A

Yes.

98
Q

Are the most important antimicrobial proteins interferons and complement proteins?

A

Yes.

99
Q

Can viruses generate ATP or synthesise proteins?

A

No.

100
Q

How do viruses do their dirty work in the body?

A

By invading tissue cells and taking over the cellular metabolic machinery to reproduce themselves

101
Q

Can some infected cells secrete small proteins called interferons (IFNs) to protect cells that have not yet been infected?

A

Yes.

102
Q

Can IFNs diffuse to nearby cells, which they stimulate to synthesize proteins that block further protein synthesis and degrade viral RNA? In this way, do they interfere with viral replication?

A

Yes. Yes.

103
Q

Because IFN protection is not virus specific, can IFNs produced against a particular virus protect against other viruses too?

A

Yes.

104
Q

Are the IFNs a family of immune modulating proteins produced by a variety of body cells, each having a slight physiological effect? Do IFN alpha and IFN beta have these antiviral effects and activate NK cells?

A

Yes. Yes.

105
Q

Does another interferon, IFN gamma, or immune interferon, secreted by lymphocytes and have widespread immune mobilizing effects, such as activating macrophages?

A

Yes.

106
Q

Because both macrophages and NK cells can also directly act against cancerous cells, do the interferons have a direct role in fighting cancer?

A

Yes.

107
Q

Are IFNs used to treat several disorders including hepatitis C, genital warts, and multiple sclerosis?

A

Yes.

108
Q

What does the term complement system refer to?

A

A group of at least 20 plasma proteins that normally circulate in the blood in an inactive state.

109
Q

What do the 20 plasma proteins in the complement system include?

A

C1 through C9 plus several others that act as regulatory proteins and other factors.

110
Q

Does complement provide a major mechanism for destroying foreign substances in the body?

A

Yes.

111
Q

Does the activation of complement also unleash inflammatory chemicals that amplify virtually all aspects of the inflammatory process?

A

Yes.

112
Q

Does activated complement also lyse and kill certain bacteria and other cell types?

A

Yes.

113
Q

Although complement is a nonspecific defense system, does it complement (enhance) the effectiveness of both innate and adaptive defenses?

A

Yes.

114
Q

What are the three pathways by which complement can be activated?

A

The classical pathway
The lectin pathway
The alternative pathway

115
Q

What does the membrane attack complex (MAC) do?

A

Forms and stabilises a hole in the membrane that allows a massive influx of water, lysing the target cell.

116
Q

Does cell lysis begin when C3b binds to the target cell’s surface and triggers the insertion of a group of complement proteins?

A

Yes.

117
Q

Do the C3b molecules also act as opsonins?

A

Yes.

118
Q

What do opsonins do?

A

Coat the microorganism, providing handles that receptors on macrophages and neutrophils can adhere to. This allows them to engulf particles more rapidly.

119
Q

What do C3a and other molecules formed during complement activation do?

A

They amplify the inflammatory response by stimulating mast cells and basophils to release histamine and by attracting neutrophils and other inflammatory cells to the area.

120
Q

What is fever?

A

An abnormally high body temperature, a systemic response to invading microorganisms.

121
Q

When leukocytes and macrophages are exposed to foreign substances in the body what chemicals do they release?

A

Pyrogens.

122
Q

What do pyrogens do?

A

They act on the body’s themostat - a cluster of neurons in the hypothalamus - raising the body’s temperature above normal (37 degrees celsius)

123
Q

What does fever do?

A

It causes the liver and spleen to sequester iron and zinc, which may make them less available to support bacterial growth. Additionally, fever increases the metabolic rate of tissue cells, and may speed up repair processes.

124
Q

What does our adaptive immune system do?

A

It stalks and eliminates with nearly equal precision any type of pathogen that intrudes into the body, and is the third line of defense.

125
Q

When it operates effectively what does the adaptive immune system do?

A

It protects us from a wide variety of infectious agents as well as abnormal body cells.

126
Q

Do devastating diseases such as cancer and AIDS result when the adaptive immune system is disabled or fails?

A

Yes.

127
Q

Does the activation of the adaptive immune system tremendously amplify the inflammatory response, and is it responsible for most complement activation?

A

Yes.

128
Q

Must the adaptive system meet or be primed by an initial exposure to a foreign specific substance (antigen) before it can protect the body against that substance, and does this priming take precious time?

A

Yes.

129
Q

What are the four key characteristics that set the adaptive immune system apart from the innate defenses?

A
  1. It involves lymphocytes called B and T Lymphocytes
  2. It is specific
  3. It is systemic
  4. It has “memory”
130
Q

What are antigens?

A

Antigens are substances that can mobilise the adaptive defenses. They are the ultimate targets of all adaptive immune responses.

131
Q

What is the word “antigen” a contraction of?

A

Antigen generating

132
Q

Are most antigens large, complex molecules that are foreign, and consequently nonself?

A

Yes.

133
Q

Can antigens be complete or incomplete?

A

Yes.

134
Q

What two important functional properties do complete antigens have?

A

Immunogenicity

Reactivity

135
Q

What is immunogenicity?

A

The ability to stimulate specific lymphocytes to proliferate (multiply)

136
Q

What is reactivity?

A

the ability to react with the activated lymphocytes and the antibodies released by immunogenic reactions.

137
Q

What is a hapten or incomplete antigen?

A

A hapten or incomplete antigen is when small molecules – peptides, nucleotides and many hormones are not immunogenic, and link up with the body’s own proteins.

138
Q

Unless attached to protein carriers do haptens have reactivity but not immunogenicity?

A

Yes.

139
Q

Besides certain drugs what other places can chemicals that act as haptens be found?

A

Poison ivy, animal dander, detergents, cosmetics and a number of common household and commercial products.

140
Q

Does the ability of a molecule to act as an antigen depend on both its size and its complexity?

A

Yes.

141
Q

Are only certain parts of the antigen, called antigenic determinants, immunogenic?

A

Yes.

142
Q

“Are only certain parts of the antigen, called antigenic determinants, immunogenic?” Do antibodies or lymphocyte receptors bind to these antigenic determinants in much the same manner that an enzyme binds to a substrate?

A

Yes.

143
Q

Why are large simple plastic molecules, which have no immunogenicity, used to make artificial implants?

A

Because the substances are not seen as foreign and rejected by the body.

144
Q

Assuming your immune system has been properly “programmed”, are your self-antigens not foreign or antigenic to you, but are strongly antigenic to other individuals?

A

Yes.

145
Q

Among the cell surface proteins that identify a cell as self is there a group of glycoproteins called MHC proteins?

A

Yes.

146
Q

“Among the cell surface proteins that identify a cell as self is there a group of glycoproteins called MHC proteins?” Do genes of the major histocompatibility complex (MHC) code for these proteins?

A

Yes.

147
Q

Does each MHC protein have a deep groove that holds a peptide, either a self-antigen or a foreign antigen?

A

Yes.

148
Q

Can T Lymphocytes only bind antigens that are presented on MHC proteins?

A

Yes.

149
Q

Do B Lymphocytes oversee humoral immunity?

A

Yes.

150
Q

Are T Lymphocytes non antibody producing lymphocytes that constitute the cellular arm of adaptive immunity?

A

Yes.

151
Q

Do APCs not respond to specific antigens as lymphocytes do? Do they instead play essential auxiliary roles?

A

Yes.

152
Q

Can T cells not recognise their antigens without APCs?

A

Yes.

153
Q

What are the five general steps of lymphocyte development, maturation and activation?

A
  1. Origin
  2. Maturation: immunocompetence and self-tolerance
  3. Seeding secondary lymphoid organs and circulation
  4. Antigen encounter and activation
  5. Proliferation and differentiation
154
Q

What do antigen presenting cells (APCs) do?

A

Engulf antigens and then present fragments of them, like signal flags on their own surfaces where T cells can recognise them.

155
Q

The major types of cells presenting as antigen presenting cells are:

A

dendritic cells, macrophages and B lymphocytes.

156
Q

Where are dendritic cells found?

A

At the body’s frontiers (skin for example) where they act as mobile sentinels.

157
Q

Is migration of dendritic cells to secondary lymphoid organs now recognised as the most important way of ensuring lymphocytes encounter invading antigens?

A

Yes. This early alert spares the body a good deal of tissue damage that might otherwise occur.

158
Q

Are macrophages widely distributed throughout the lymphoid organs and connective tissues?

A

Yes.

159
Q

Do macrophages present antigens to T cells for different reasons to dendritic cells? What are these reasons?

A

Yes. to maintain T cell activation or be activated themselves.

160
Q

Do certain effector T cells release chemicals that prod macrophages to become activated macrophages?

A

Yes.

161
Q

Are activated macrophages true “killers” - insatiable phagocytes that also trigger powerful inflammatory responses and recruit additional defenses?

A

Yes.

162
Q

Do B cells activate naive T cells?

A

No.

163
Q

Do B cells present antigens to a certain kind of T cell (a helper T cell) in order to obtain help in their own activation?

A

Yes.

164
Q

Does the two-fisted adaptive immune system use lymphocytes, APCs and specific molecules to identify and destroy all substances - both living and nonliving - that are in the body but not recognised as self?

A

Yes.

165
Q

Does the immune system’s response to threats depend on its ability to 1) recognise antigens by binding to them and 2) communicate with one another so that the whole system mounts a response specific to those antigens?

A

Yes.

166
Q

List the characteristics of B lymphocytes compared to T lymphocytes:

A 
B lymphocytes:
Humoral immune response
Antibody secretion
Primary targets are extracellular pathogens (e.g., bacteria, fungi, parasites and some viruses in extracellular fluid)
Site of origin: red bone marrow
Site of maturation: red bone marrow
Effector cells: plasma cells
Memory cell formation: yes
T lymphocytes:
Cellular immune response
No antibody secretion
Primary targets: intracellular pathogens (e.g. virus-infected cells) and cancer cells
Site of origin: red bone marrow
Site of maturation: thymus
Effector cells: Cytotoxic cells, Helper cells, Regulatory cells
Memory cell formation: yes.
167
Q

When a B cell encounters its antigen does that entigen provoke the humoral immune response, in which antibodies specific for that antigen are made?

A

Yes.

168
Q

Is an immunocompetent but naive B lymphocyte activated when matching antigens bind to surface receptors and cross-linked adjacent receptors are bound together?

A

Yes.

169
Q

Is antigen binding quickly followed by receptor mediated endocytosis of the cross-linked antigen-reception complexes?

A

Yes.

170
Q

“Is antigen binding quickly followed by receptor mediated endocytosis of the cross-linked antigen-reception complexes?” Is this called clonal selection, and is it followed by proliferation and differentiation into effector cells?

A

Yes.

171
Q

Do most cells of the clone differentiate into plasma cells, the antibody secreting effector cells of the humoral response?

A

Yes.

172
Q

What do clone cells that do not become plasma cells turn into?

A

Long-lived memory cells.

173
Q

What can memory-cells do?

A

They can mount an almost immediate humoral response if they encounter the same antigen again in the future.

174
Q

What constitutes the primary immune response?

A

Cellular proliferation and differentiation constitutes the primary immune response, which occurs on first exposure to a particular antigen.

175
Q

How long does the primary response typically last?

A

It typically lasts for a period of 3 to 6 days after the antigen encounter.

176
Q

“It typically lasts for a period of 3 to 6 days after the antigen encounter.” What does this lag period reflect?

A

It reflects the time required for the few B cells specific for the antigen to proliferate and for their offspring to differentiate into plasma cells.

177
Q

After the mobilisation period, do plasma antibody levels rise, and reach peak level in about 10 days, and then decline?

A

Yes.

178
Q

If and when someone is reexposed to the same antigen, whether its the second or twenty-second time, does a secondary immune response occur?

A

Yes.

179
Q

Are secondary immune responses faster, more effective and more prolonged to primary immune responses, and are sensitized memory cells already “on alert”, and do these memory cells provide immunological memory?

A

Yes.

180
Q

When your B cells encounter antigens and produce antibodies against them, are you experiencing active humoral immunity?

A

Yes.

181
Q

What are the two ways that active immunity is acquired?

A
  1. Naturally acquired when you get a bacterial or viral infection, during which time you develop symptoms of disease and suffer a little
  2. Artificially acquired when you receive a vaccine.
182
Q

What two benefits do vaccines provide?

A
  1. Their weakened antigens provide functional antigenic determinants that are both immunogenic and reactive.
  2. They spare us most of the symptoms and discomfort of the disease that would otherwise occur during the primary response.
183
Q

Do antibodies, also called immunoglobins, constitute the gamma globulin part of blood proteins?

A

Yes.

184
Q

Does each antibody consist of four looping polypeptide chains linked together by disulfide bonds? Do the four chains combined form a molecule, called an antibody monomer, with two identical halves?

A

Yes. Yes.

185
Q

What is the common event in all antibody-antigen interactions?

A

The formation of antigen-antibody (or immune) complexes.

186
Q

What do defensive mechanisms used by antibodies include?

A

Neutralisation, agglutination, precipitation and complement activation, with the first two most important.

187
Q

What is neutralisation?

A

Neutralisation, the simplest defensive mechanism, occurs when antibodies block specific sites on viruses or bacterial exotoxins (toxic chemicals secreted by bacteria). As a result, the virus or exotoxin cannot bind to receptors on tissue cells. Phagocytes eventually destroy the antigen-antibody defenses.

188
Q

What is agglutination?

A

Because antibodies have more than one antigen-binding site, they can bind to the same determinant on more than one antigen as a time. Consequently antigen-antibody complexes can be cross-linked into large lattices. When cell-bound antigens are cross-linked the process causes clumping, or agglutination, of the foreign cells. Agglutination occurs when mismatched blood is transfused (the foreign red blood cells clump) and is the basis of tests used for blood typing.

189
Q

What is precipitation?

A

In precipitation, soluble molecules are cross-linked into large complexes that settle out of solution. Like agglutinated bacteria, precipitated antigen molecules are much easier for phagocytes to capture and engulf than are freely moving antigens.

190
Q

What is complement activation?

A

Complement activation is the chief antibody defense used against cellular antigens, such as bacteria or mismatched blood cells. When several antibodies bind together on the same cell, the complement-binding sites on their stem regions align and complement is activated. Membrane attack complexes may insert into the cell’s surface, triggering cell lysis.

Anatomy and Physiology 2 (10 decks)

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