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HDM > Midterm > Flashcards

Midterm Flashcards

1
Q

Why do warm-blooded, long-lived animals require complex immune systems?

A

Infectious agents such as bacteria can rapidly divide in warm-blooded creatures

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2
Q

What are examples of some viruses?

A

polio, pox viruses, influenza, hepatitis B, HIV

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3
Q

What are examples of protozoans?

A

trypanosomes, leishmania, malaria

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4
Q

What are examples of some fungi?

A

candida, aspergillus

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5
Q

What are examples of some worms?

A

tapeworms, filaria

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6
Q

How many bacteria are there in the world?

A

~4-6 x 10^30 bacteria

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7
Q

What is the term for the community of microorganisms that live in a particular habitat? What are examples of some of these habitats in the bod?

A

microflora

skin, oral, respiratory tract, GI tract, urogenital and eye microflora

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8
Q

What percent of our intestinal contents are intestinal microflora?

A

20%

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9
Q

What is one reason we really need microflora?

A

provides molecular signals for the development of the immune system

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10
Q

What are three characteristics of germ-fee animals?

A
  • mucosal immune system is undeveloped
  • spleen and lymph nodes are undeveloped
  • serum hypgammaglobinemia (low antibody levels)
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11
Q

Can you reverse the undeveloped mucosal immune system, spleen, and lymph nodes in an adult germ-free animals?

A

not all abnormalities can be reversed

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12
Q

Can all bacteria cause diseases in humans?

A

nope

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13
Q

Who are the most prominent scientists in the history of the germ theory?

A

Joseph Lister
Robert Koch
Louis Pasteur

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14
Q

Who established that a particular germ could cause a specific disease?

A

Koch

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15
Q

What are the four Koch’s postulates?

A
  • infected tissue must show the presence of a particular microorganism not found in healthy animals
  • the microorganism must be isolated and grown in a pure culture
  • when injected into a healthy animal, the microorganism must cause the disease associated with it
  • this “second generation” microorganism should then be isolated and shown to be identical with the microorganism found in I
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16
Q

What is the study of a cause of disease including its origin and what pathogens, if any, are involved?

A

etiology

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17
Q

What do gram negative bacteria have that gram positive bacteria do not have?
What color do gram negative bacteria stain?

A

lipopolysaccharide outer leaflet of outer membrane

pink

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18
Q

Which has a thicker peptidoglycan layer? What does peptidoglycan function as? What color do these bacteria stain?

A

gram positive

purple- violet binds to peptidoglycan

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19
Q

What are ways that our body kill cytoplasmic pathogens? What pathogens would you find in the cytoplasm?

A

CTLs, NK cells, T cells, macrophages

bacteria, protozoa, viruses

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20
Q

What is an example of a pathogen that is vesicular?

A

mycobacteria

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21
Q

What are ways to kill extracellular pathogens? What are examples of extracellular pathogens?

A

antibodies, PMN (?), complement

bacteria, protozoa, viruses, fungi, worms/helminthes

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22
Q

How are extracellular microbes able to survive?

A

they grow extracellular being simply immersed in nutrients

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23
Q

How do intracellular microbes survive?

A

They invade and replicate intracellular within animal cells were they utilize host-cell energy sources

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24
Q

What is the only way to eliminate intracellular bacteria? How is tissue damage caused?

A

cellular immune response- they’re shielded from antibodies

tissue damage is caused by the host response- inflammation rather than by bacterial factors

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25
Q

What does Mycobacterium tuberculosis cause? Is it intracellular or extracellular? What is the mechanism of pathogenicity?

A

(intracellular)
tuberculosis, leprosy
macrophage activation resulting in granulomatous inflammation and tissue destruction

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26
Q

What does Legionella pneumophila cause? Is it intracellular or extracellular? What’s the mechanism of pathogenicity?

A

(intracellular)
Legionnaire’s disease
cytotoxin lyses cells and causes lung injury and inflammation

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27
Q

What are the two principal pathogenic mechanisms extracellular bacteria cause disease?

A
  • induces inflammation, which results in tissue destruction at site of infection
  • bacteria produces toxins with pathologic effects
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28
Q

What are exotoxins? What are endotoxins?

A

exotoxins are actively secreted by the bacteria

endotoxins are components of bacterial cell walls

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29
Q

What disease does Staph aureus cause? Is it intracellular or extracellular? What is the mechanism of pathogenicity?

A

extracellular
skin and soft tissue infections, lung abscess
systemic: TSS, food poisoning
enterotoxin-induced inflammation and cytokine release causing skin necrosis, shock diarrhea

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30
Q

What disease does Clostridium tetanus cause? Is it intracellular or extracellular? What is the mechanism of pathogenicity?

A

tetanus
extracellular
tetanus toxin causes irreversible muscle contraction

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31
Q

What disease doe Neisseria meningitidis cause? Is it intracellular or extracellular? What is the mechanism of pathogenicity

A

meningitis
extracellular
acute inflammation and systemic disease caused by potent endotoxin

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32
Q

What disease does Escherichia coli cause? Is it intracellular or extracellular? what is the mechanism of pathogenicity?

A

UTIs, gastroenteritis, septic shock
extracellular
toxins increased chloride and water secretion; endotoxin (LPS) stimulates cytokine secretion by macrophages

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33
Q

Is E coli gram positive or negative?

A

negative- LPS is its endotoxin

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34
Q

What are noninfectious foreign substances that can also elicit an immune response?

A

antigens (Ags)

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35
Q

What elicits autoimmune responses?

A

self Ags

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36
Q

What are the primary and secondary fixed elements of the immune system?

A

Primary: BM, thymus
Secondary: spleen and lymph nodes, mucosal immune tissues

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37
Q

What are examples of mobile elements of the immune system?

A

immune cells

soluble (humoral components): antibodies, complement, acute phase proteins

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38
Q

What are the granulocytes?

A

neutrophils, eosinophils, basophils

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39
Q

What are the lymphocytes?

A

B cells, T cells, NK cells

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40
Q

What are two types of cells found in the blood that can phagocytize?

A

neutrophil, monocyte

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41
Q

What are the primary lymphoid organs? What are their functions?

A

thymus and bone marrow

produce the cellular components of the immune system

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42
Q

What are the secondary lymphoid organs? What are their functions?

A

adenoids, lymph nodes, spleen

locations where the immune responses occur

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43
Q

Where can you find diffuse scattering of lymphoid cells?

A

deep to the epithelium in the connective tissue

GI tract, GU tract, respiratory passages

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44
Q

Which is more common: primary or secondary nodules?

A

secondary nodulars

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45
Q

What do primary nodules consist of? When in our lifetime would you have them?

A

consist of only small lymphocytes, no germinal center

prenatal

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46
Q

What type of nodule contains germinal centers? What do you find in the outer rings of these nodules?

A

secondary nodule
lymphoblasts
lymphocytes and memory cells collect in the outer ring

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47
Q

Tonsils are what type of tissue

A

partially encapsulated aggregates of lymphoid nodular tissue

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48
Q

What infiltrates the epithelium of the tonsils

A

lymphocytes

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49
Q

What two things would you see if you looked at pharyngeal tonsils under a microscope

A

pseudo stratified columnar ciliated epithelium
germinal center
no crypts

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50
Q

What would see if you looked at palatine tonsils under a microscope

A

stratified squamous epithelium
thick partial connective tissue capsule
germinal centers
10-15 invaginations called crypts

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51
Q

What would you see if you looked at lingual tonsil under a microscope

A

stratified squamous epithelium
no well defined capsule
germinal centers
one crypt per tonsil

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52
Q

How many palatine, pharyngeal, lingual tonsils does everyone have

A

2
1
1

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53
Q

Where do you find MALT?

A

GI tract, respiratory tract, urinary tract

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54
Q

What is the type of MALT that is found in Peyer’s patches in the ileum

A

GALT

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55
Q

What would you see if you looked at GALT from Peyer’s patches under a microscope

A

abundance of villi
single or clusters of lymphoid nodules
simple columnar epithelium with Goblet cells

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56
Q

What would you see if you looked at GALT from the appendix under a microscope

A

no villi
crypts
simple columnar epithelium with Goblet cells

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57
Q

What are types of apical specializations?

A

microvilli, stereo cilia, cilia, flagella

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58
Q

What are the functions of microvilli

A

to increase cell surface area

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59
Q

What are the majority of the immune cells produced from? CD?

A

CD34+ hemopoietic stem cell (HSC)

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60
Q

Where can you find hemopoietic stem cells?

A

fetal liver/spleen

neonate and adult bone marrow

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61
Q

What do stromal cells do?

A

interact with HSC and produce

  • stem cell factor (SCF)
  • granulocyte-colony stimulating factor (G-CSF)
  • monocyte colony-stimulating factor (M-CSF)
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62
Q

What are examples of stroll cells?

A

epithelial cells, fibroblasts, macrophages

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63
Q

What are stem cell factors needed for?

A

HSC self-renewal

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64
Q

What is G-CSF needed for?

A

the development of neutrophils

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65
Q

What is M-CSF needed for?

A

development of monocytes

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66
Q

What does CD stand for? What does it indicate?

A

cluster of differentiation

indicates a defined subset of cellular surface receptors that identify cell type and stage of differentiation

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67
Q

What lab order would provide the complete hematologic picture of a case at least from the morphologic standpoint?

A

DIFF (differential leukocyte count) and CBC (complete blood count)

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68
Q

What is the stain that is usually used for blood smears? What is it a mixture of?

A

Gismo smear

basic stain methylene blue and acidic stain eosin

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69
Q

What two white blood cells would dominate a blood smear compared to other WBCs?

A

neutrophils (40-60%)

lymphocytes (20-40%)

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70
Q

What are the markers (CDs) for T cells?

A

CD3
CD4
CD8

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71
Q

What are the markers (CDs) for B cells?

A

CD19

CD20

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72
Q

What are the markers (CDs) for NK cells?

A

CD56

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73
Q

What are the markers (CDs) for macrophage/monocytes?

A

CD14

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74
Q

What is another name for neutrophils? What do their nucleus look like? What do they mediate?

A

polymorphonuclear leukocytes
neutrophil is segmented into 3-5 connected lobules
mediate the earliest phases of inflammatory reactions

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75
Q

Where do we make neutrophils? What cytosine stimulates the production of neutrophils? How long can a neutrophil circulate in the blood? After entering tissue, how long can they function?

A

bone marrow
G-CSF
circulate for hours or few days
die within 1-2days of entering tissue

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76
Q

What do we call a WBC count that is above the normal range in the blood? What is it usually in response to?

A

leukocytosis
bone marrow’s response to infection and inflammation caused by trauma, gout, rheumatoid arthritis, rheumatic fever, thyroiditis, acute stress or primary bone marrow disease (CML)

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77
Q

What allows for the rapid response to the demand for increased WBCs? How big of a response can we get and how quickly?

A

bone marrow stores a lot of maturing cells

2-3 fold increase (leukocytosis) possible in 4-5 hours

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78
Q

In response to infection/inflammation the bone marrow is release immature WBCs. What do we call this?

A

left shift

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79
Q

What do we call the reduction in the circulating WBC count to

A

leukopenia

neutropenia

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80
Q

What is another name for neutropenia? If severe what can it cause? What often causes neutropenia? What would a patient present with that would make you suspect neutropenia?

A

agranulocytosis or granulocytopenia
life-threatening infection
chemotherapy or radiation therapy
frequent or unusual infections

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81
Q

What is the main function of neutrophils? What else can they do? What are in the granulocytes of neutrophils?

A

main function is phagocytosis
produce inflammatory mediators-cytokines, prostaglandins, leukotrienes
granules contain: peroxidase, lysozyme, degradative enzymes, defensins

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82
Q

What is protein contained within neutrophils that act against bacteria, fungi, and many enveloped/nonenveloped viruses?

A

defensins

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83
Q

What granulocytes are stained by:

1) neutral dyes
2) eosin
3) basic dyes

A

1) neutrophils
2) eosinophils
3) basophils

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84
Q

What do you use to stain lysosomes that contain enzymes and other microbicidal substances?

A

azure dye to give azurophilic granules

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85
Q

What are three ways neutrophils kill bacteria?

A

phagocytosis
degranulation
NETs

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86
Q

What are NETs? What is the main function of NETs? What do neutrophils do after producing NETs?

A

neutrophils release neutrophil extracellular traps (NETs) and continue directional chemotaxis (spread NETs) and phagocytosis
main function of NETs is preventing bacterial dissemination

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87
Q

What do cell of the macrophage lineage arise from? Where?

A

M-CSF

bone marrow

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88
Q

Would you see monocytes or macrophages in the circulating blood normally? What would you find in the tissue?

A

mature monocytes enter the blood circulation then migrate into tissues where they mature into macrophages

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89
Q

What is an increased number of monocytes called? What is it in response to usually?

A

monocytosis
chronic infections, autoimmune disorders, certain cancers, proliferation of macrophages can occur in tissues (sarcoidosis)

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90
Q

What is a low number of monocytes in the blood called? what can cause this?

A

monocytopenia

can occur in response to endotoxemia or chemotherapy

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91
Q

What are macrophages in the connective tissue called?

A

histiocytes

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92
Q

what are macrophages in the liver called?

A

kupffer cells

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93
Q

What are macrophages in the lungs called?

A

alveolar macrophages

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94
Q

what are macrophages in the CNS called?

A

microglial cells

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95
Q

What are the functions of tissue macrophages?

A

phagocytic cells and antigen-presenting cells

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96
Q

What do macrophages release?

A 
cytokines and chemokine
reactive oxygen intermediates (ROI)
nitric oxide (NO)
defense's
enzymes: lipases, galactosidases
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97
Q

What do tissue macrophages produce to drive Th1 cell responses?

A

TNF, IL-12, IL-23

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98
Q

What do Th1 cells produce that provide a positive amplification loop that increases microbicidal and tumoricidal activity of tissue macrophages?

A

interferon-y

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99
Q

What do tissue macrophages produce that makes them important drivers of chronic inflammatory and autoimmune diseases?

A

TNF and IL-1B

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100
Q

How do tissue macrophages help with wound repair?

A

secrete cytokines/chemokines, matrix metalloproteinases and their tissue inhibitors that regulate the recruitment of cells to and deposition of ECM components at site of tissue injury

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101
Q

How do macrophages activate T lymphocytes at the site of infection?

A

present Ags

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102
Q

What do the granules in eosinophils contain?

A

basic proteins, peroxides, antimicrobial substances

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103
Q

In what type of reactions do we see a lot of eosinophils?

A

allergic reactions and reactions to parasite infections

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104
Q

What do eosinophils produce?

A

granules for extracellular digestion of infectious pathogens

inflammatory mediators- cytokines, prostaglandins, leukotrienes

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105
Q

What are the functions of mast cells and where do you find them? What do they express receptors for?

A

They serve functions that can amplify or suppress innate or acquired immune responses
They are tissue-fixed, at sites exposed to environment
express receptors for pathogen associated (PAMP) and damage-associated molecular patterns (DAMP)

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106
Q

What do mast cells release that attract neutrophils?

A

IL-8

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107
Q

Why would you want mast cells to be located close to blood vessels?

A

they can regulate vascular permeability and effector-cell recruitment

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108
Q

How do mast cells control the behavior of surrounding cells?

A

through the release of mediators

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109
Q

Do neutrophils and monocytes require activation to be recruited into tissue sites?

A

nope

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110
Q

How do neutrophils and monocytes enter the tissue?

What does this migration cause?

A

through post-capillary venues except parenchymal tissues (liver, lungs, kidney) where all blood cells enter through capillaries
inflammation

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111
Q

For neutrophil recruitment cascade, what is rolling dependent on? What about adhesion, crawling, and transmigration?

A

selectin-dependent

integrin-dependent

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112
Q

What lines the luminal part of the endothelium to induce conformation changes in neutrophil integrins? What do these interactions result in?

A

IL-8 (neutrophils have IL-8 receptor)

result in arrest, adhesion, crawling, and transmigration of neutrophils

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113
Q

What guides neutrophils to the preferential site for transmigration?

A

chemokine gradient

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114
Q

What is produced by tissue macrophages that induce rapid induction of pre-formed p-selectin on the surface of endothelial cells?

A

TNF and IL-1

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115
Q

What selection initiates rolling on the endothelium? What selection stabilizes the rolling?

A

P-selectin initiates

L-selectin stabilizes

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116
Q

What controls transmigration of monocytes?

A

CCL2 and MCP-1

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117
Q

What shape do cells adopt following diapedesis?

A

amoeboid shape

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118
Q

What do leukocytes migrate on once under the basement membrane to get to the site of infection?

A

migrate along collagen fibrils

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119
Q

Where on a leukocyte would you expect to find chemotactic receptors?

A

located on the leading edge

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120
Q

What are the cytotoxic mechanisms of NK cells? DO they have Ag receptors? Do they belong to innate or adaptive immunity?

A

secretion of perforin
no
innate

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121
Q

What are targets of NK cells?

A

virus-infected cells, cancer cells, transplant cells

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122
Q

Do NK cells arise from precursors in the same lineage of B or T cells?

A

nope it’s unique!

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123
Q

Do we see NK cells in adults only? How can we increase their numbers/activity?

A

we see them in the body at birth

IL-15 and IL-2 increase number/activity but do NOT activate them. they’re always active.

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124
Q

What is the difference between stereo cilia and regular cilia?

A

stereocilia are non-motile whereas cilia are

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125
Q

What are the functions of stereocilia? Cilia?

A

stereocilia work in absorption and secretion

cilia generate currents for movement of fluids and particulate matter

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126
Q

What is the function of tight junctions?

A

prevent movement of membrane proteins between apical and lateral domains
prevent water-soluble materials from passing through

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127
Q

Whats another name for zonula adherens? What are their functions?

A

anchoring junctions

fasten cells to each other or to extracellular material

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128
Q

What types of plaques do zonula adherens use?

A

myosin, tropomyosin, vinculin

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129
Q

What’s another name for macula adherens? What is their function?

A

desmosomes

provide firm cell-to-cell adhesion

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130
Q

What make up gap junctions? What’s the function?

A

connexions

mediate intercellular communication by allowing rapid spread of information

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131
Q

What do hemidesmosomes bind to in the basal lamina?

A

fibronectin in lamina lucida

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132
Q

What makes up the basement membrane?

A

basal lamina and reticular lamina

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133
Q

What in the thick skin gives it fingerprints?

A

epidermal ridges and furrows that correspond to the dermal papillae

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134
Q

What type of glands do we find in thin skin?

A

sweat and sebaceous glands

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135
Q

What layer of skin is only found in thick skin?

A

stratum lucidum

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136
Q

What are the five layers of epidermis from deep to superficial? What can you find in the epidermis?

A 
basale
spinosum
granulosum
lucid
corner

free nerve endings (unencapsulated)

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137
Q

What layer of the epidermis is bound to the basal lamina by hemidesmosomes? What is it bound to keratinocytes by? Is it mitotically active

A

stratum basale
desmosomes
it’s mitotically active

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138
Q

What gives the stratum spinosum cells a prickly appearance? Are they mitotically active? What does it produce when it thickens with pressure?

A

tonofilaments
yes
corns and calluses

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139
Q

What is the function of the stratum granulosum?

A

uses granules to be a barrier to foreign material and protect body from dehydration

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140
Q

What makes the stratum lucid translucent?

A

no organelles or nuclei

has lots of keratin

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141
Q

What cells are continuously exfoliated? What are they filled with?

A

stratum corner

mature keratin

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142
Q

Of the keratinocytes, melanocytes, langerhans, and merkel cells, which is most abundant in the epidermis? What does it make? What is it the final location of?

A

keratinocytes
makes keratin and lamellar granules
final location of melanin

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143
Q

What layer do you find melanocytes? What do they do?

A 
stratum basale (No desmosome)
make melanin then transfer it to keratinocytes
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144
Q

What is the function of melanin?

A

protects cell nuclei from UV radiation
tyrosinase enzyme is UZ sensitive
cytocrine secretion

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145
Q

What are dendritic cells in the epidermis? What layer do you find them?

A

langerhans cells

stratum spinosum

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146
Q

What are langerhans cells involved in? What are they easily damaged by?

A

immunologic skin reactions

UV radiation

147
Q

What do Langerhans cells look like under a microscope?

A

pale cytoplasm with long processes

contain Birbeck’s granules

148
Q

What cells do you expect to respond to an infection in the first few hours?

A

innate immunity- phagocytes, complement pathway, NK cells

149
Q

What cells do you expect to finish off an infection but won’t show up for at least a day after the beginning of the infection?

A

B lymphocytes -> antibodies

T lymphocytes -> effector T cells

150
Q

What makes B and T cells highly selective?

A

the antigen receptors they have on their surfaces

151
Q

When do we stop developing B lymphocytes? What about T lymphocytes?

A

B lymphocytes develop throughout lifetime

T lymphocytes are generated in the thymus during fetal stage

152
Q

What type of antigens can B cells recognize?

A

proteins, carbohydrates, lipids, nucleic acids

153
Q

Does an individual B cell express a bunch of different B cell receptors? What are the functions of BCRs?

A

no they express identical receptors

recognition of antigens

154
Q

What are the functions of antibodies?

A

neutralize and eliminate extracellular microbes and microbial toxins
prevent dissemination of microbes

155
Q

What kind of antigens can TCRs recognize? What do they require to “see” antigens?

A

peptides only

antigen-presenting cells

156
Q

What do cytolytic T lymphocytes (CTLs) kill?

A

infected host cells (intracellular microbes)

157
Q

What are the three types of professional APCs? What are their functions?

A

dendritic cells, macrophages, and B cells

when activated, they activate T helper lymphocytes

158
Q

What are non-professional APCs? What do they activate?

A

any infected nucleated cell in the body

activate cytolytic T lymphocytes

159
Q

What reside in the epithelium to capture microbes?

A

dendritic cells

160
Q

After they capture microbes, where do dendritic cells go and what do they do?

A

transport the Ags to the lymph nodes where protein Ags are displayed for recognition by T lymphocytes

161
Q

Where are blood borne Ags presented by APCs?

A

spleen

162
Q

PALS + lymphoid follicles =

A

white pulp

163
Q

White pulp is surrounded by ____ which is rich in ____ ?

A

red pulp

vascular sinusoids

164
Q

What surrounds splenic arterioles? What does this thing contain?

A

periarteriolar lymphoid sheath (PALS)

T and B cell zones

165
Q

Which MHC class do non-professional APCs express?

A

class I MHC only

166
Q

Which MHC class do professional APCs express?

A

classes I and II MHC

167
Q

What do T helper cells recognize? What do they express?

A 
Ads presented by class II MHC
they express CD4+
168
Q

What do cytolytic T cells recognize? What do they express?

A

express CD8+ that directs them to Ags presented by class I MHC

169
Q

How do cytolytic T lymphocytes know to kill infected cells?

A

infected cells will display the peptide Ags in the class I MHC (all nucleated cells have class I MHC so they can all present to CTLs)

170
Q

What are the phases of adaptive responses

A
  • recognition of Ag by specific lymphocytes
  • activation of lymphocytes (clonal expansion and differentiation)
  • effector phase (elimination of Ag)
171
Q

What causes immune response to decline? What happens to antigen-stimulated lymphocytes?

A

declines as antigens are eliminated

some die by apoptosis and some survive as memory cells

172
Q

What part of the antibody determines the effector property of the antibody?

A

the constant region (Fc)

173
Q

What does the hinge domain of the antibody provide?

A

flexibility to allow optimal Ag binding

174
Q

What does it mean when an antibody neutralizes a virus or toxin?

A

blocks its interaction with cell surface receptors

175
Q

What antibody can activate the complement cascade?

A

IgM

176
Q

What does opsonization by antibodies mean?

A

Abs bind to Fc receptors on tissue macrophages and neutrophils that enhances phagocytosis

177
Q

How does antibody-dependent cell-mediated cytotoxicity work?

A

Ab tags tumor cells and virus-infected host cells

NK cells bind Fc receptors on Ab and kills the infected/tumor cell

178
Q

How does an antibody assist with degranulation?

A

mast cells, basophils, and eosinophils have Fc receptors that are bound by IgE which makes them degranulate

179
Q

What about epithelial cells forms as a mechanical barrier?

A

the tight junctions that connect them

180
Q

In what three ways does the innate immune system provide natural immunity against microorganisms?

A

phagocytes and intracellular killing
recruitment of other inflammatory cells
presentation of antigens

181
Q

What two general types of cells are the first line of immune defense? What are examples of each type?

A

leukocytes; neutrophils, monocytes, tissue macrophages, eosinophils
lymphocytes: NK cells

182
Q

What does activation of neutrophils lead to?

A

respiratory bursts and release of granules to control bacterial growth

183
Q

What are the first cells to arrive on scene?

A

neutrophils

184
Q

What three things will macrophages do for the innate immune system?

A

engulf organisms
release inflammatory mediators
act as professional APCs to link innate and adaptive immunity

185
Q

What do NK cells kill and how?

A

kill infected host cells by a cytolytic mediator perforin

186
Q

What is the term for transmigration through endothelium?

A

diapedesis

187
Q

What activates the integrins on blood leukocytes? What state are they normally in? What does this state look like?

A

the binding of chemokines to the chemokine receptors on the leukocyte
normally in a low-affinity state
low-affinity is bent
high-affinity is extended

188
Q

Which molecules regulate chemotaxis?

A

chemokine, C3a, C5a, leukotrienes

189
Q

Which cells express E-selectin?

A

endothelial cells

190
Q

Which cells express integrins?

A

leukocytes

191
Q

How do defensins work? What are they effective against? Where do you find it?

A

they are a cationic (rich in Arg) antibiotic peptide
they insert into microbial membranes and destabilize ion channels
effective against ALL bacteria, fungi, and enveloped viruses
found in neutrophil granules

192
Q

What does bactericidal permeability increase protein (BPI) do and where do you find it?

A

increases permeability of bacterial membrane

in granules of neutrophils

193
Q

Where do you find lysozyme and lactoferrin and what do they do?

A

in neutrophil granules

bactericidal and bacteriostatic proteins

194
Q

What does cathepsin G do and where do you find it?

A

a serine protease that digests collagen and proteoglycans

in granules of neutrophils

195
Q

How do monocytes transmigrate?

A

same as neutrophils! except their chemoattractants are different

196
Q

What are the chemoattractants for monocytes?

A

macrophage inflammatory protein-1a (MIP-1a) and MIP-1B

197
Q

What induces classical macrophage activation? By what cytokine?

A

induced by TLRs and by cytokine IFN-y

198
Q

What is another name for classically activated macrophages? What are their functions?

A

M1

involved in destroying microbes and inflammation

199
Q

What induces alternative macrophage activation?

A

IL-4 and IL-13

200
Q

What is another name for alternative macrophages? What are their functions?

A

M2

tissue repair and control of inflammation

201
Q

What signaling molecule is very important in wound healing? what is it a chemoattractant for?

A

TGF-B

fibroblasts

202
Q

What is in prokaryotes but not eukaryotes that phagocytes use to help distinguish self from non-self?

A

N-formylmethionyl peptide (fMet)

203
Q

What are the NK cells direct involvement in immune response

A

NK cells recognize infected or stressed cells

release granules and kill dysfunctional cells

204
Q

What are the NK cells indirect involvement in immune response?

A

NK cells are activated by IL-12 produced by macrophages

they secrete IFN-y that activates phagocytosis and killing of pathogens by macrophages

205
Q

What activates NK cells and what produces it?

A

IL-12 produced by macrophages

206
Q

How are NK cells activated by a virus-infected cell?

A

virus inhibits class I MHC expression on infected cell so the inhibitory receptor on NK cell is not engaged and allows the activating receptor to dominate activating NK cells to destroy the target cell

207
Q

Are the activating receptor and inhibitory receptor of NK cells always on?

A 
The activating receptor is on
Inhibitory receptor is on as long as it's engaged by normal class I MHC expression by target cells
208
Q

What enzyme is associated with the activating receptor of NK cells?

A

protein tyrosine kinase is activated by the activating receptors

209
Q

What inhibits the PTK of NK cells?

A

PTK is inhibited by inhibitory receptors that recognize class I MHC molecules and active protein tyrosine phosphatase (PTP)

210
Q

What is the goal of the complement system?

A

to form the membrane attack complex (MAC) which creates holes in plasma membranes and kill pathogens

211
Q

What initiates classical activation of the complement system?

A

binding of C1 protein complex to IgM or IgG which are deposited on the bacteria

212
Q

What happens to the products of C3 being cleaved?

A

C3a plays a role in chemotaxis and inflammation

C3b is deposited on the surface of the bacteria and serves as an opsonin and can form a complex to make C5 convertase

213
Q

What does C3b acting as an opsonin do?

A

increases phagocytosis by phagocytic cells

214
Q

What makes up C5 convertase

A

C4b2a3b

215
Q

What happens to the products of C5 being cleaved?

A

C5b is responsible for initiating the self-assembly of the MAC
C5a anaphylatoxin is a potent mediator of inflammatory responses

216
Q

What all is the MAC composed of?

A

C5b, C6, C7, C8, and numbers C9

217
Q

What is 3d’s involvement with B cells?

A

It binds CR2 and lowers the threshold for activity on B cells
this links innate to adaptive immunity

218
Q

What does C3b bind to on macrophages to increase phagocytosis?

A

CR1

219
Q

What is the result of solubilization and clearance of immunocomplexes? What complement proteins do this?

A

prevention of aggregation and spreads inflammation

C3a and C3b

220
Q

What is production of acute phase proteins regulated by? What are APPs produced by? What do they accompany?

A

IL-6
hepatocytes
inflammation for SYSTEMIC acute-phase response

221
Q

What causes activation and maturation of antigen-presenting cell?

A

pathogen recognition through PRRs

222
Q

What TLR recognizes gram-positive bacteria?

A

1, 2, 6

223
Q

What TLR recognizes dsRNA?

A

3

224
Q

What TLR recognizes gram-negative bacteria?

A

TLR4

225
Q

What TLR recognizes flagellin?

A

TLR5

226
Q

What TLR recognizes unmethylated CpG DNA?

A

TLR9

227
Q

What receptors recognize microbial Ags?

A

BCRs and TCRs

228
Q

In BCR, the NH-terminus of what are highly variable?

A

H and L chains (Vh and VL)

antigen binding site

229
Q

In TCR, the NH-terminus of what are highly variable?

A

Va and VB

230
Q

Is the constant (c) region very variable?

A

noooooope!

231
Q

What is another name for a BCR?

A

Ig molecule

232
Q

Even though individuals codominantly express maternal and paternal sets of alleles for L and H chains, only one of the VLCL and VHCH alleles (either maternal or paternal) is expressed in a single B cell. Why?

A

allelic exclusion

233
Q

What does allelic exclusion refer to?

A

individual B cells express only on of the VLCL or VHCH alleles (either maternal or paternal) even though individuals codominantly express maternal and paternal alleles for L and H chains

234
Q

What things is allelic exclusion applied to?

A

TCRs and BCRs

235
Q

What determines the variable regions of the chains in TCRs and BCRs?

A

rearrangement of the DNA

236
Q

What is the major mechanism of epitope-specific diversity of BCR and TCR?

A

DNA chromosomal rearrangement

237
Q

What initiates rearrangement of BCR or TCR?

A

somatic recombination

238
Q

What are RAG1 and RAG2? What cells is the expression of RAG1 and RAG2 restricted to and during what stage?

A

recombination-activating genes 1 and 2 encode enzymes performing recombination of BCR and TCR during the process of VDJ recombination
B and T lymphocytes during developmental stages

239
Q

How many separate gene segments are in a chromosome 14 on a heavy chain? What are they?

A

4

V, D, J, C (constant)

240
Q

What’s the difference between an immature B cell DNA segment for heavy chain and a mature B cell?

A

all copies but one are randomly deleted giving a single B cell a unique combination of V-D-J

241
Q

What is the test for productive rearrangement? What is the chance of producing a productive rearrangement?

A

transcription and translation

10%

242
Q

Why can B cells recognize any Ag possible?

A

the number of combinations possible is very big for the V, D, J genes

243
Q

Where is junctional diversity generated?

A

at the points between the joining genes

244
Q

What does junctional diversity result from?

A

loss of nucleotides by exonuclease

addition of N and P nucleotides

245
Q

What are P nucleotides derived from?

A

asymmetric opinion of hairpin loops

246
Q

What does the opening of the hairpin loops produce for junctional diversity?

A

single stranded extensions that can be added into junctions or alternatively removed by exonuclease activity

247
Q

What aids the addition of N nucleotides?

A

terminal deoxynucleotidyl transferase (TdT)

248
Q

Does junctional diversity work for BCR or TCR

A

both

249
Q

What is the cause of Omenn syndrome?

A

missense mutation -> only partial rag1/rag2 activity

250
Q

What are symptoms of Omenn syndrome?

A

lack of B cells
decrease in T cell counts
severe immune deficiency with failure to thrive, diarrhea, red rush

251
Q

What defect causes severe combined immune deficiency?

A

null mutation in rag1 and rag2 genes
NO enzymatic activities
(deficiency in adenosine deaminase)

252
Q

What are symptoms of SCID?

A

total lack of B and T cells

defect in both humoral and cell-mediated immunity

253
Q

What do CD4+ T cells require?

A

APC and co-stimulation

254
Q

Resting APCs express low levels of what?

A

co-stimulatory molecules

255
Q

Activated APCs express high levels of what?

A 
class II MHC
co-stimulatory molecules called B7-1 and B7-2 (CD80 and CD86)
256
Q

Costimulation involves a protein ___ on APC and a protein ___ on T cells

A

B7 on APC

CD28 on T cells

257
Q

What is the immunological synapse?

A

close contact between T cell and APC

258
Q

What three molecular pairs participate in the immunological synapse?

A

TCR/MHC-peptide pair
Co-stimulatory pair CD28(T cell)/B7(APC)
Adhesion pair LFA-1(T cell)/ICAM-1(APC)

259
Q

What does the immunological synapse ensure?

A

effector molecules (cytokines) released by the cells are not affecting bystander cells

260
Q

What is an analog for CD28 that can be found on T cells?

What is its function?

A 
CTLA-4
signal transduction (negative regulation)
261
Q

Where are plasma cells mostly found?

A

lymphoid organs NOT in the plasma

262
Q

What is one of the main functions of B cells? What can they do once activated and after performing this function?

A

professional APC to T cells

can develop into memory B cells

263
Q

What is the specific marker for B cells? What else does it do other than serving as a marker?

A

CD19

coreceptor for BCR

264
Q

What else do B cells need to be activated by protein Ags? What do we call protein Ags?

A

assistance of T helper cells

thymus dependent or TD Ags

265
Q

What do we call antigens of lipid, carbohydrate, or polynucleotide nature? Why?

A

thymus-indepdnet or TI Ags

activate B cells without help of T cells

266
Q

What generates a signal for B cell activation by TI Ags?

A

cross-linking

267
Q

What is cross-linking when it comes to B cell activation by TI Ags?

A

multiple BCRs bind to a repetitive epitope on bacterium

268
Q

What transduces the signal generated by cross-linking in B cell activation by TI Ags? What

A

Iga and IgB

269
Q

Enzymes attached to the cytoplasmic portion of Iga and IgB catalyze what?

A

phosphorylation of signaling molecules

270
Q

What is the co-stimulatory signal from T helper cells for B cell activation by TD Ags?

A

Th2 cell delivers second signal via CD40L (B cell has CD40)

271
Q

What if a T cell receives a specific signal but never receives a co-stimulatory signal?

A

T cell becomes anergia (does not react)

272
Q

What if a T cell receives a co-stimulatory signal but no specific signal?

A

there’s no effect on T cell

273
Q

In antibody-dependent cell-mediated cytotoxicity, what part of the antibody binds to what cell that will kill the target?

A

Fc region of bound Ig binds CD16 of NK cell

274
Q

What are some examples of autocoids?

A

nitric oxide, eicosanoids, histamine, serotonin

275
Q

What are the sequential enzymatic reactions that generate eicosanoids referred to as?

A

arachidonic acid cascade

276
Q

What are eicosanoids?

A

a family of antacid lipid mediators derived from oxidative metabolism of a polyunsaturated fatty acid substrate with 20 carbons (arachidonic acid)

277
Q

How do we get prostaglandin (PG)H2 endoperoxide?

A

cell membrane phospholipids—> arachidonic acid (via phospholipase A2)
arachidonic acid —> prostaglandin (PG)H2 endoperoxide (via COX cyclooxygenase)

278
Q

What type of enzymes give us prostacyclin or thromboxane from the same substrate? What is the substrate?

A

tissue isomerases

prostaglandin (PG)H2 endoperoxide

279
Q

What enzyme inactivates prostaglandins?

A

15-OH PG dehydrogenase

280
Q

When are PG or Tx made?

A

only upon stimulation which activates phospholipase A2 to liberate AA from cellular phospholipids

281
Q

Are Pgs or Tx stored in cells?

A

noooooooope

282
Q

What does autocoid inactivation involve?

A

rapid metabolic degradation of PGs or spontaneous hydrolysis of Tx and PGI2

283
Q

How can different cells make different eicosanoids?

A

expression of isomerases and synthase enzymes vary among cells

284
Q

What G protein is associated with thromboxane? What are some downstream effects?

A

Gq —> PLC —> DAG and IP3 —> ^Ca

smooth muscle contracts

285
Q

What G protein is associated with prostaglandin? What are some downstream effects?

A

Gs —> AC —> cAMP

smooth muscle relaxes

286
Q

Why can most cell types make eicosanoids?

A

most cell types express COX

287
Q

What cells in cardiovascular physiology produce thromboxane? what enzyme do they express?

A

platelets in the blood

express Tx synthase

288
Q

What cells in cardiovascular physiology produce prostacyclin? What enzyme do they express?

A

vascular endothelium

express PGI2 synthase

289
Q

What cells in cardiovascular physiology express thromboxane receptors?

A

platelets and vascular smooth muscle

290
Q

What cells in cardiovascular physiology express prostacyclin receptors?

A

platelets and vascular smooth muscle

291
Q

If someone’s heart had an excess of TxA2 and a deficit of PGI2 what condition would they have?

A

coronary spasm such as angina pectoris

292
Q

What receptors when occupied by their cognate ligands typically relax smooth muscles and cause vasodilation?

A

EP2, EP4, IP

293
Q

What receptors when occupied by their ligands contract smooth muscles and cause vasoconstriction?

A

FP and TP

294
Q

How can EP sub-types vary in dilation or constriction?

A

vary in G protein coupling

295
Q

What is the eicosanoid for vasculature and what is its action?

A

PGE2

permeability

296
Q

What is the eicosanoid for the gut and what is its action?

A

PGE2

mucosal cytoprotection, muscle tone, motility

297
Q

What are the eicosanoids for the kidney and what are their actions?

A

PGI2, PGE2

Na+, H2O excretion

298
Q

What are the eicosanoids for the uterus and what are their actions?

A

PGF2a, PGE2

uterine contraction

299
Q

What is the eicosanoid of the CNS and what is its action?

A

PGE2

temperature

300
Q

What is the eicosanoid of the PNS and what is its action?

A

PGE2

pain sensitization

301
Q

What inhibits platelet aggregation?

A

PGI2

302
Q

Platelets being exposed to what stimulates TxA2 formation?

A

collagen in the connective tissue

303
Q

How does thromboxane take care of bleeds?

A
  • amplifies platelet aggregation
  • constricts blood vessel
  • slows bleeding
304
Q

What stops the thromboxane process from spreading throughout the blood stream? What keeps it local?

A

stimulus (collagen) is local

PGI2 made by downstream endothelial cells opposes the action of TxA2 on blood vessels and platelet

305
Q

When is COX-1 expressed?

A

constitutive-all the time

306
Q

What does COX-1 synthesize in the gut? What is the stimulus? what is the role of this prostaglandin?

A

PGE2
gastric acid
mucosal cytoprotection, gut motility

307
Q

IF you have a deficit of PGE2 in the gut what happens? What if you have an excess of PGE2?

A

deficit: ulcers
excess: diarrhea, cramps

308
Q

What does COX-1 synthesize in the uterus? What is the stimulus? What is the role of this prostaglandin?

A

endocrine hormones and mechanical stretch
PGE2 and PGF2
dilate the cervix, contract the uterus —> delivery

309
Q

If you have a deficit of PGE2 or PGF2a in the uterus what will happen? What if you have an excess of PGE2 and PGF2a?

A

pre-mature labor

birth

310
Q

What does fetal lung maturation cause?

A

withdrawal of PGE2 —> ductus arterioles closes

311
Q

What does a deficit of PGE2 in the kidneys cause? what special enzyme can produce PGE2 in the kidneys?

A

leads to Na+ and H2O retention (edema), mild hypertension

COX-2

312
Q

Where does COX-2 complement the role of COX-1?

A

kidney and brain

313
Q

When is COX-2 expression induced?

A

prominent role responding to pathological stimuli (cancer, inflammation)

314
Q

Where can you find 15-OH-PGDH? What does it do?

A

lungs

limits the systemic administration of PGs

315
Q

Are autocoids hormones?

A

NO

316
Q

How does inflammation stimulate production of PGs?

A

stimulates AA release

317
Q

What would be the advantage of a selective COX2 inhibitor?

A

it would inhibit COX2 in the knee but leave COX1 in the tummy alone

318
Q

What do SH2 domains bind?

A

phosphotyrosine-containing polypeptides

319
Q

What do SH3 domains recognize?

A

proline-rich stretches in polypeptides

320
Q

What do PH domains recognize?

A

PIP3 or other phosphatidylinositol-derived lipids

321
Q

What domains are present on Syk and ZAP-70 tyrosine kinases? What motifs do they bind to in the Ag receptor complex?

A

SH2 domains bind phosphotyrosine motifs in the Ag receptor complex

322
Q

What tyrosine kinase family recognizes PIP3 on the inner leaflet of the plasma membrane?

A

TEC family tyrosine kinase Btk

323
Q

What are the adaptor proteins for B cells? What about T cells?

A

BLNK (B cell linker)

LAT (linker for the activation of T cells)

324
Q

What can adaptor proteins contain?

A

SH2 or SH3 domains
or proline-rich stretches
or tyrosine residues that can be phosphorylated by tyrosine kinases

325
Q

Explain the process of attaching adaptor proteins in T cell activation starting with LAT

A

LAT is phosphorylated and recruits PLC (Ca signaling) and GADS adaptor
SLP-76 (proline-rich stretch) binds GADS’s SH3 domain and recruits VAV after being tyrosine phosphorylated -> actin-cytoskeletal rearrangment

326
Q

What are on the cytosolic side of activating/inhibiting immune receptors?

A

ITAMs

ITIMs

327
Q

What inhibitory receptor is found on B cells and myeloid cells?

A

FcyRIIB

328
Q

How can a coreceptor increase cellular activation?

A

coreceptor with its signaling enzymes can increase ITAM phosphorylation and activation of the antigen receptor

329
Q

What are the coreceptors for T helper and cytotoxic T cells?

A

CD4 and CD8

330
Q

What is the coreceptor on B cells?

A

complement receptor type 2 (CR2/CD21)

331
Q

What is an inhibitor of T cell receptors?

A

CTLA-4 (analog CD28)

332
Q

What are inhibitory receptors in B cells?

A

CD22 and FcyRIIB

333
Q

What is another name for CD80/CD86?

What does it bind on T cells?

A

B7

CD28

334
Q

Why do the aB chains of a TCR need CD3 and the squiggle proteins?

A

TCR a and B chains have cytoplasmic tails that are too small to transduce signals so CD3 and squiggle proteins serve as signal-transducing subunits of TCR complex

335
Q

How many polypeptides chains make up CD3 and what are they? On what cells do we find CD3?

A

three: y, d, E

CD4 and CD8 T cells

336
Q

What protein is in charge of adhesion on T cells? What does it bind to on an APC?

A

LFA-1

binds ICAM-1 on APC

337
Q

What is the negative regulation accessory molecule on TCR that is bound by ligands on tumor cells, tissue cells, and APCs?

A

program death-1

PD-1

338
Q

What does the CD4 coreceptor look like?

A

four extracellular Ig-like domains, hydrophobic transmembrane region, highly basic cytoplasmic tail (38 AAs long)

339
Q

What does the CD8 co receptor look like?

A

composed of two related chains called CD8a and CD8B
they have a single extracellular Ig domain
highly basic cytoplasmic tail that is 25 AAs long

340
Q

Describe early events in T cell activation starting with Ag recgonition

A
  • recognize Ag, TCR complexes cluster with CD4 or CD8
  • CD4-associated Lck becomes active and phosphorylates ITAMs of CD3 and squiggle chains
  • ZAp-70 binds phophotyrosines of squiggle chains and is phosphorylated/activated
  • ZAP-70 activates various adaptors such as LAT
  • adaptors become docking sites for PLCy1 and exchange factors that activate Ras and MAP kinases
341
Q

What is the function of activated Akt kinase?

A

contributes to T cell survival by inactivating pro-apoptotic proteins

342
Q

How do we activate Akt kinase in T cells?

A

activated PI3-kinase is recruited to TCR complex and generates PIP3 from PIP2
PDK1 is PIP3-dependent which phosphorylates/activates Akt kinase

343
Q

What protein is associated with LFA-1? So in what cell do you find it?

A

talin

T cell

344
Q

How does Lck activate MAP kinase? What transcription factor is synthesized and activated by the MAP kinase cascade?

A

Lack activates ZAP-70 upon Ag recognition
ZAP-70 phosphorylates LAT (adaptor protein)
LAT binds Grb-2 adaptor
Grb-2 docks the GTP/GDP exchange factor SOS
SOS converts Ras-GDP to Ras-GTP
Ras-GTP activates MAP kinase and ERK
cascade activates AP-1

345
Q

How does a T cell use PLCy1 to induce numerous cellular responses? How do we activate PLCy1?

A

activated LAT binds PLCy1 and it is activated by ZAP-70
PLCy1 hydrolyzes PIP2 to generate IP3 and DAG
IP3 stimulates increase in cytosolic Ca
DAG activates PKC
PKC and Ca ions induce numerous cellular responses

346
Q

What are two ways to generate AP-1?

A

calcium-calmodulin activates Nuclear factor of activated T-cells (NFAT)
Ras and Rac pathways

347
Q

What kinase is important in activating NF-kB

A

PKC

348
Q

What inactivates NF-kB?

A

IkB

349
Q

How does PKC activate NF-kB?

A

PKC phosphorylates IkB and activated NF-kB can go to the nucleus

350
Q

What transcription factors regulate gene expression in T cells?

A

AP-1 and NF-kB

351
Q

Why does TCR engagement alone cause anergy?

A

calcium-mediated signals induce the activation of NFAT only
NFAT alone elicits the expression of a distinct set of anergy-inducing genes which inhibit T-cell function at different levels and induce a status of T-cell unresponsiveness

352
Q

Iga and IgB on B cell surfaces are associated with what? How are Iga and IgB linked? What do they contain?

A

Membrane IgM and IgD
disulfide linked
contain ITAMs in their cytoplasmic tails

353
Q

What complex has Src-Syk activation? What does Src-Syk activation lad to?

A

BCRs!

activation of PLCy and Ras and Rac small GTPase which will be followed by activation of transcription factors

354
Q

The activation of what three transcription factors follow Src-Syk activation? What do these transcription factors promote?

A

NFAT, Nf-kB, AP-1

cell growth, differentiation, survival

355
Q

what are examples of some Src kinases in BCR signaling?

A

Lyn, Fyn, Blk

356
Q

What activates Src kinases? What do these activated Src kinases do? Where do you find them?

A

cross-linking by multivalent Ags brings together and activates Src kinases
which phosphorylate the ITAMs of Iga and IgB
BCR signaling

357
Q

What’s the point of phosphorylating the ITAMs of Iga and IgB? Where do you find them?

A

they provide a docking site for the tandem SH2 domains of the Syk tyrosine kinase
(remember Src kinases phosphorylate the ITAMs)
BCR signaling

358
Q

Who activate the Syk kinase? What are they?

A

Lyn, Fyn, Blk kinases activate Syk kinase-associated with ITAMs
these three things are Src kinases

359
Q

What enzymes are in charge of inhibitory signaling in lymphocytes?

A

E3 ubiquitin ligases

360
Q

What do inhibitory receptors do?

A

recruit and activate phosphates that counter signaling events induced by Ag receptors

361
Q

Ligand binding to an inhibitory receptor results in what?

A

phosphorylation of the ITIM tyrosine by a Src family kinase

362
Q

What do the phosphorylated ITIMs recruit?

A

SH2 domain containing tyrosine phosphatase that can attenuate immune receptor signaling

363
Q

TLRs, BCR, and TCR are all a part of the canonical or non canonical NF-kB signaling pathways?

A

canonical

364
Q

What are features of the canonical NF-kB signaling pathways?

A
  • rapid and transient
  • independent of protein synthesis
  • respond to numerous stimuli
  • diverse functions

HDM (3 decks)

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