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Microbio Immuno > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

According to Sir William Osler, what is humanity’s greatest enemy?

A

Fever

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2
Q

Who are considered the grandfathers of microbiology?

A

Pasteur and Koch

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3
Q

The period that spanned from 1875-1910 was known as what? Why?

A

First golden age of Microbiology bc many bacteria/pathogens were defined

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4
Q

Who discovered Penicillin? When?

A

Alexander Fleming, 1929

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5
Q

When was Penicillin-resistant Staph discovered?

A

1940

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6
Q

Who purified penicillin for mass production? When?

A

Howard Florey and Ernst Boris Chain in 1944

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7
Q

What resistant strain resulted from Tetracycline

A

Shigella

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8
Q

What resistant strain resulted from Erythromycin

A

Streptococcus

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9
Q

What resistant strain resulted from Methicillin

A

Staphylococcus

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10
Q

What resistant strain resulted from Gentamicin

A

Enterococcus

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11
Q

What resistant strain resulted from Vancomycin

A

Enterococcus

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12
Q

Name a nitrogen-fixing bacteria and its symbiotic plant

A

Rhizobia, legumes

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13
Q

Ruminants are bacteria that break down what?

A

Cellulose

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14
Q

What must be used to visualize bacteria?

A

Light microscope

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15
Q

What must be used to visualize viruses?

A

EM

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16
Q

What are the largest classes of microbes?

A

Protozoa and fungi

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17
Q

Most complex and diverse microorganism?

A

Parasite

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18
Q

C. albicans is a causative agent for what types of infection?

A

Thrush, vaginal yeast infection

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19
Q

Smallest independently living cell

A

bacteria

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20
Q

bacterial cell division

A

binary fission

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21
Q

Viruses ability to only infect certain types of cells is known as:

A

tissue tropism

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22
Q

Define symbiotic bacteria and give example

A

Benefit host. Gut bacteria that participate in digestion.

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23
Q

Define comensals and give example

A

Neutral relationship with host. Oral streptococci

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24
Q

Define parasitic relationship and give example

A

Harm to host. Tape worms

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25
Q

Define residents

A

Established niche at particular body site

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26
Q

Define transients

A

Acquired from environment and establish themselves briefly before being inhibited by residents or immune system.

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27
Q

Define carrier state and give example

A

Potentially pathogenic organism becomes a resident. S. mutans

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28
Q

Example given as a possible microorganism treatment for autoimmune disease

A

Tape worm - decreases inflammation

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29
Q

First microbes are acquired when

A

Mother’s vaginal canal

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30
Q

Principal bacteria genus in vagina

A

Lactobacilus

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31
Q

Principal bacterial genuses in male urethra

A

Similar to colon - Enterococcus, Mycobacterium, E. coli

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32
Q

Principal skin bacterium

A

S. epidermidis

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33
Q

Where might Staph aureus be found?

A

Nose, skin

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34
Q

At what body sites should potential pathogens not be found?

A

Blood, tissues, stomach, small intestine

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35
Q

Where on skin is bacterial flora concentration highest?

A

Moist areas - armpits, perineum, between toes

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36
Q

What type of bacteria can grow on sebum? Why are they not subject to bactericidal effects of skin lipids?

A

Gram-positive rods break down skin lipids to fatty acids. Proprionibacteria are also resistant.

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37
Q

Three principal bacteria types of mouth and pharynx

A

Streptococci first. Also Neisseria and Moraxella

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38
Q

Principal organism of stomach and small bowel

A

H. pylori

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39
Q

Where in body is the most abundant and diverse microbiota?

A

Colon

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40
Q

Primary site of carriage for pathogens

A

anterior nares

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41
Q

Three principal bacterial species in nasopharynx

A

Pneumoccoci, menigococi, Haemophilus

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42
Q

What protects accessory sinuses from colonization?

A

Epithelium and Eustachian tubes

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43
Q

Describe the microbiota of the urinary tract

A

Bladder and upper urinary tract are sterile. 1 cm of distal urethra has similar flora to perineum.

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44
Q

What influences concentration of vaginal flora

A

Hormonal fluctuations

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45
Q

At what points in life does the vaginal tract display mixed, nonspecific and relatively scanty microbiota

A

Pre-puberty and after menopause.

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46
Q

Why are lactobacilli able to thrive in the vagina during childbearing years?

A

High estrogen concentration causes deposition of glycogen (food source) in vaginal epithelium.

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47
Q

Explain exclusionary effect

A

Competition between normal flora and invaders. Pathogens may gain advantage from antibiotics killing normal flora.

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48
Q

What separates a pathogen from a commensal

A

Pathogen must cause damage to host

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49
Q

How might an S. pneumoniae infection in lungs cause damage?

A

Lungs fill with neutrophils - can’t exchange O2.

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50
Q

How does Diptheria affect cellular machinery

A

Toxin released inhibits host protein synthesis

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51
Q

Bacterial enzymes that degrade host tissues (3)

A

Collagenases, proteases, hydrolytic enzymes

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52
Q

Four ways pathogens can evade immune response

A

1) Attack immune effector cells
2) Secrete enzymes that degrade antibodies
3) Camouflage by changing surface structure
4) Hide inside host cells

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53
Q

Three methods of specimen collection? Which method presents highest quality, but also highest risk?

A

1) Direct - localized in sterile locations (CSF)
2) Indirect - Passes through site containing normal flora (Sputum, urine)
3) Site with normal flora - pathogen and nonpathogen are mixed (throat and stool)

1 is highest quality and risk*

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54
Q

How soon must isolation occur after sample collection?

A

3-4 hours

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55
Q

What bacterium requires special transport media to survive isolation?

A

Neisseria gonorrhoeae

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56
Q

Bacterial growth is a problem during isolation after collection. What normal flora is known to overgrow a sample?

A

Enteric gram-negative rods

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57
Q

2 functions of transport media

A
  • maintain neutral pH to prevent sample from drying out

- contain minimal nutrients to prevent overgrowth

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58
Q

A gram stain uses what material? What does it stain? what color

A

Crystal violet. Ribonuclear intracellular proteins. Purple

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59
Q

An acid-fast stain uses what material? What does it stain? Color?

A

Carol-fuchsin. Stains mycolic acid. Red

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60
Q

Two counter stains used in gram stain and acid-fast stain respectively?

A

Safranin, methylene blue

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61
Q

General composition of direct immunofluorescence

A

Fluorescein-labeled antibody binds to fixed antigen on slide

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62
Q

General composition of indirect immunofluorescence

A

Fluorescein-labeled immunoglobulin binds to fixed antibody which is bound to antigen on slide (antigen-antibody complex)

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63
Q

Potassium Tellurite is a selective media that inhibits growth of what

A

Gram-negative bac

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64
Q

Define differential media

A

Distinguishes between closely related

species of bacteria based on characteristics on media

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65
Q

What provides evidence for viral infection

A

cytopathic effect

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66
Q

Which bac form endospores

A

Gram +

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67
Q

Which bac have periplasm

A

Gram -

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68
Q

DNA structure in bacteria

A

Circular supercoiled double-stranded

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69
Q

What structure is more prevalent in bacteria than eukaryotes

A

Ribosomes

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70
Q

Granules that contain reserve materials

A

inclusion bodies

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71
Q

Are there sterols in a bacterial cell membrane?

A

No, except mycoplasma

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72
Q

What cell wall components vary by species

A

Polysaccharides and proteins

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73
Q

Principal components of peptidoglycan

A

Teichoic acid (may help with attachment or secretion) and lipotechoic acid (Anchors cell wall to membrane through glycolipids)

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74
Q

Alternating sugars in Peptidoglycan glycan chains. What crosslinks them

A

NAG and NAM. Peptide side chain and pentaglycine interbridge

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75
Q

Instead of lycine, what might be observed in Gram - cell wall

A

DAP

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76
Q

Lysozyme is present in what? What does it do?

A

Tears, saliva and mucus. Cleaves beta 1-4 glycosidic bonds betwen NAG and NAM

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77
Q

What does Penicillin do? How?

A

affects Gram +. Blocks cell wall synthesis by inhibiting transpeptidase enzymes that form crosslinks between glycan chains

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78
Q

Which Gram (-) cell wall component in impermeable? How does it allow things in and what?

A

Outer membrane has porins. Allows diffusion of hydrophilic solutes.

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79
Q

Role of periplasmic space

A

Contains proteins important for transport and chemotaxis

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80
Q

Describe LPS structure

A 
-O antigen polysaccharide side chain-linked
sugars- antigenic determinant
- Core Polysaccharide- similar between
species
-Lipid A (toxin)- phospholipid with
glucosamine instead of glycerol (located
in outer membrane)
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81
Q

What’s the smallest known bacterial species? How is it different and what does it do?

A

Mycoplasma. Sterol-containing membrane, no cell wall. Parasitizes host cells - causes walking pneumonia

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82
Q

Thick hydrophilic gel that surrounds bac cell? What’s it made of? Function?

A

Capsule (if discrete); slime layer (if amorphous). Made of polysaccharides, sometimes polypeptides. Protection from immune system

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83
Q

What environmental condition is required for S. mutans to form a capsule?

A

Sucrose

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84
Q

Function of fimbriae

A

Attachment

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85
Q

Pili functions

A

Attachment/DNA transfer

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86
Q

What species is known for sporulating?

A

Bacillus

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87
Q

Bacterial metabolism differences from eukaryotes

A
  • Faster (10-100x)
  • Can use many energy sources
  • No organelles so macromolecule synthesis is streamlined
  • Synthesis of Peptidoglycan/LPS
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88
Q

Three pathways for energy generation

A

1) E-M (glycolysis)
2) Pentose phosphate - generates NADPH* and ribose-5-phosphate for nucleotide synthesis
3) Krebs

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89
Q

“Strict anaerobe” is a designation based on the lack of what?

A

Catalase and superoxide dismutase

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90
Q

Obligate anaerobes and Aerotolerant anaerobescan only use___ for energy

A

Fermentation (substrate-level phosphorylation)

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91
Q

Enzyme that introduces supercoils in replication

A

DNA gyrase

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92
Q

Enzyme that relaxes upercoils in replication?

A

Topoisomerase

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93
Q

Prok. replication is what two things

A

Bidirectional, semi-conservative

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94
Q

What gene controls homologous recombination

A

recA

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95
Q

Define transduction

A

Bacterial DNA transfered via phage (lytic and lysogenic)

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96
Q

What binds to promoter

A

RNA polymerase

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97
Q

Two components in TCS

A

Protein kinase, response regulator

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98
Q

First immune response

A

Innate

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99
Q

Innate vs. Adaptive: response time and specificity?

A

Innate: fast, non-specific.
Adaptive: Delayed, antigen-specific

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100
Q

Two lines of white blood cell hematopoieses

A

Myeloid, lymphoid

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101
Q

With age, hematopoiesis occurs in what types of bones chronologically?

A

Young -> old:

  • tibias
  • femurs
  • ribs
  • sternum
  • vertebrae

Long bones -> flat bones

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102
Q

Most abundant granulocyte

A

Neutrophil

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103
Q

Involved in inflammatory and allergy (granulocyte)

A

basophil

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104
Q

Granulocyte involved in parasite/allergy

A

eosinophil

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105
Q

Two general cell types from myeloid lineage?

A

Phagocytes, granulocytes

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106
Q

Phagocyte that can activate naive T cells

A

Conventional dendritic cells

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107
Q

Only granulocytic myeloid cell that isn’t considered a granulocyte? What’s its role?

A

Mast cell - parasite/allergy

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108
Q

What turns the immune response off?

A

Regulatory T cell

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109
Q

Are memory cells associated with T or B cells?

A

Both

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110
Q

First responder

A

Neutrophil

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111
Q

Three types of T cells

A

Cytotoxic (CD8)
Helper (CD4)
Suppressor/regulatory

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112
Q

B cells differentiate into what that produce what?

A

Plasma cells, antibodies

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113
Q

NK cells are involved with what immune system?

A

Innate

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114
Q

Molecule capable of

inducing an immune response

A

Antigen

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115
Q

How many antigens does an antibody recognize?

A

Just 1, specific.

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116
Q

Activation of receptors occurs where most often?

A

Extracellularly

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117
Q

Signaling molecules (2)

A

Chemokines, cytokines

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118
Q

4 functions of cytokines

A

1) Activation/proliferation
2) Inflammation
3) Motility
4) Immunosuppresion

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119
Q

Organized clusters

A

Follicles

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120
Q

Follicles grouped together

A

Patches

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121
Q

Encapsulated follicles

A

Organs

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122
Q

Two structures of primary lymphoid tissue

A

Bone marrow, thymus

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123
Q

T cell arises in _____ and matures in ____

A

Bone marrow, thymus

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124
Q

4 types of MALT

A

Nasopharynx, bronchial, gut, skin

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125
Q

Outline infection response

A

1) Phagocytosis by DC
2) Presentation to T cells in lymph node
3) Clonal expansion of T cell
4) Migration of T cell to infection

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126
Q

Non-inducible immune components

A

Skin/mucus/commensal bacteria (physical)

Lysozyme, antimicrobial peptides (a and b-defensins, cathelicidin)

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127
Q

Inducible immune components

A

Innate immune cells, neutralizing antibodies (secetory IgA)

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128
Q

4 bacterial PAMPs

A

LPS, peptidoglycan, CpG DNA, flagellin

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129
Q

2 viral PAMPs

A

dsRNA, ssRNA

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130
Q

2 fungal PAMPs

A

Chitin, zymosan

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131
Q

6 classes of DAMPs

A
  • Complement (C3b, C4b)
  • ROS
  • Stress-induced molecules
  • Metabolites
  • Nucleic acids
  • Exogenous (alum, silica, asbesots)
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132
Q

What TLRs are bacteria-associated? Virus associated?

A

Bac: 1,2,4,5,6,9

Virus: 3, 7, 8

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133
Q

TLR2, 4, and 5 roles

A

2 - peptidoglycan
4 - LPS
5 - flagellin

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134
Q

TLRs are highly expressed in what 3 cells

A

DC, Monocytes/mac, neutrophils

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135
Q

Inflammasomes are formed from what? What does this lead to? This activation can also lead to what?

A

Nod-like receptor complexes. Caspase 1 activation to activate IL-1 and IL-18. NLR activation can also lead to apoptosis

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136
Q

What receptors recognize viral RNA? Activation leads to production of what?

A

RIG. IFN-a and IFN-b

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137
Q

Carbohydrate-based DAMPs and PAMPs are recognized by what?

A

CLRs

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138
Q

Scavenger receptors bind to what?

A

lipids

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139
Q

Collectins are comprised of what two components? Where are they found? What can they do once activated?

A

1) Collagen and lectin
2)blood
3:
a) activate complement
b) Phagocytosis
c) agglutination

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140
Q

4 outcomes of complement activation

A

1) Pathogen destruction
2) Pathogen opsonization
3) Clearance of immune complexes
4) Creation of peptides to help inflammatory response

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141
Q

What starts classical complement pathway

A

recognition of antigen-antibody complexes

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142
Q

What starts lectin complement pathway

A

mannose-binding ligand bound to pathogen

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143
Q

What activates alternative complement pathway

A

Binding of C3 to pathogen

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144
Q

The product of all 3 complement pathways that begins pathogen destruction/inflammtion

A

C3b

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145
Q

Which complement pathway is delayed? Why?

A

Classical, bc antibodies specific to antigen must be made.

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146
Q

Cleavage of C3 yields what 2 products? What are their roles?

A

C3a: inflammation
C3b: opsonization/phagocytosis

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147
Q

What leads to production of membrane attack complex (MAC)? What does mac do?

A

C5a. Lysis of microbe

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148
Q

What term describes engulfment of fluid and macromolecules? What process is similar, but receptor-mediated?

A

Macropinocytosis, Clathrin-Mediated Endocytosis

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149
Q

What method of pathogen capture requires a surface receptor

A

phagocytosis

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150
Q

Trace the process of phagocytosis

A

Binding of microbe to receptor, microge ingested into phagosome

  • Phagosome fuses with lysosome
  • bacteria killed by lysosomal enzymes and ROS.
  • By-products can be uses as PAMPs or expelled
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151
Q

Cell recycling

A

Autophagy

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152
Q

A membrane-bound Ig is known as? Non-membrane-bound?

A

Bound: BCR
Non: antibody

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153
Q

How many different kinds of heavy and light chains can a B cell produce?

A

1

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154
Q

What attaches a heavy and light chain

A

disulfide bond

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155
Q

What connects two heavy chains?

A

2 disulfide bonds

156
Q

Enzyme used to digest antibody

A

Papain

157
Q

Enzyme digestion of Ig yields what two fragments? Which is involved in opsonization? Which is involved with Ag binding?

A

Fc - constant, opsonization

Fab - variable (distal half), Ag binding

158
Q

The hinge region of an Ig is what

A

linking of heavy chains

159
Q

Most variable hypervariable region? What’s the purpose of hypervariable regions?

A

CDR3, antigenic diversity

160
Q

The constant region can give rise to different what?

A

Isotypes

161
Q

Two light-chain isotypes? which is more common in humans?

A

kappa and lambda. Kappa is

162
Q

Heavy chain isogypes

A

IgM, IgD, IgG, IgE, IgA

163
Q

What isotype is first produced upon encounter with Ag

A

IgM

164
Q

Which structural isoform has a transmembrane domain?

A

Membrane-bound Ig

165
Q

Where are Membrane-bound Ig(mig) found

A

B cell plasma membrane (BCR)

166
Q

Where are secreted ig (sig) found

A

blood

167
Q

Where are secretory ig (Sig) found

A

secretions (tears, mucus, saliva)

168
Q

Most common polymeric immunoglobulins? (2) What keeps them together?

A

IgM pentadimer
IgA dimer

J chain

169
Q

Receptor activation and subsquent intracellular phosphorylation results in what 3 things

A

1) gene transcription
2)actin rearrangement
or
3) mediator release

170
Q

What transmembrane proteins are associated with BCR? What do they do

A

Ig-alpha, Ig-beta. Activate ITAMs

171
Q

Variable regions are made up of what gene segments? Which chain is missing one and what is it?

A

Variable (V), Diversity (D) and Joining (J)

Light chain does not have D

172
Q

What occurs in every naive B cell

A

VDJ recombination

173
Q

Is vdj recombo permanent

A

yeah

174
Q

Antigenic determinant is called:

A

epitope

175
Q

What specificially do antigens tend to bind to

A

CDR3 of Ig heavy chain

176
Q

The strength of the non-covalent
association between one
antigen-binding site and one
antigenic epitope

A

affinity

177
Q

The overall strength of the bond
between a multivalent Ab and
multivalent Ag.

A

avidity

178
Q

Define cross reactivity

A

when one epitope is shared by two Ag, or when two epitopes

on separate Ag are similar in structure.

179
Q

Outline 2 stages of B cell development

A

1) Maturation - begins in bone marrow and ends in periphery. *B cell is still naive here.

2) Differentiation – Begins once a B cell recognizes its specific Ag, ends
with the generation of Ag-specific plasma cells and memory B cells.

180
Q

Outline stages of B cell maturation

A
  • Hematopoietic stem cell
  • Multipotent progenitor cell
  • Common lymphoid progenitor
  • Progenitor B cell (pro-B cell)
  • Precursor B cell (pre-B cell)
  • Immature naïve B cell
  • Mature naïve B cell
181
Q

What’s the first hematopoietic cells that are recognizable as B cells? What’s the status of Ig genes here?

A

Pro. Ig genes still in germline configuration.

182
Q

Pre B cells are marked by what 2 things?

A

VDJ recombination is complete.

-Late pre B cells will produce membrane-bound IgM and Ig-alpha/Igbeta

183
Q

2 things happening in Immature B cell stage

A
  • Development of central tolerance

- Immature B cells get last chance to rearrange Ig loci via receptor editing.

184
Q

What percentage of immature B cells survive positive/negative selection?

A

2-5%

185
Q

Where does a transitional type 1 traditional B cell go?

A

red pulp then PALS

186
Q

What’s expressed by transitional type 2 B cells? What do they become?

A

Both IgM and IgD.

Become follicular B cells or marginal zone B cells

187
Q

3 points for mature B cells

A

1) express both Igm and IgD
2) can’t undergo further VDJ rearrangements
3) Considered naive

188
Q

Distinguish between two types of B cell antigens

A

1) T-dependent - usually follicular B cells

2) T-independent - usually marginal zone B cells

189
Q

End result of T-dependent B cell activation?

A

Isotype switched (to different Ig), high-affinity antibodies, memory B cells

190
Q

End result of T-independent B cell activation?

A

Mainly IgM, low-affinity antibodies, short-lived plasma cells

191
Q

T-dependent involves what kind of antigen

A

Protein

192
Q

Where does B cell activation occur?

A

Lymphoid tissues

193
Q

3 steps of B cell activation

A
  • Antigen binding
  • Costimulation - activated Th effectors
  • Cytokine help (Released from T cell)
194
Q

Outline the 3 signals in B cell activation

A

Signal 1 - Ag binds to BCR. Signal transmitted via Igalpha/Igbeta. Precedes T cell binding

Signal 2 - Interaction with Ag-specific Th cell; TCR (T) binds to MHC-II (B) and CD40L (T) binds to CD40 (B)

Signal 3 - Cytokine stimulation by Th cell. Involvement of IL-4, IL-2, IL-5 and IL-10. Macrophages and DC also contribute cytokines

195
Q

During clonal expansion, a secondary follicle becomes what?

A

Germinal center

196
Q

Three events within germinal centers

A

1) Somatic hypermutation
2) Affinity maturation
3) Isotype switching

197
Q

Germinal centers give rise to what two types of cells?

A

Long-lived memory B cell
or
Long-lived class switched plasma cell (IgA, IgG, or IgE)

198
Q

4 functions of antibodies

A
  • neutralization
  • classical complement activation
  • opsonization
  • antibody-dependent cell-mediated cytotoxicity
199
Q

Outline antibody neutralization

A

Pathogens that are usually endocytosed after binding to cell receptor are blocked from attachment via the action of binding antibodies that provide steric interference and induce capsid stabilization and structurral changes

200
Q

4 antibodies that activate classical complement

A

IgM, IgG1, IgG2, IgG3

201
Q

2 antibodies involved in opsonization

A

IgG1, IgG3

202
Q

Outline antibody-dependent cell-mediated cytotoxicity and examples

A

Antibody binds large pathogen and presents to NK cells, which activates them to release granules to kill pathogen.

Pathogen/antigen undergoes this process bc it’s too big for conventional phagocytosis.

E.g. Parasitic worms, virally infected cells, tumor cells

203
Q

How was MHC discovered

A

Due to importance during tissue rejection

204
Q

Where is MHC encoded

A

HLA complex, chromosome 6

205
Q

3 qualities of MHC genes

A

-polygenic
0-polymorphic
-codominantly expressed

206
Q

On what cells are MHC Class I found?

A

All nucleated cells

207
Q

To what does MHC Class I present? What kind of peptides are presendted?

A

CD8+ T cells. Endogenous

208
Q

On what cells are MHC class II found

A

APCs

209
Q

What kind of peptides are displayed by MHC Class II? What do they present to?

A

Exogenous. CD4+ T cells

210
Q

Difference in structure between MHC I and II

A

I: 3 alpha subunits and B2-microglobulin subunit

II: 2 alpha subunits, 2 beta subunits

211
Q

MHC I or II, larger binding region?

A

II

212
Q

Antigen processing involves:

A

• The breaking down of macromolecules into smaller fragments in
order to prepare them for presentation to a T cell

213
Q

4 pathways of Ag processing

A

Exogenous, endogenous, cross-presentation, autophagic

214
Q

Autophagy Ag processing switches from _ to _

A

Endogenous to exogenous pathway

215
Q

Cross-presentation Ag processing switches from _ to _

A

Exogenous to endogenous pathway

216
Q

Rank APCs from high to low levels of MHC II

A

DC, macrophage, B cell

217
Q

Rank APCs from high to low level of constitutive costimulatory molecules

A

DC, Macrophage, B cell

218
Q

Rank APCs from high to low capability of cross-presentation

A

DC, Macrophage, B cell

219
Q

What APC activates naive T cell

A

DC

220
Q

What APCs activate effector and memory T cells

A

all of them

221
Q

Macrophage APC is involved with what type of immunity

A

cell-mediated

222
Q

B cell APC is involved with what type of immunity

A

humoral

223
Q

When is a dendritic cell most expressing Fc receptors

A

in tissue, resting, unactivated

224
Q

Trace exogenous pathway

A
  • Endocytosis
  • antigen degradation.
  • assembly of MHC II molecules (assembled in ER, travel to golgi then lysosome)
  • Complex takes endosome to surface to present to CD4
225
Q

What’s the MHC II Ag binding issue? How’s it solved?

A

Invariant chain blocks binding. Invariant chain is cleaved in vesicle, leaving CLIP FRAGMENT. CLIP blocks binding but it’s released via action of HLA-DM. Then antigen can bind

226
Q

Trace endogenous pathway

A
  • Proteins degraded by proteasome and transported to ER via TAP.
  • MHC I loaded in ER
  • Complex transported to golgi then membrane to present to CD8
227
Q

Outline cross-presentation

A

APC ingests and processes virally infected cell. Viral proteins
enter the cytosol and is process via endogenous pathway to
activate a CD8 T cell via MHC I.

228
Q

Trace Autophagic pathway

A
  • Collection of cellular degradable components
  • Completion of autophagosome
  • Fusion of autophagosome and lysosome
  • Degradation
229
Q

Two classes of TCR and their characteristics

A

1) alphabeta (90%) - recognize MHC/Ag and reside in secondary lymphoid tissue.
2) gammadelta (10%) - recognizes ligands. Intraepithelial tissues

230
Q

TCR complex is what with respect to membrane

A

spanning

231
Q

What happens in T cell after antigen presentation

A

TCR complex and coreceptors are clustered within membrane lipid rafts by antigen recognition.
Then Lck protein (intracellular) phosphorylates tyrosines in ITAMs

232
Q

Do TCR do VDJ recombo

A

yes

233
Q

4 ways that T cell development is similar to B cell development

A
  • Begins in bone marrow
  • V(D)J recombination of variable region of TCR leads to antigenic diversity
  • At one point cells express both CD4 and CD8 (double positive)
  • Undergo positive and negative selection
234
Q

4 ways that T cell development is different from B cell development

A

• Begins with NK/T precursor cell
• After leaving the bone marrow thymocytes move to thymus to finish
development
• MHC molecules are involved in the establishment of central tolerance
• No possibilities for somatic hypermutation

235
Q

What TCR is involved in cell adhesion? What TCR is an IL-2 receptor?

A

CD44, CD25

236
Q

RAG expression is associated with what?

A

VDJ recombination

237
Q

Stages of T cell differentiation

A
  • Stem cell
  • Pro-T
  • Pre-T
  • Double positive
  • Single positive (immature)
  • Mature T cell
238
Q

At what T cell development stage is has cell moved to thymus?

A

Pro-T

239
Q

At what T cell development stage is IL-2 receptor expressed?

A

Pro-T

240
Q

At what T cell development stage does Beta chain rearrangement begin to occur?

A

Pro-T

241
Q

What T cell development stage is a checkpoint? What does this mean?

A

Pre-T. Determination of viability of T cell

242
Q

At what T cell development stage does first semblance of a TCR appear

A

Pre-T

243
Q

At what T cell development stage does alpha chain begin to undergo VDJ recombination?

A

End of Pre-T

244
Q

At what T cell development stage does positive/negative selection occur?

A

Double positive

245
Q

What T cells are negatively selected?

A

Self-reactive

246
Q

Outline the mechanics of negative T cell selection

A

MHC presentation to a T cell. If affinity is too strong, it’s negatively selected

247
Q

At what T cell development stage doesw a T cell become Cd4 or Cd8

A

Single positive (immature)

248
Q

What’s the distribution of CD4 to CD8 in body

A

2x CD4

249
Q

To where does a mature T cell travel?

A

Secondary lymphoid organ; usually lymph node

250
Q

What cytokine does a naive T cell release to become effector?

A

IL-2

251
Q

CD28 coreceptor binds to what on APC?

A

B7

252
Q

Effector function of CD4

A

Activation of macrophages, B cells. Inflammation

253
Q

Effector function of CD8

A

Killing of infected cells, macrophage activation

254
Q

Four types of Th cells

A

Th1, Th2, Th17, iTreg

255
Q

Name cytokine involved with differentiation to Th1

A

IFN-gamma

256
Q

Name cytokine involved with differentiation to Th2

A

IL-4

257
Q

Name cytokine involved with differentiation to Th17

A

TGF-beta

258
Q

Name cytokine involved with differentiation to iTreg

A

TGF-beta

259
Q

Function of Th1

A

T help for Tc responses against intracellular pathogens. Classical macrophage activation.

260
Q

Function of Th2

A

T help for B cell responses against extracellular pathogens (humoral immunity).

261
Q

Function of Th17

A

Combats infections of skin and mucosa. Autoinflammation, neutrophil recruitment, barrier function.

262
Q

Function of iTreg

A

Peripheral tolerance

263
Q

3 cytokines needed for CD8 T cells

A

IL-2, IL-12, Type 1 IFN

264
Q

Type 1 mucosa and where it’s found

A

Single layer of columnar epithelial cells in the gut and lungs

265
Q

Type II mucosa and where it’s found

A

Mnany layers, top layer is squamous epithelial cells - mouth and nose

266
Q

Main Ab of type I mucosa

A

SIgA

267
Q

MAin antibody of Type II mucosa

A

IgG

268
Q

4 non-inducible defenses of GI tract

A
  • Acidity
  • Motility
  • Mucus layer and underlying glycocalyx
  • tight junctions
269
Q

what secretes mucin

A

goblet cell

270
Q

In what layer are immune cells of GALT

A

lamina propria

271
Q

What DC is important in inducing Treg and sampling gut epithelial tissue.

A

CD103+

272
Q

What type of mucosa is associated with NALT? BALT?

A

Type II, Type I

273
Q

Adaptive response in the gut is usually biased toward what Ab

A

SIgA

274
Q

If inflammatory respone is needed in gut, what Th are activated?

A

Th1/Th17

275
Q

What kind of immunity is involved with intracellular vs extracellular pathogens?

A

Cell-mediated, humoral

276
Q

Is SigA antigen-specific?

A

yes, but can bind to adhesion molecules found on many pathogens

277
Q

What is SIgA’s role in complement activation?

A

Does not activate complement well

278
Q

What Ig is notably very resistant to host and microbial proteases?

A

SIgA

279
Q

Drawback to initiating inflammatory response at mucosal surfaces?

A

Inflammatory cytokines (TNF-alpha) can disrupt epithelial cell tight junctions

280
Q

What lymphoid tissue has little to no B cells?

A

SALT

281
Q

2 parameters of pathogenicity

A
  • Bacterial species is able to cause disease

- Human host must be susceptible

282
Q

Lowly virulent bacterium in oropharyngeal flora

A

S. salivarious

283
Q

Moderately virulent bacterium in colon. Harmless there, but where can it cause acute infection?

A

E. coli. Bladder

284
Q

Highly virulent bacterium that causes whooping cough

A

B. pertussis

285
Q

5 modes of infection transmission

A
  • airborne
  • food borne
  • vector borne
  • water borne
  • blood borne
286
Q

Three stages to establish infection

A
  • adherence
  • colonization
  • damage
287
Q

Pili role in bacterial entry-adherance

A

Bind to cell-specific receptors (mannose, fibronectin) - attach cell and pull closer so second adhesin can bind host receptor

288
Q

3 bacteria that use sIgA protease to cleave SIgA hinge region

A

N. gonorrhea
H. influenza
S. pneumonia

289
Q

What keeps iron levels low in EC fluid? Why?

A

Lactoferrin, to prevent bacterial growth

290
Q

How do pathogens sequester iron

A

Production of siderophores to compete with human proteins for Fe

291
Q

3 methods of evasion from macrophages

A
  • hide in host cells
  • avoid contact
  • inhibition
292
Q

Three varieties of pathogens

A

Extracellular- not able to invade host cells
• Facultative intracellular bacteria- can invade host cells, but can also survive in extracellular
environment
• Obligate intracellular bacteria- require host cells for survival

293
Q

Good example of obligate intracellular bacterium

A

Chlamydia

294
Q

What class of pathogen can escape the phagosome

A

facultative intracellular bacteria

295
Q

What class of bacteria utilizes a type III secretion system to inject effector proteins

A

Gram (-)

296
Q

What do effector proteins do?

A

Promote invasion of host/suppress host cell defenses

297
Q

After being phagocytosed, what does a bacterium do to survive? what’s it known as?

A

Invasion - process by which bacteria modifies endosome, OR escapes it, replicates in cytoplasm, OR blocks endosome-lysosome fusion

298
Q

What describes efficiency of a pathogen?

A

Number of organisms required to cause disease

299
Q

What structure might a bacterium use to prevent phagocytosis? How does this work?

A

Capsule can interfere with complement deposition; capsule binds Factor H to degrade C3b

300
Q

What’s a notable area not patrolled by phagocytes

A

bladder

301
Q

4 ways to avoid contact with phagocytes

A
  • invade locations not surveilled by phagocytes
  • Avoid inducing inflammatory response
  • inhibit phagocyte chemotaxis (Streptococcus using Streptolysin).
  • Bind host molecules to hide antigenic surface (T. pallidum (Syphilis))
302
Q

3 ways manipulating pamps and amps helps bacteria’s survival

A

1) Poorly recognized lipid A portion
2) Lipid A modification affects surface charge
3) Alter cell wall teichoic acids

303
Q

How do bacteria avoid innate and adaptive immunity? give examples

A

Antigenic variation

  • change pili structure (Neisseria)
  • Vary M proteins (STrep)
  • Change VSG coat (T. brucei)
  • Change coat proteins (P. falciparum - Malaria)
  • Mutated hemagglutinin and neuraminidase (Flu)
304
Q

Induction of host apoptosis examples

A
  • Strep and Staph make streptolysin and leukocidin respectively to target neutrophils.
  • Psudomonas makes Exotoxin A to kill macrophages
305
Q

5 ways bacteria cause host injury

A

• Exotoxins- bacterial secreted proteins- local and systemic if in blood
Endotoxin- lipid A portion of LPS of Gram-negative bacteria- stimulates cytokine release (inflammation)
• Hydrolytic enzymes- (i.e. collagenase or hyaluronidase)- facilitate tissue invasion
• Superantigen exotoxins- stimulate massive cytokine secretion (toxic shock)
• Inflammation- prolonged immune response to bacteria can damage host tissues (periodontal disease)

306
Q

Do exotoxins bind to specific cell receptors

A

yes

307
Q

Subunits of exotoxins and their roles

A

B and A
B binds surface receptor
A gets transported by endocytosis

308
Q

What causes loss of cell integrity and leakage through pore? What would the immune system recognize this as?

A

Membrane active exotoxins that create pores in hose cell membranes (S. aureus, Group A Strep, E. coli)

DAMPs

309
Q

Very prominent endotoxin that causes fever through release of what

A

Lipid A toxin of LPS - phospholipid with glucosamine instead of lycerol. Induces fever through release of IL-1 and TNF from macrophages

310
Q

Action of superantigen. What do they cause?

A

Superantigens are polyclonal stimulators of T cells; they bind to MHC II to activate T cells. S. aureus and Group A strep do this to cause Toxic shock syndrome

311
Q

Principal physiological function of immune system

A

defense against pathogens

312
Q

Three high-affinity receptors on bacterial cell

A

1) Mannose
2) Mac-1 Integrin (Opsonized with complement proteins)
3) Scavenger receptor - non-mannose

313
Q

Define respiratory burst

A

Conversion of O2 into ROS

314
Q

Chemostatic neutrophil factors

A

IL-8, IFN-gamma, C5a

315
Q

How can neutrophils kill microbes without ROS (4)

A
  • degranulation
  • defensins
  • myeloperoxidase
  • neutrophil extracellular traps (NETs)
316
Q

Ab involved in B cell neutralization

A

IgG, IgM, IgA

317
Q

Ab involved in opsonization and Fc receptor-mediated phagocytosis

A

IgG

318
Q

Ab involved in phagocytosis of C3b-coated bacteria

A

IgM, IgG

319
Q

CD4 make what inflammatory cytokines. When they make these, what are they called

A

IFN-gamma and TNF-alpha. Now called Th1 cells

320
Q

CD4 make what B cell promoting cytokines? When they make these, what are they called?

A

IL-4, IL-5 IL-10

Th2

321
Q

3 intracellular pathogens

A

-mycobacteria
L. monocytogenes
Salmonella

322
Q

What cytokines are secreted by NK and why

A

IFN-gamma for macrophage and Th1 development

323
Q

Outline T cell vs intracellular microbes

A

CD4 binds APC, releases IFN-gamma. Bacteria are liberated from phagolysosome into cytoplasm. CD8 binds APC and kills it

324
Q

CD4 are _____ t cells

A

helper

325
Q

TH1 CD4 produce what and promote what

A

IFN-gamma and TNF-alpha, cell-mediated immunity

326
Q

TH2 CD4 produce what and promote what

A

IL-4, antibody-mediated (humoral)

327
Q

CD8 are called ___ t cells and secrete what? Particularly important in what kind of immunity?

A

Effector. Anti-viral (IFN-gamma, TNF-alpha)

328
Q

Define inflammation

A

A non-specific response to infection or injury that is characterized by
enhanced accumulation of immune cells and plasma proteins.

329
Q

5 marks of inflammation

A 
Redness (rubor)
Heat (calor)
Swelling (tumor)
Pain (dolor)
Loss of function (functio laesa)
330
Q

Primary difference between acute and chronic inflammation? What type of immunity is involved in each?

A

Acute - innate
Chronic - adaptive

Chronic experiences ongoing stimulus

331
Q

3 proinflammatory cytokines

A
  • TNF-alpha
  • IL-1Beta
  • IL-6
332
Q

3 inflammatory mediators involved in vasodilation

A

Histamine, bradykinin, leukotrines

333
Q

What causes histamine release by mast cells?

A

Interaction with microbes, ligation of C5a, or interaction with IgE

334
Q

What are prostaglandins derived from? What do they do?

A

Derived from cell membrane phospholipids - involved in inflammatory response

335
Q

Complement protein involved in monocyte/neutrophil recruitment

A

C5a

336
Q

Complement proteins that can trigger mast cell degranulation

A

C3a, C5a

337
Q

Two cytokines involved in turning off inflammation

A

IL-10, TGF-beta

338
Q

Treatment for acute inflammation

A

Ice/elevation, NSAIDS

339
Q

Treatment for chronic inflammation

A

Steroids, immunosuppressants, anti-leukotrienes

340
Q

Outline first step of neutrophil migration to infection

A

Tethering/rolling - slows leukocyte down within post-capillary venule. Halted by selectins on endothelial surface that bind cell.

341
Q

Affinity of selectins?

A

low

342
Q

What do selectins recognize?

A

sialylated crabohydrates

343
Q

Three types of selectins and where they’re found

A

P and E on endothelial cells; L on leukocytes/lymphocytes

344
Q

Activator for P selectin?

A

Histamine/thrombin

345
Q

Activator for E selectin

A

Cytokines, microbial byproducts

346
Q

Outline second step of migration to infection

A

Integrin activation:

Chemokines from infected tissue signal to leukocyte. Integrin affinity becomes high to bind to endothelium

347
Q

2 notable integrins and their selectin ligands

A

LFA-1 (I) : ICAM-1 (S)

VLA-4 (I) : VCAM-1(S)

348
Q

Outline third step of migration to infection

A

Adherence:

Integrin/selectin binding. Leukocyte stops rolling. cytoskeleton rearrangement

349
Q

Outline fourth step of migration to infection

A

Migration:

Leukocyte diffuses into tissue to follow chemokine scent after cytoskeleton rearrangement and tight junction loosening

350
Q

8 prominent phyla of oral bacteria

A
  • firmicutes
  • fusobacteria
  • bacterodetes
  • actinobacteria
  • proteobacteria
  • spirochaetes
  • synergistetes
  • TM7
351
Q

What bacterium is found in every location in the mouth? What two are on every tooth surface?

A

S. mitis

S. anguinis and S. gordonnii

352
Q

Most common species in plaque

A

Mitis group Strep:

S. sanguinis, S. gordonii
S. oralis

353
Q

Minor species in healthy plaque

A

Mutans group Strep:

S. mutans and S. sobrinus

354
Q

3 early colonizers of plaque and a brief role

A

Strep (produce H2O2, co-aggregation)

  • Veillonella - maintains neutral pH by metabolizing lactic acid
  • Actinomyces - coaggreation
355
Q

Late colonizers of plaque

A
  • F. nucleatum (Removes oxygen)
  • P. gingivalis - strict anaerobe
  • T. denticola
  • Prevotella
356
Q

NOn-specific plaque hypothesis

A

Caries result from perturbation in bacterial populations due to disruption in enviornment. Not a specific bacteria

357
Q

As dental caries progress, bacterial diverstiy _________

A

decreases

358
Q

4 virulence factors of S. mutans

A
  • acidogenic
  • acid tolerant
  • glycosyltransferases
  • glucan binding proteins
359
Q

What serotype of S. mutans is most common in oral cavity

A

C

360
Q

Ubiquitous commensal that antagonizes bad oral species

A

S. sanguinis

361
Q

Socransky’s Red complex (3) - associated with periodontal disease

A

P. gingivalis
T. forsythia
T. denticola

362
Q

What inhibits host immune response to oral flora? What’s the morphology and oxygen demand of this org.

A

P. gingivalis. Gram - rod. Obligate anaerobe

363
Q

Distingujish between disinfection and sterilization

A

D; kills everything except spores

S: kills everything

364
Q

Disinfectant that can be used on living tissue

A

Antiseptic

365
Q

Prevention measures for contact with microorgs.

A

Asepsis

366
Q

Hospital-acquired infections

A

Nosocomial

367
Q

A higher MIC would mean what

A

Non-sensitivity and resistance to microbial growth

368
Q

4 general targets of antibiotics

A
  • cell wall synthesis
  • protein synthesis (70s ribosome)
  • Nucleic acid synthesis/folate synthesis
  • cell membrane integrity
369
Q

B- lactams inhibit what

A

Cell wall synthesis (penicillin)

370
Q

How do b-lactams work?

A

Bind to transpeptidases and interfere cross-linking of amino acid side chains

371
Q

How do non-B lactams work

A

inhibit assembly of peptidoglycan by binding to AA side chains to prevent cross linking (Vancomycin)
*Treatment for MRSA

372
Q

What inhibits AA synthesis

A

Chloramohenicol

373
Q

What inhibits 50s and 30sribosome

A

Aminoglycosides

374
Q

What inhibits 30s ribosome

A

tetracylcine

375
Q

What inhibits RNA polymerase

A

Rifampin

376
Q

What breaks DNA

A

Metronidazole

377
Q

What inhibits DNA topoisomerase and gyrase

A

Quinolones

378
Q

What inhibits folate synthesis

A

Sulfonamides, Trimethoprin

379
Q

What targets fungal cell membrane

A

amphotericin

380
Q

what targets gram neg outer membrane

A

polymyxins

381
Q

5 mechanisms of antibiotic resistance

A

-efflux pump
-blocked penetration
altered target
-enzymatic inactivation
genetic resistance

382
Q

Why can’t methicilin bind MRSA?

A

Altered PBPs

383
Q

Treatment for MRSA?

A

Non-B-lactams (Vancomycin, Teicoplanin)

384
Q

Why can’t Vancomycin bind VRSA?

A

Altered peptide

385
Q

Give example of enzymatic inactivation

A

B-lactamase is bacterial enzyme that breaks B-lactam ring

Microbio Immuno (1 decks)

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