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Unit 4 > Immunology > Flashcards

Immunology Flashcards

1
Q

What cells are included in granulocyte?

A

Neutrophils/eosinophils/basophils

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2
Q

What kind of cells are included under myeloid cells?

A

Monocyte/granulocyte/erythrocyte/platelet

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3
Q

What kind of cells are included under lymphoid stem cells?

A

Plasma cells/T cells/natural killer cells

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4
Q

What is the normal white blood cell count?

A

4,000 to 10,000/uL

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5
Q

What cells are included in leukocyte (WBC)?

A

Granulocyte/T cell/monocyte

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6
Q

What causes hypereosinophilia?

A

NAACP

Neoplastic/asthma/allergic reaction/collagen vascular disease/parasites

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7
Q

Histamine increase ___ production in the stomach and causes ___?

A

Gastric acid/peptic ulcer

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8
Q

Where are basophil and mast cells found in the body?

A

Basophil—>mature in bone marrow and stay in blood

Mast cell—>mature in tissues and stay in tissues

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9
Q

How does dendritic cell present antigens to B and T cell?

A

It carries it through lymphatic system to the lymph nodes

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10
Q

Where do B and T cell mature?

A

B—>bone marrow

T—>thymus

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11
Q

Which cell’s nuclei has a clock face appearance?

A

Plasma cell

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12
Q

What are primary and secondary follicles in the lymph nodes?

A

B cells reside in there
Primary—>dense center (nonactive)
Secondary—>pale center (active)

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13
Q

Where are B/T/plasma cells in the lymph nodes?

A

B—>cortex
T—>paracortex
Plasma cell—>Cord of the medulla

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14
Q

Where do B/T cells enter the lymph node?

A

High endothelial venules (in paracortex)

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15
Q

Why don’t you biopsy testicular cancer?

A

Because testicle and scrotum drains into different lymph nodes
Testicle—>periaortic
Scrotum—>superficial inguinal

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16
Q

Where do the lymph of right arm and head drain into?

A

Right lymphatic duct—>right subclavian vein

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17
Q

What cells are in red pulp/white pulp/PALS in the spleen?

A

Red—>RBC
White—>WBC
PALS—>T cells

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18
Q

Why is pt with asplenia is more susceptible to encapsulated bacteria?

A

Spleen makes IgM—>activate complement

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19
Q

What are the 3 signs of asplenia?

A

Howell-Jolly bodies/target cell/thrombocytosis

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20
Q

What happens in the cortex/corticomedullary junction/medulla in the thymus?

A

Immature T cells in cortex/T cell maturation in corticomedullary junction/mature T cell in medulla

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21
Q

Where are Hassall’s corpuscles found?

A

Medulla of the spleen

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22
Q

What are the positive and negative selection of T cells?

A

Positive—>see if T cell bind to self MHC—>yes then survive
Negative—>see if it binds too strongly—>get rid of the ones that bind too strongly

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23
Q

List 3 examples of innate immunity

A

Lysosome/defencin (inside neutrophilic granules—>break cell wall)/surfactin

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24
Q

What are the 3 chemotaxis for neutrophil?

A

IL-8 (macrophages)/C5a/LTb4

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25
Q

What surface receptor do neutrophil use to attach to the bacteria?

A

TLR/C3b/IgG

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26
Q

What is the process of O2 dependent killing in the phagolysosome?

A

NADPH is oxidized to NADP+ in the cytoplasm—>H+ goes into the phagolysosome—>NADPH oxidase combine e- from NADPH with O2 to produces superoxide anion (O2-)—>superoxide dismutase combine O2- and H+ into H2O2—>break down to hydroxal (OH-) radical—>kill the bacteria

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27
Q

How does myeloperoxidase kill bacteria in the phagolysosome?

A

It converts H2O2 and Cl into OCl- (hypochloride)—>kill the bacteria

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28
Q

How does mast cells respond to inflammation?

A

C5a is released from the infected region—>C5a binds to C5a receptor on mast cell—>degranulation

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29
Q

What does histamine do to the endothelial cells of the blood vessel?

A

It regulates P-selectin

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30
Q

How does neutrophil bind to endothelial cell of the blood vessel?

A

Through P and E-selectin (low affinity) via integrin on neutrophil—>rolling on the surface (slow down leukocyte)—>

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31
Q

How does neutrophil diapedesis happens?

A

IL8 binds to proteoglycan on the endothelial cell—>neutrophil binds to IL8 (high affinity binding)

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32
Q

What is chronic granulomatous disease?

A

Inherited disease with defective NADPH oxidase—>can’t produce superoxide (O2-) anion—>chronic infection of catalase + bacteria

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33
Q

Why is chronic granulomatous disease pt not susceptible to catalase - bacteria?

A

Catalase - bacteria produces H2O2—>MPO convert it to OCl- in phagolysosome and then kill the bacteria

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34
Q

Why is MPO deficiency usually asymptomatic?

A

Because NADPH oxidase can still produce OH- to kill the bacteria

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35
Q

What bacteria infection is MPO deficiency susceptible to?

A

Candida

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36
Q

What is type I leukocyte adhesion deficiency?

A

Beta 2 integrin (low affinity) (CD18) deficiency on leukocyte—>recurrent infection and delay in umbilical cord separation

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37
Q

Where do you find MHC class II protein?

A

On APCs

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38
Q

Where are the antigen loaded and presented to for MHC class I and II protein?

A

Class I—>loaded in rough ER and presented to CD8 cells

Class II—>loaded in endosomes and presented to CD4 cells

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39
Q

What are class I and II MHC structure compose of ?

A

Class I—>alpha chain and beta microglobulin

Class II—>alpha chain/beta chain/invariant chain (released when antigen is loaded)

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40
Q

What disease does the pt in risk for with HLA-B27?

A

Seronegative spondyloarthropathy (ankylosing spondylitis/inflammatory bowl disease/reactive arthritis/psoriasis)

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41
Q

What disease does the pt in risk for with HLA-DR3 and DR4?

A

DR3—>type I DM/Hashimoto

DR4—>type I DM/rheumatoid arthritis

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42
Q

Is natural killer cell a part of innate or adaptive immune response? and what protein does it look for?

A

Innate/MHC class I

43
Q

What happens when natural killer cell encounter a normal cell?

A

Normal cell express MHC class I—>natural killer cell express KIR (killer cell immunoglobulin like receptor)—>normal cell bind to KIR and inhibit natural killer cell

44
Q

What happens when natural killer cell encounter a foreign cell?

A

No MHC class I/no KIR—>KAR receptor is activated on natural killer cell—>attack by producing perforin (poke a hole) and then insert granzyme (induce apoptosis)

45
Q

What is the most prominent cell present in graft vs. host disease?

A

Natural killer cell

46
Q

What are the interleukens that are responsible for Th1 and Th2 cell differentiation?

A

Th1 cell—>IL-12

Th2 cell—>IL-4

47
Q

What is the first signal for the activation of T cell by APCs?

A

MHC class II on the APCs bind with TCR (then CD4 binds to it) and the help of CD3 on the T cell surface

48
Q

What is the costimulatory signal that is needed to activate T cell along with the first signal?

A

CD28 on the T cell surface binds with B7 on the APCs

49
Q

What are the first and second signal that are needed to activate CD8 cells?

A

First signal—>Infected cells present antigen to CD8 through Class I MHC
Second signal—>Helper T cell secretes IL-2—>IL-2 binds to CD8 cells

50
Q

Which T helper cells activate CD8 cells and which one for B cell?

A

Th1—>activate CD8 cells

Th2—>activate B cells

51
Q

What are the 2 signals for activation of B cells?

A 
1st--->CD40 ligand from Th2 cells bind to CD40 on B cell
2nd--->Interleukens (IL-4/5/6/13) are secreted from Th2 cells for B cell class switch
52
Q

Where does B cells activation occur?

A

Lymph nodes/spleen

53
Q

What do Th1 and Th2 cell secrete to inhibit each other?

A

Th1—>IFN gamma

Th2—>IL-10

54
Q

How do CD8 cells kill?

A

Same as natural killer cells

55
Q

What are the 2 types of antibody light chain?

A

Kappa and lambda

56
Q

What are the 2 ends of a antibody and what do they consist?

A

Fab—>top—>bind to antigen

Fc—>bottom—>bind to APC—>determine if the antibody is IgA/G/A/D/E

57
Q

What are the 4 ways to create antibody diversity?

A
  1. Random recombination of genes:
    light chain — VJ recombination (v-variable/j-joined region)
    heavy chain — VDJ recombination (d-diversity region)
  2. Random recombination of chains
  3. Somatic hypermutation:
    B cell stimulation—>B cell proliferation—>sloppy proofreading—>mutations—>more diverse antibodies produced
  4. TdT add random nucleotide into the DNA
58
Q

What are the 3 functions of antibody?

A

Opsonization/neutralization/complement activation

59
Q

Which Ig can cross placenta and which is secreted as a dimer and which forms pentamer?

A

IgG/IgA/IgM

60
Q

What cell does IgE bind to to initiate allergic reaction?

61
Q

What are thymus independent and dependent antigens?

A 
Independent (no peptide component)--->can not be presented to T cell (e.g. LPS of gram - rod)/stimulate IgM--->no immunologic memory
Dependent (has peptide component)--->allow antibody class switch--->has immunologic memory
62
Q

What are the 2 IL secreted by macrophages that are responsible for fever during inflammation?

63
Q

Which cytokine secreted by macrophages that is responsible for sepsis?

64
Q

Which 5 main cytokines do macrophages secrete?

A

IL-1/IL-6/IL-8/IL-12/TNF-alpha

65
Q

Wh does cytokines do Th1 and Th2 cell secrete?

A

Th1—>IL-2 (activate CD8 cells)/IL-3/IFN-gamma (activate macrophages)
Th2—>IL-4 (IgE and IgG production)/5 (IgA production)/10 (inhibitory)

66
Q

What do IFN alpha and beta do?

A

They inhibit viral protein synthesis and are used to treat many viral infections

67
Q

What are the 3 CD markers for B cells?

A

CD19/20/21

68
Q

What are the CD marker in macrophage and what does it bind?

A

CD14—>bind to LPS—>release IL-1 and TNF-alpha

69
Q

What is the CD marker for NK cell?

70
Q

What does anergy of T cell mean?

A

Self reactive T cell bind to APC without costimulatory signal—>die

71
Q

How does superantigen work? and does it relate to any specific antigen?

A 
Cross link TCR with MHC class II--->over activation of T cells
No, it crosses link without any antigen
72
Q

What are the 3 bacteria/1 virus/2 parasites that exhibit antigenic variation?

A

Salmonella/Borrelia/Gonorrhea
Influenza
Trypanosoma brucei rhodesiense
Trypanosome brucei gambiense

73
Q

What is passive immunity and what infection do we use this to treat?

A

Inject preform antibodies/C. tetani, rabies, hep B, C. botulinum

74
Q

What are the 3 pathways of complement activation?

A

Classical—>C1 attaches to IgG or IgM that is bound to the bacteria/virus
Lectin—>activated by lectin that binds to the mannose residuals on the surface of bacteria/fungi/viruses
Alternative—>activated by C3b binding to bacteria (mediated by properdin)

75
Q

What does complement accomplish?

A
  1. Makes C3b and mark it onto the target cell for opsonization
  2. Makes and cleave C5 into C5a and C5b—>C5b combines with C6/7/8/9 to form membrane attack complex—>kill the bacteria
76
Q

Which 3 anaphylatoxins do the 3 complement pathway produce and what do they do?

A

C3a/4a/5a—>promote inflammatory response

77
Q

Deficiency in C1 inhibitor gives?

A

Hereditary angioedema

78
Q

Deficiency in classical pathways give?

A

SLE and recurrent encapsulated bacteria

79
Q

Complement deficiency pt is susceptible to what bacteria infections?

A

Neisseria/H. influenza/S. pneumoniae

80
Q

Deficiency in alternative pathway indicate a deficiency in what enzyme? and what does it cause?

A

Properdin/fulminant N. menigitidis

81
Q

What are the assay that are used to test the classical and alternative pathway?

82
Q

When do you know the immunodeficiency is acquired?

A

When both CH50/AH50 are below 50% but still detectable

83
Q

What is the process of antigen presenting?

A

Phagocytes eat a bacteria—>phagolysosome kills it—>MHC class II comes into it and pick up some antigen and go to the cell surface

84
Q

What is the progression of B cell activation?

A

B cell is activated—>proliferation—>differentiation—>antibody production

85
Q

What is TAP protein?

A

It’s located in the ER to allow antigen in to be presented on MHC class I

86
Q

Pt with MHC class I deficiency is susceptible to ___ infection and thus ___ vaccine?

A

Viral/live attenuated

87
Q

What are the 3 bacteria/1 virus/2 parasites are known for their antigen variation?

A

Salmonella (2 different flagella)/Borrelia (change surface protein)/gonorrhea (pili protein)
Influenza
Trypanosoma brucei rhodesiense
Trypanosome brucei gambiense

88
Q

What type of hypersensitivity is responsible for serum sickness (foreign protein) or arthus reaction (local reaction)?

89
Q

What is the most common example of arthus reaction?

A

Tetanus vaccine

90
Q

What kind of immune deficiency is more prone to type III hypersensitivity reaction?

A

C3 deficiency

91
Q

What are common examples of type IV hypersensitivity?

A

Transplant rejection (excluding hyperacute)/PPD test/contact dermatitis

92
Q

For type I hypersensitivity reaction, what is the first antibody produced?

93
Q

Which cytokine would inhibit type IV hypersensitivity reaction?

94
Q

Which antibody is against which antibody in rheumoatoid arthritis?

A

IgM against IgG

95
Q

Antimitochondria antibody is associated with which disease?

A

Primary biliary cirrhosis

96
Q

What is B (boy) ruton’s agammaglobulinemia?

A

X-linked/defect in BTK gene/B cell unable to differentiate

97
Q

What is hyper IgM syndrome?

A

Defect in CD40L which is necessary for B cell class switch/B cell unable to differentiate into other Igs

98
Q

DNA in Heterochromatin is methylated or acetylated? what about euchromatin?

A

Methylated/acetylated

99
Q

What’s the difference between nucleoside and nucleotide?

A

Nucleoside—>base/ribose

Nucleotide—>base/ribose/phosphate

100
Q

Carbamoyl phosphate is involved in what 2 pathways?

A

De novo pyrimidine synthesis/urea cycle

101
Q

Ornithine transcarbamylase deficiency has a build up of ___?

A

Carbamoyl phosphate

102
Q

Thymidylate synthase depends on ___?

A

Folic acid

103
Q

What does C3a and C5a activate?

Unit 4 (28 decks)

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