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SFM-Kayla > Quiz 2- immunity > Flashcards

Quiz 2- immunity Flashcards

1
Q

What is in a neutrophil granule?

A

Peroxidase, lysozyme, degradative enzymes, defensins

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2
Q

How do neutrophils act to kill pathogens?

A

Phagocytosis, degranulation, or NETs

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3
Q

What is the lifespan of a neutrophil?

A

Hours to a couple of days

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4
Q

What is the lifespan of monocyte?

A

If you days normally, can live longer during inflammation

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5
Q

Is the lifespan of a macrophage?

A

Long lifespan, can live up to years in tissues

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6
Q

What kinds of things do macrophages do?

A

Respond to PAMPs/DAMPs, regulate extravasation of white blood cells, phagocytosis, tissue repair, produce inflammatory mediators, present antigens, and immunomodulation

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7
Q

What types of dendritic cells are there?

A

Myeloid, plasmacytoid, Langerhans

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8
Q

What do basophils do?

A

Parasite defense, allergic reaction

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9
Q

What do mast cells do?

A

Parasite defense, allergic reactions

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10
Q

What is the lifespan of a mast cell?

A

Long-lived cells

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11
Q

What type of cell regulates vascular permeability?

A

Mast cells

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12
Q

What type of cells are polymorphonuclear?

A

Eosinophils and neutrophils

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13
Q

What do eosinophils do?

A

Parasite defense, allergic reactions

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14
Q

What types of WBCs work in parasite defense and regulate allergic reactions?

A

Basophils, mast cells, eosinophils

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15
Q

What are the clusters of differentiation for pluripotent stem cells, natural killer cells, T cells, and B cells?

A

Pluripotent stem cells - 34
NK - CD 56
T - 3, 4, 8
B - 19, 20

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16
Q

What do eosinophil granules contain?

A

Histamine, peroxidase, lipase, and major basic protein

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17
Q

What do basophil/mast cell granules contain?

A

Histamine, serotonin, heparin, cytokines, chemokines

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18
Q

What are the hallmark signs of inflammation?

A

Heat, redness, swelling, pain, loss of function

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19
Q

What type of WBC is involved in inflammation and what does it release?

A

Mast cell, releases prostaglandins, leukotrienes, and histamine

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20
Q

What are the pyrogenic cytokines that are produced by macrophages?

A

TNF, IL-1, IL-6

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21
Q

Examples of pattern recognition receptors

A

Mannose receptor, f-met receptor, toll-like receptors, NOD-like receptors

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22
Q

TLR1/TLR2

A

Recognizes bacterial lipopeptides and GP1 of parasites

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23
Q

TLR2/TLR6

A

Recognizes lipoteichoic acid of G+ bacteria and zymosan of yeasts (fungi)

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24
Q

TLR3

A

Double stranded viral RNA

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25
Q

TLR4

A

LPS of G- bacteria

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26
Q

TLR5

A

Flagella of motile bacteria

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27
Q

TLR7

A

ssRNA of viruses

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28
Q

TLR8

A

ssRNA of viruses

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29
Q

TLR9

A

Unmethykated CpG-rich DNA of bacteria and viruses

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30
Q

What do DAMPs interact with to start inflammatory process?

A

PRRs

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31
Q

What types of cells are phagocytes?

A

Neutrophils, monocytes, and macrophages

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32
Q

What types of cells are involved in cell-mediated innate immune responses?

A

Neutrophils, monocytes, and macrophages act as phagocytes. Mast cells, basophils, and eosinophils defend against multicellular parasites and play a role in allergy response. Natural killer cells eliminate infected/malignant cells

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33
Q

What types of responses are involved in humoral innate immunity?

A

Complement system, acute phase proteins, and natural antibodies generated against antigens in GI tract

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34
Q

What does CRP do?

A

It is an acute phase protein that promotes phagocytosis as an opsonin

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35
Q

How does the humeral response of adaptive immunity work?

A

B cell receptors bind to specific antigens which causes them to undergo clonal expansion and differentiation into plasma cells that secrete antibodies

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36
Q

How does the cell-mediated response of adaptive immunity work?

A

T cells are activated by APCs and then undergo clonal expansion. Cytotoxic T cells kill infected host cells, helper T cells involved in B cell high affinity antibodies

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37
Q

What types of cells are APCs?

A

Macrophages, dendritic cells, and B cells

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38
Q

Tissue macrophage in CNS

A

Microglia

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39
Q

Tissue macrophage in liver

A

Kuppfer cells

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40
Q

Tissue macrophage in lung

A

Alveolar macrophages

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41
Q

Tissue macrophage in bone

A

Osteoclast

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42
Q

Tissue macrophage in spleen

A

Sinusoidal macrophages

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43
Q

Tissue macrophage in connective tissue

A

Histocyte

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44
Q

For recurrent sinopulmonary bacterial infections, you screen…?

A

Screen humoral immunity

45
Q

For recurrent viral/fungal infections, you screen…?

A

Screen cellular immunity

46
Q

For recurrent skin abscesses/fungal infections, you screen…?

A

Screen for phagocyte defect

47
Q

For bacteremia or meningitis with encapsulated bacteria, you screen…?

A

Screen for complement deficiency

48
Q

What does a diff test look for?

A

T-cell, B-cell, T/B cell defects

49
Q

What does a DTH skin test look for?

A

T cell defects, only works if previously immunized

50
Q

What does serum IgG, IgM, and IgA look for?

A

Humoral immunodeficiency

51
Q

What does Ab testing to a specific Ag after immunization look for?

A

Humoral immunodeficiency

52
Q

What does total hemolytic complement assay look for?

A

Functional status of complement system

53
Q

What does nitroblue tetrazolium test look for?

A

Phagocytic disorder

54
Q

What disease is typically associated with severe lymphopenia?

A

SCID

55
Q

Paroxysmal Nocturnal Hemoglobinuria

A

Failure to regulate MAC formation. Unable to anchor complement regulatory proteins like DAF and CD59 to cell membrane due to lack of GPI anchor. RBCs most susceptible

56
Q

MyD88 deficiency

A

Severe pyogenic infections but normal resistance to other infections. Patients lack fevers or elevated CRP/ESR w/ infection.

57
Q

TLR3 deficiency

A

Increased susceptibility to HSV encephalitis

Autosomal dominant

58
Q

Type 1 hypersensitivity

A 
Immediate reaction, (need cross-linking) pre-formed IgE antibodies bound to mast cells crosslink with antigen upon exposure. Mast cell degranulation (histamine, proteases, prostaglandins, leukotrienes, cytokines) = symptoms
IL-4 triggers B cells to class switch to IgE
59
Q

Atopy

A

Genetic predisposition to hypersensitivity

60
Q

Type 2 hypersensitivity

A

IgG/IgM directed against self tissues/antigens.
Phagocytosis via Ig opsonization (FcRgamma or CR1 receptors - ROS and lysosomal enzymes released), complement-mediated lysis, or ab-dependent cytotoxicity
Complement system activation - C3a and C5a (anaphylatoxins) induce inflammation
– Complement-mediated cytotoxicity and antibody-dependent cellular cytotoxicity (ADCC)

61
Q

Type 3 hypersensitivity

A

Antigen-antibody (IgG) complexes form (deposit in blood vessels) which activates complement system —> tissue/cell damage
Complement system activation - C3a and C5a (anaphylatoxins) induce inflammation.
Fc receptor-mediated inflammation.
Generalized: serum sickness
Localized: arthus reaction

62
Q

Type 4 hypersensitivity

A

Delayed. Cell-mediated, no antibodies. Memory T-cells initiate immune response (ex: TB test). Triggers include autoimmunity, exaggerated/persistent responses to environmental antigens, and some microbial antigens. Tissue injury caused by inflammation induced by Th1 and Th17 cytokines, by macrophages, or by CD8+ killing

63
Q

Type 1 examples

A

Asthma = spasmodic contraction of smooth muscle around bronchi. Can have non-immunologic stimuli like cold and exercise
Systemic: anaphylaxis - food allergen intake = massive release of vasoactive amines and cytokines from mast cells.

64
Q

Allergen-specific immunotherapy (allergen-SIT)

A

curative approach to allergic diseases by administering increasing doses of allergen to induce peripheral T cell tolerance, increase thresholds for mast cell activation, and decrease IgE-mediated histamine release by mast cells

65
Q

Type 2 examples

A

Antibodies stimulate TSH receptor without ligand = hyperthyroidism (Graves disease)
Antibodies inhibit binding of acetylcholine NT to ACh receptor = myasthenia gravis

66
Q

Autoimmune hemolytic anemia

A

RBC membrane proteins opsonized for phagocytosis causing hemolytic anemia. Type 2 hypersensitivity.

67
Q

Autoimmune thrombocytopenic purpura

A

Platelet membrane proteins opsonized for phagocytosis causing bleeding. Type 2 hypersensitivity.

68
Q

Goodpasture’s syndrome

A

Non-collagenous protein in basement membrane of kidney glomeruli/lung alveoli have complement-mediated inflammation or Fc receptor-mediated inflammation causing nephritis/lung hemorrhage. Type 2 hypersensitivity.

69
Q

Grave’s disease

A

TSH receptor stimulated by antibodies causing hyperthyroidism. Type 2 hypersensitivity.

70
Q

Myasthenia gravis

A

Ach receptor inhibited by antibody which downregulates it and causes muscle weakness and paralysis. Type 2 hypersensitivity.

71
Q

Pemphigus vulgaris

A

Antibody-mediated activation of proteases causes skin vesicles

72
Q

Rheumatic fever

A

Antibodies produced against strep start cross-reacting with heart causing myocarditis. Type 2 hypersensitivity.

73
Q

Systemic Lupus Erythematosus

A

Antibodies for DNA cause nephritis, arthritis, vasculitis. Type 3 hypersensitivity.

74
Q

Polyarteritis nodosa

A

Microbial antigens cause vasculitis. Type 3 hypersensitivity.

75
Q

Post-streptococcal glomerulonephritis

A

Streptococcal cell wall antigens cause nephritis. Type 3 hypersensitivity.

76
Q

Serum sickness

A 
Various protein antigens cause systemic vasculitis, nephritis, and arthritis. Type 3 hypersensitivity.
Immune complexes (ab-ag) in bloodstream are deposited which triggers complement response/macrophages and neutrophils
77
Q

Arthus reaction

A

Various protein antigens cause cutaneous vasculitis. Type 3 hypersensitivity.
Local tissue reaction usually on skin. Ag-ab complexes form in tissues

78
Q

DTH

A

Delayed-type hypersensitivity = T-cell mediated inflammatory reaction. Type 4 hypersensitivity.

79
Q

MS

A

T-cells specific to myelin proteins causes demyelination in CNS and sensory motor dysfunction. Type 4 hypersensitivity.

80
Q

RA

A

T-cells specific to antigens in joints causes inflammation of synovium and erosion of cartilage/bone in joints. Type 4 hypersensitivity.

81
Q

DM I

A

T-cells specific to pancreatic islet antigens causes impaired glucose metabolism and vascular disease. Type 4 hypersensitivity.

82
Q

Crohn’s disease

A

T-cells specific to unknown intestinal microbes causes inflammation of bowel wall. Type 4 hypersensitivity.

83
Q

Contact sensitivity

A

T-cells specific to modified skin proteins (ex: haptogen added) causes skin rash (ex poison ivy rxn). Type 4 hypersensitivity.

84
Q

Chronic infections

A

T-cells specific to microbial proteins causes chronic inflammation (ex TB). Type 4 hypersensitivity.

85
Q

Which enzymes act before Pro-T phase?

A

Gamma-chain, JAK3, ADA, PNP

86
Q

Which enzymes act before Pre-B/Pre-T?

A

RAG1/RAG2, ARTEMIS

87
Q

Which enzymes act before Immature B (Pre-BCR checkpoint)?

A

BTK

88
Q

Which enzymes act before double positive T cell (Pre-TCR checkpoint)?

A

CD3

89
Q

Which enzymes act before single positive T cell?

A

ZAP70, TAP1,2

90
Q

Typical signs of SCID

A

Severe, persistent (opportunistic) infections, oral thrush, chronic diarrhea, failure to thrive

91
Q

Adenosine Deaminase Deficiency

A

T-, B-, NK-
No Igs
Autosomal recessive, no live vaccines, HSCT
Accumulation of toxic doxyadenosine leads to lymphocyte apoptosis
2nd most common form of SCID

92
Q

Purine Nucleotide Phosphorylase Deficiency

A

T-, B-, NK+/-
Normal Igs
Autosomal recessive, no live vaccines, HSCT
Accumulation of intracellular dGTP which is toxic to lymphocytes. Commonly associated w/ autoimmune disorders.
Very rare

93
Q

ARTEMIS Deficiency

A

T-, B-, NK+
Low Igs
Autosomal recessive, no live vaccines, HSCT
Enzyme that repairs double strand breaks during VDJ recombination. Presentation - diarrhea, candidiasis, and opportunistic pneumocystis jiroveci (fungus). Risk for developing lymphomas.

94
Q

RAG1/RAG2 Deficiency

A

T-, B-, NK+
No Igs
Autosomal recessive, no live vaccines, HSCT
Impaired V(D)J recombination, development of B/T cells stopped. Presentation - diarrhea, candidiasis, and opportunistic pneumocystis jiroveci.
LEAKY allows for Omenn Syndrome (partial dysfunction w/ severe erythroderma)

95
Q

Jak3 Deficiency

A

T-, B+, NK-
Low IgM produced
Autosomal recessive, no live vaccines, HSCT
Janus Kinase 3 mutation (part of IL-2 receptor) - T-cell growth factor

96
Q

Most common immunodeficiency (cell type)

A

B lymphocyte immunodeficiencies

97
Q

Agammaglobulinemia

A

T+, B-, NK+
No Igs
X-linked OR autosomal recessive, no live vaccines, HSCT
B-cell development arrested at Pre-B due to BTK deficiency. No rearrangement in Ig heavy chains

98
Q

Isolated IgG Subclass Deficiencies

A

T+, B+, NK+
Low IgG, normal IgM, IgA, IgE
Autosomal recessive, no vaccine restrictions, symptomatic treatment
Caused by “several” gene defects. Usually asymptomatic, sometimes associated w/ recurrent URIs

99
Q

IgA Deficiency

A

T+, B+, NK+
NO IgA, Normal IgM, IgG
Autosomal (high in male), no vaccine restrictions, symptomatic treatment
B cells don’t mature to plasma cells. 50% asymptomatic. Symptomatic show recurrent encapsulated bacterial infections. Patients develop anti-IgA antibodies which can cause anaphylactic response to IVIG transfusions

100
Q

DiGeorge Syndrome

A

T-, B+, NK+
Normal Igs
Autosomal dominant, vaccines depend on T-cell count
Micro-deletion of chromosome 22 causes undeveloped thymus = progenator T cells can’t develop. Frequent URIs.
Classic TRIAD- cardiac anomalies, hypocalcemia, and hypoplastic thymus

101
Q

Hyper IgM Syndrome

A

T+, B+, NK+
High IgM, low IgG and IgA
X-linked (CD40L) AND autosomal (CD40), no polio vaccine, symptomatic treatment
Susceptible to bacterial infection. No class switching/somatic hypermutation = only IgM present.

102
Q

Transient Hypogammaglobulinemia of Infancy

A

T+, B+/-, NK+
Normal IgM, low IgG and IgA
Polio vaccine not recommended, symptomatic treatment
Maternal IgG disappears after 6 months, IgG production delayed for up to 3 years. Susceptible to sinopulminary infections

103
Q

Common Variable Immune Deficiency

A

T+, B+/-, NK+
Low IgG and IgA, normal IgM
Autosomal recessive, HSCT
Mutations in receptors for B-cell growth factor and costimulators. Defect in Ig production (like hypogammaglobulinemia). Recurrent infections (sinopulminary), autoimmune disease association, and risk for lymphoma. Dx at 20-30 y/o.

104
Q

Common Gamma Chain Deficiency

A

T-, B+, NK-
Very low Igs
X-linked, no live vaccines, HSCT
Most common SCID. IL-2Rgamma (T-cell growth factor receptor) deficiency. No functional B cells since T cells can’t help them. Presentation - failure to thrive, severe thrush, opportunistic infections, chronic diarrhea

105
Q

IL-7R Alpha Chain Deficiency

A

T-, B+, NK+
Very low Igs
Autosomal recessive, no live vaccines, HSCT
Receptor for early T-cell development defective, no co-stimulation for B-cells.

106
Q

Bare Lymphocyte Syndrome

A

CD4-, B+, NK+
Low Igs
Autosomal recessive, no live vaccines, HSCT
No MHC class II expression on professional APCs due to transcription factor defect = affects CD4 T-cells. Recurrent URI, GI, UTI

107
Q

MHC Class I Deficiency

A

CD8-, B+, NK-
Normal Igs
Autosomal recessive, no restrictions of vaccines, symptomatic treatment
TAP1 mutation for peptide txfr to ER = deficient CD8+ cells = recurring viral infections

108
Q

CD3 Complex Deficiencies

A

T-, B+, NK+
Low Igs
Autosomal recessive, no live vaccines, HSCT
Deficiency in subunit of CD3 coreceptor (delta, gamma, epsilon, zeta) means no T-cell activation. Causes failure to thrive, opportunistic infections, chronic diarrhea.

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