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Dermatology Board Prep > DERM (01) Cutaneous Basic Science > Cutaneous Immunology > Flashcards

Cutaneous Immunology Flashcards

1
Q

What are the two main “branches” of innate immunity?

A

Cellular vs non-celullar

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2
Q

What cells make up cellular innate immunity?

A

Macrophages, neutrophils, NK cells, mast cells, eosinophils, lymphocytes (especially cytotoxic T-cells)

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3
Q

What are some important components of non-cellular innate immunity?

A

Antimicrobial peptides - cathelicidins and defensins

Cytokines (IL-1, IL-10, IL-12, IFNa, IFNb)

Complement

TLR

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4
Q

What are the 3 primary complement pathways?

A

Classical, alternative, and mannose-binding lectin pathways

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5
Q

What is the difference between classical complement and alternative/mannose-binding lectin pathway activation?

A

Classical requires antibodies (It is activated by Antigen-Ab complexes [IgM or IgG])

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6
Q

Which IgG does not activate complement?

A

IgG4

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7
Q

In what order (strength) do IgG’s activate complement?

A

IgG3>IgG1>IgG2

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8
Q

What are the purposes of the complement cascade?

A
  1. opsonization, C3b>>C5b
  2. Lyse pathogen (membrane attack complex)
  3. increase chemotaxis (c3a, c5a) known as anaphalaxins.
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9
Q

What is the alternative pathway activated by?

A

Viral or bacterial products

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10
Q

What is the mannose-binding lectin pathway activated by?

A

Microbial carbohydrates like mannose and other monosaccharides on the bacterial wall

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11
Q

What cells are Toll-like receptors mostly expressed on?

A

Dendritic cells and macrophages

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12
Q

What pathway does activation of TLR activate?

A

NF-kB (Nuclear factor kappa beta)

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13
Q

Which TLR does NOT use MyD88 for intracellular signaling?

A

TLR3

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14
Q

Which TLR is activated by triacylated lipoproteins?

A

TLR1/TLR2

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15
Q

Which TLR is activated by diacylated lipoproteins?

A

TLR2/TLR6

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16
Q

Which TLR is activated by flagellin?

A

TLR5

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17
Q

Which TLR is activated by imidazoquinolines (imiquimod) and ssRNA?

A

TLR7/TLR8

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18
Q

Which TLR is activated by CpG DNA?

A

TLR9

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19
Q

Which TLR is activated by dsRNA?

A

TLR3

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20
Q

Which TLR is activated by LPS?

A

TLR4

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21
Q

Which TLR is affected by retinoids?

A

TLR2

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22
Q

Which TLR is involved in inflammatory acne?

A

TLR2 (As expected, this TLR is also affected by retinoids)

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23
Q

Which dermatologic medication affects TLR7?

A

Imiquimod (synthetic TLR7 analog)

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24
Q

Which complement fragment is the most potent anaphylatoxin?

A

C5a

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25
Q

Which complement fragments are anaphylatoxins?

A

C3a/C5a

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26
Q

List some important innate antimicrobial peptides that are important in dermatology and what secretes them

A

Human beta-defensin 1 (hbd-1) (keratinocytes)

  • Human beta-defensin 2 (hBD-2) inducible by bacteria or cytokines
  • Cathelicidin (LL-37) secreted by keratinocytes and granulocytes, upregulated in rosacea
  • Psoriasin- inducible by bacteria or cytokines
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27
Q

Which defensins are affected in AD? And how?

A

cathelicidin (LL-37) and hBD-2 (human beta defensin2) are decreased in AD. (increased risk of infection)

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28
Q

Which innate immune defensins are affected in psoriasis?

A

Cathelicidin (LL-37) and hBD-2 (human beta defensin2) are increased in psoriasis (Thought to play a role in the decreased number of infections seen as compared to atopic dermatitis)

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29
Q

What cells produce the most cytokines?

A

T-cells

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30
Q

What is the main neutrophil chemoattractant/cytokine?

A

IL-8

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31
Q

True/False, do neutrophils express receptors for a complement?

A

Yes, they express receptors the Fc receptor for IgG and complement

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32
Q

In general terms, what do NK cells do?

A

Recognize antigen via opsonization (ab-dependant) or killer-activating /inactivating receptors.

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33
Q

How does MHC-1 expression change to activate NK cells?

A

Increased surface MHC-1 expression leads to cell death via granzymes (apoptosis), perforins (pores in cell membranes) and FAS and TRAIL ligand pathways

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34
Q

What are the primary immunohistologic markers for Langerhans cells?

A

CD1a, S100, vimentin, langerin

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35
Q

What is the main cytokine that modulates eosinophils?

A

IL-5 (Th2-cytokine)

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36
Q

What cells in the skin produce IL-1?

A

Monocytes, macrophages, and keratinocytes

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37
Q

What does IL-1 do?

A

Is proinflammatory –> induces fever, increases the production of acute-phase reactants, and increases expression of vascular endothelial cell adhesion molecules

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38
Q

Which interleukins are pro-inflammatory?

A

IL-1, IL-4, IL-6, TNFa

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39
Q

Which interleukins are “anti-inflammatory”?

A

IL-10, TGF-beta

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40
Q

What does IL-2 do and what cell produces it?

A

Activated T cells produce it –> Increased growth and activation of T, NK, and B cells

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41
Q

What does IL-3 do and what cell produces it?

A

T cells and stimulated myeloid cells –> Promotes growth of mast cells and enhances basophil production

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42
Q

What does IL-4 do and what cells produce it?

A

Th2 T helper cells –> Increases Th2 response, induces B cell class switching to increase IgE and increase MHC II production

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43
Q

What does IL-5 do and what cell produces it?

A

TH2 T-cells and mast cells –> stimulates eosinophils and stimulates B cells + Ig production (increases IgA too)

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44
Q

What does IL-6 do and what cell produces it?

A

Lymphoid cells and endothelial cells –> leads to the production of acute-phase proteins, stimulates B cells to differentiate to plasma cells and increases antibody secretion, and increases neutrophil production

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45
Q

What does IL-8 do and what cell produces it?

A

Keratinocytes and endothelial cells –> Neutrophil chemotaxis, member of the CXC chemokine family

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46
Q

What does IL-10 do and what cell produces it?

A

Th2 T-cells and keratinocytes –> Anti-inflammatory cytokine, inhibits pro-inflammatory cytokines along with inhibition of macrophages/dendritic cells; activates B cells, downregulates TH1 response

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47
Q

What does IL-12 do and what cells produce it?

A

Mononuclear phagocytes, dendritic cells –> Proinflammatory cytokine. It induces cell-mediated immunity like NK cells. Increases synthesis of IFNgamma and TNFa

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48
Q

What does IL-15 do and what cells produce it?

A

Mononuclear phagocytes –> Proliferative cytokine, increases NK cell proliferation, plus/minus T-cell growth factor

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49
Q

What does IL-18 do and which cells produce it?

A

Activated T-cells –> Proinflammatory, IFN-gamma inducing factor

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50
Q

What does TNF-alpha do and what cells produce it?

A

T-cells, mononuclear/phagocytes, mast cells, keratinocytes –> Proinflammatory, releases other proinflammatory cytokines like IL-1, IL-6 increases MHC I/II, activates T/B cells, induces fever and catabolism (cachexia)

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51
Q

What does IFNa/IFNb do and what cells produce it?

A

Leukocytes, fibroblasts –> Antiproliferative, antiviral, anti-oncogenic. Increase in I/II MHC expression, activates NK cells, has antifibrotic properties, and inhibits angiogenesis

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52
Q

What does IFN-gamma do and what cells produce it?

A

T-cells, NK cells –> Increased TH1 response –> primes macrophages, causes B-cell type switching to produce Ab

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53
Q

What does TGF-beta do and what cells produce it?

A

Activated platelets, keratinocytes –> Antiinflammatory, induces apoptosis, inhibits the growth of many cell lines/types, counteracts proinflammatory cytokines

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54
Q

What drugs trigger mast cell degranulation?

A

NSAIDs, opiates, asprin, vancomycin, polymyxin B, curare

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55
Q

What non-drug things can trigger mast cell degranulation?

A

Specific antigens (bridging of FceRI), anti-FceRI autoantibodies, IL-3, stem cell factor, C3a, C4a, C5a, radiocontrast media, and some neuropeptides

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56
Q

What two main branches make up the adaptive immune response?

A

Humoral (Antibodies) and cellular (T/B cells)

57
Q

What two major/basic classes of T-cells exist?

A

CD4+ T-helper cells and CD8+ cytotoxic T-cells

58
Q

What are the two major classes of CD4+ T-cells

A

TH1: Increases cell-mediated immunity, involved in delayed hypersensitivity reactions (type IV), and activates macrophages

TH2: Increases humoral mediated immunity through IL-4 and IL-5, switching to IgG4a and IgE, suppress macrophage activity.

Other important classes include T-reg, Th17, and other subtypes

59
Q

Which cytokines favor the Th1 axis?

A

IL-2, IL-12, IFN-gamma, and TNF-a (High-Yield!)

60
Q

Which cytokine(s) downregulate the Th2 axis?

A

IFN-gamma

61
Q

Which cytokine(s) favor the Th2 axis?

A

IL-4, 5,6,and 10 (High-Yield)

62
Q

Which cytokine downregulates the Th1 axis?

A

IL-10

63
Q

What diseases are associated with Th1 dysfunction?

A

Allergic contact dermatitis, tuberculoid leprosy, leishmaniasis, psoriasis

64
Q

What diseases are associated with Th2 dysfunction?

A

AD, lepromatous leprosy, dessminated leishmaniasis, sezarry syndrome, parasityci infection

65
Q

What important cytokine in psoriasis favors the Th17 pathway?

A

IL-23

66
Q

What drugs act on the IL-12/23 pathway in psoriasis?

A

Ustekinumab (Stelara) (also used in inflammatory bowel disease)

67
Q

What cells express MHC-1?

A

All nucleated cells

68
Q

What cell(s) recognize MHC-1?

A

CD8+ T-cells, NK cells

69
Q

Where are antigens for MHC-1 processed?

A

In the cytosol

70
Q

Qhat HLA types are associated with MHC-1?

A

HLA A/B/C

71
Q

Which HLA MHC I subtype is associated with psoriasis?

A

HLA-Cw6

72
Q

Which HLA MHC I subtype is associated with psoriatic arthritis and reactive arthritis?

A

HLA B-27

73
Q

Which HLA MHC I subtype is associated with Behcets?

A

HLA-B51

74
Q

What cells express MHC-II?

A

Antigen-presenting cells

75
Q

Where do antigens get processed for MHC-II?

A

Endocytic vesicles

76
Q

What cells recognize/respond to antigens on MHC II receptors?

A

CD4+ T-cells –> Promote a TH2 patheway–>more B cell activation –> antibody

*Dz’s with autoantibody follow this general pathway

77
Q

What HLA subtypes are involved with MHC-II?

A

HLA DP/DQ/DR

78
Q

Which HLA subtype is a/w lichen planus?

A

HLA-DR1

79
Q

Which HLA subtype is a/w pemphigus vulgaris?

A

HLA-DR4

80
Q

Which HLA subtype is a/w chronic urticaria?

A

HLA-DR4

81
Q

Which HLA subtype is a/w dermatitis herpetiformis?

A

HLA-DQ2

82
Q

What are the receptors and co-receptors that act as costimulatory molecules that are only found on T-cells?

A

CD 80 (B7-1) and CD86 (B7-2) which are co-receptors with CD28, and CD152 (CTLA-4) [both]

83
Q

What receptor and co-receptor costimulatory molecules are ligands on T- and B-cells?

A

CD274 (PD-L1, B7H1) and CD273 (PD-L2, B7DC) and co-recpetor molecules CD279 (PD-1)

84
Q

What are the main neutralizing antibodies?

A

IgA1/IgA2 (mucosal); IgG2/IgG4 (tissue)

85
Q

What are the preformed mast cell mediators?

A

Tryptase, histamine, serotonin, and heparin

86
Q

What factors are newly formed mast cell mediators (not pre-formed)?

A

Prostaglandin D2, Leukotriene C4, and Platelet-activating factor

87
Q

What antibody class can cross the placenta?

A

IgG

88
Q

Most abundant antibody class found in the circulation?

A

IgG

89
Q

What complement pathways can IgA activate?

A

IgA can agglutinate with antigens and activate the alternate but not the classic pathway

90
Q

What interleukins do keratinocytes produce?

A

IL-1, IL-6, IL-8, IL-10, IL-12, and TNF-alpha

91
Q

What interleukins do keratinocytes respond to?

A

IL-2, IL-4, IL-13, IL-22, and TNF-alpha

92
Q

What are the principal effects of IL-1 alpha/beta

A

Increase production of acute-phase proteins, fever, lymphocyte activation, macrophage activation, increased leukocyte/endothelial adhesion; involved in the innate immune inflammatory response

93
Q

What is the function of IL-2?

A

The proliferation of T, B and NK cells. T-cell differentiation into different subsets including memory t-cells

94
Q

What is the primary purpose of IL-4?

A

Isotype switching to IgE upon stimulation of B-cells. This increases Th2 cellular proliferation and differentiation

95
Q

What is the primary purpose of IL-5?

A

Eosinophil activator, b-cell activation, increased IgA

96
Q

What is the primary function of IL-6?

A

Involved in innate immune response and neutrophil production, b-cell differentiation and induction of acute-phase reactants

97
Q

What is the main function of IL-8?

A

Chemokine –> Increases neutrophil chemotaxis

98
Q

What are the main functions of IL-10?

A

Inhibition of macrophages/dendritic cells and proinflammatory cytokine production. Decreased expression of IL-12/Th1 response

99
Q

What is the primary function of IL-12?

A

Activator of the Th1 response, increased interferon-gamma/TNF-alpha, enhances the cytotoxic activity of T and NK cells (cell-mediated immunity)

Has both a p40 and p35 subunit, which is important because IL-23 also has the p40 subunit

100
Q

What is the primary function of IL-17?

A

Increases cytokine and chemokine production by keratinocytes and macrophages

this one is a key pathways in psoriasis

101
Q

What is the main effect of IL-22?

A

Activation and proliferation of B-cells; proliferation of Th17 cells; stimulation of NK cells

102
Q

What is the primary effect of IL-23?

A

Promotes Th17 proliferation and differentiation

Also has the p40 subunit like IL-12 (This is why ustekinumab interacts w/ IL-12 and IL-23)

this one has a key role in psoriasis

103
Q

What is the main effect of TNF-alpha?

A

Activation of macrophages and T and B lymphocytes, increased proinflammatory cytokine production, leukocyte/endothelial cell adhesion, cachexia, pyrexia, induction of acute-phase proteins and increased MHC class I induction

104
Q

What is the main effect of interferon-alpha?

A

Activation of antiviral/antitumor state (antiproliferative), Increased MHC I expression, NK-cell activation

105
Q

What is the main effect of interferon-beta?

A

Activation of antiviral/antitumor state (antiproliferative), Increased MHC I expression

106
Q

What is the main effect of interferon-gamma?

A

MHC class I and II induction, macrophage activation and cytokine synthesis, increased endothelial cell/lymphocyte adhesion antiviral state, antiproliferative (Th1 cells), differentiation of the Th1 cells, isotype switching with opsonization activity, macrophage activation, increased MHC I/II expression; downregulation of Th2 pathway

107
Q

What are the main cytokines released by macrophages?

A

IL-1a/b, IL-10, IL-12, IL-18, TNF-alpha, G-CSF, GM-CSF

108
Q

What are the main cytokines released by T-cells?

A

Th2: IL-4, IL-5, IL-22

Th17: IL-17, IL-22

Treg: IL-10,

T-cells (general): IL-2, IL-3, IL-6, IL-8, IFN-gamma

109
Q

What cytokines are released by monocytes?

A

IL-8, IL-15

110
Q

What cytokines are released by B-cells?

A

IL-1a/b, IL-6, TNF-alpha (lymphocytes)

111
Q

What component of complement binds antibodies?

A

C1q binds the Fc portion of the antigen-bound antibodies, the other components of the C1 3 protein complex are C1r and C1s. C1s cleaves C4 and then c2 to make the C3 convertase (C4b/c2a which then turns C3 to C3a and C3b

112
Q

What complement components make up the MAC?

A

C5b, C6, C7, C8, and C9

113
Q

What cell lineage are NK cells from?

A

They are lymphocytes

114
Q

What are the primary B-cell immunohistochemical markers?

A

FC receptor, MHC class II, complement receptors, CD19, CD20, CD79a

115
Q

What is required for a T-cell receptor to recognize an antigen?

A

TCR’s require the antigen to be teamed with an MHC I/II receptor and costimulatory signals

116
Q

What are the main co-stimulatory receptors located on the T-cell and what do they interact with?

A
  • CD28 on the T-cells binds with B7-1 and B7-2 on APC’s
  • CD2 on T-cells binds to LFA-3 on APC’s
  • LFA-1 on T-cells binds to ICAM-1 on APC’s
117
Q

What are some co-inhibitory receptors on the T-cell and what do they interact with?

A

CTLA4 is on the T-cell and interacting with B7-1 and B7-2 and leads to inhibition.

118
Q

What cytokine is released when T-cells are activated and what does it do?

A

IL-2 is released and it leads to the proliferation of antigen-specific T-cells

119
Q

What are the main Immunohistochemical markers on T-cells?

A

CD2, CD3, CD4 (helper t-cells), CD8 (on cytotoxic t cells)

120
Q

How are Th1 cells activated and what is their primary function?

A

Activated by intracellular pathogens, these activate macrophages, and then the Th1 response is mediated by macrophage activity

  • the Th1 response is important for cell-mediated immunity and delayed-type hypersensitivity reactions
  • Stimulate IgG2 and IgG3 class switching
  • Promote phagocytic activity through INF-gamma mediated macrophage activation, FcgammaRIII crosslinking, complement deposition, opsonization
  • Requires stimulation by IL-12 and INF-gamma (mediated through T-bet, STAT1, and STAT4 signaling)
  • Th1 cells produce INF-gamma, IL-2, IL-12, and TNF-alpha
121
Q
A
122
Q

What is the function of the Th2 response, how is it triggered, what chemokines are produced as a result?

A

Th2 cells activate eosinophils which help mediate systemic immune responses against helminthic parasites and downregulate macrophage activity.

  • Also important in humoral immunity
  • IL-4 is the key cytokine that stimulates Th2 proliferation by activating STAT6 and GATA-3
  • Th2 cells produce: IL-4, IL-5, IL-6, IL-10 (decreases Th1 response), IL-13 (important in allergies, acts like IL-4)
  • Stimulates IgG4 to IgE
  • Response mediated by mast cells and eosinophils
  • Increases degranulation through FcepislonR1 cross-linking, IL-5 mediated eosinophil activation
123
Q

What activates, what is the purpose of, and what things do Th17 activate?

A

Th17 requires activation of the transcription factors RORgammT, STAT3 (mutated in job’s syndrome), and TGF-beta

  • The purpose of these cells is to recruit neutrophils to an area to destroy extracellular pathogens
  • Produce IL-6, IL-17, IL-22 (increases keratinocytes), IL-23 (essential for survival/division of cells), IL-36, and TNF-alpha
  • activate local endothelium, induce cytokine and chemokine production, increase neutrophils infiltration, activate cell-mediated inflammation
124
Q

What is the purpose of Tregs and what factors are expressed on these?

A

Downregulate immune response, express CD25 and transcription factor FOXP3

125
Q

How do CD8+ T-cells kill their target cells?

A

Via the perforin/granzyme pathway: perforin enables granzyme to enter the cytoplasm of virally infected cells leading to apoptosis.

-Also, Fas ligand on thse cells can bind Fas on target cells leading to cell death

126
Q

What is the predominant type of TCR construct of t-cells (alpha/beta vs gamma/delta)?

A

alpha/beta is the most common

127
Q

What is the purpose of gamma/delta T-cells?

A

They act like Treg’s, they suppress the immune system via IL-10 which is why they make such aggressive lymphomas (suppress immune detection and attack)

128
Q

What are the cell surface markers for NK cells?

A

CD2, CD56, CD16

129
Q

What cells do NK cells attack?

A

These attack cells which have decreased MHC-I on their surface (viral infected) and destroy via perforin/granzymes

130
Q

What cytokines activate NK cells and what cytokines do they produce?

A

NK cells are activated by: IL-12, IL-15, and type I interferons

NK cells secrete INF-gamma and enhance the phagocytic capability of macrophages and have cytoplasmic granules that are similar to CD-8+ cytotoxic t-cells

131
Q

What are the cellular markers for macrophages?

A

CD11a/b/c, CD6, Fc receptor for IgG, and MHC-II, come from CD34+ progenitor cells

132
Q

What are the immunohistological markers for Mast cells?

A

CD34/c-kit (CD117)/CD13

133
Q

What are the main neutrophil chemotactic factors?

A

C5a, IL-8, LTB4, Kallikrein

134
Q

What chemokines are required for Langerhans cell development?

A

TGF-beta and macrophage colony-stimulating factor receptor (M-CSFR) ligant for development

135
Q

What is the function of Langerhans cells

A

They are poor at phagocytosis but they are professional antigen-presenting cells. They take up antigens and then travel to the lymph nodes where the MHC-bound antigen is presented to T-lymphocytes followed by subsequent activation of T-lymphocytes

136
Q

What do Langerhans cells stain + for?

A

S100+, langerin (CD207)+ (most sensitive and specific), vimentin +, and CD1a+

137
Q

What is a major difference between the types of antigens that a B-cell will recognize and a t-cell will recognize?

A

T-cells require that the antigen be attached to an MHC molecule whereas the B-cells can pick up antigens. The response from this initial contact is not as robust and leads to IgM not the other Ig’s

138
Q

What are key differences in the antigens presented by MHC-1 vs MHC-II?

A

MHC-1 molecules are intracytoplasmic (think virus/cancer), so they get transported to the ER and then put on the receptor and shipped out.

MHC-II are for extracellular antigens that APC’s pick up, so they are engulfed and then processed in the vehicles in the cytoplasm where the receptors are loaded and presented.

139
Q

What components of the complement pathway are the main drivers of opsonization?

A

C3b>>C5b

DERM (01) Cutaneous Basic Science (4 decks)

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