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HOST AND DEFENSE > MCQ 1 > Flashcards

MCQ 1 Flashcards

1
Q

What does TH1 cell secrete?

A

IFN-gamma

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2
Q

What does TH2 cell secrete?

A

IL-4, IL-5, IL-10, IL-13

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3
Q

What does TH17 cell secrete?

A

IL-17, IL-21, IL-22

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4
Q

What does Treg cell secrete?

A

TGF-ß, IL-10, IL-35

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5
Q

Function of Th1 cell?

A

Activates macrophages
and cytotoxic T cells
to kill phagocytosed
microbes

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6
Q

What is Th1 induced by?

A

IFN-gamma, IL-12

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7
Q

What is Th1 inhibited by?

A

IL-4, IL-10 (from Th2
cell)

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8
Q

What immunodeficiency will be seen with Th1 deficiency?

A

Mendelian
susceptibility to
mycobacterial disease

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9
Q

What is the function of Th2?

A

Activate eosinophils
and promote
production of IgE for
parasite defense

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10
Q

What is Th2 induced by?

A

IL-2, IL-4

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11
Q

What is Th2 inhibited by?

A

IFN-gamma (from Th1 cell)

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12
Q

What is the function of Th17 cell?

A

Immunity against
extracellular
microbes, through
induction of
neutrophilic
inflammation

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13
Q

What is Th17 induced by?

A

TGF-beta, IL-1, IL-6

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14
Q

What is Th17 inhibited by?

A

IFN-gamma, IL-4

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15
Q

How does immunodeficiency of Th17 present?

A

Hyper-IgE syndrome

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16
Q

What is the function of Treg?

A

Prevent autoimmunity
by maintaining
tolerance to self-antigens

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17
Q

What is Treg induced by?

A

TGF-gamma, IL-2

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18
Q

What is Treg inhibited by?

A

IL-6

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19
Q

How will immunodeficiency of Treg present?

A

IPEX

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20
Q

What is the function of IFN-gamma?

A

Th1 cells secrete IFN-gamma, which enhances the ability of monocytes and macrophages to kill microbes they ingest. This function is also enhanced by interaction of T cell CD40L with CD40 on macrophages.

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21
Q

Cytotoxic T cells

A

Kill virus-infected, neoplastic, and donor graft cells by inducing apoptosis.
Release cytotoxic granules containing preformed proteins (eg, perforin, granzyme B).

Cytotoxic T cells have CD8, which binds to MHC I on virus-infected cells.

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22
Q

Regulatory T cells

A

Help maintain specific immune tolerance by suppressing CD4 and CD8 T-cell effector functions.
Identified by expression of CD3, CD4, CD25, and FOXP3.
Activated regulatory T cells (Tregs) produce anti-inflammatory cytokines (eg, IL-10, TGF-beta).

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23
Q

What are the APCs?

A

B cells, dendritic cells, Langerhans cells, macrophages

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24
Q

Describe T-cell activation

A
  1. ) Dendritic cell (specialized APC) samples antigen, processes antigen, and migrates to the draining lymph node.
  2. ) T-cell activation (signal 1): Exogenous antigen is presented on MHC II and recognized by TCR on Th (CD4+) cell.

Endogenous or
cross-presented antigen is presented on MHC I to Tc (CD8+) cell.
3.) Proliferation and survival (signal 2): costimulatory signal via interaction of B7 protein (CD80/86) on dendritic cell and
CD28 on naïve T cell.
4.) Th cell activates and produces cytokines. Tc
cell activates and is able to recognize and kill
virus-infected cell.

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25
Q

B-cell activation and class switching

A

1.) Th-cell activation as mentioned in T-cell activation
2.) B-cell receptor–mediated endocytosis; foreign antigen is presented on MHC II and
recognized by TCR on Th cell.
3.) CD40 receptor on B cell binds CD40 ligand (CD40L) on Th cell.
4.) Th cell secretes cytokines that determine Ig class switching of B cell. B cell activates and undergoes class switching, affinity maturation, and antibody production.

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26
Q

Antibody structure and function: describe fab

A

Fab (containing the variable/hypervariable regions) consisting of light (L) and heavy (H) chains recognizes antigens

Fab: Fragment, antigen binding   

Determines idiotype: unique antigen-binding pocket; only 1 antigenic specificity expressed per B cell

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27
Q

Antibody structure and function: describe Fc

A

Fc region of IgM and IgG fixes complement. Heavy chain contributes to Fc and Fab regions. Light chain contributes only to Fab region

Fc:
   Constant
   Carboxy terminal
   Complement binding
   Carbohydrate side chains
   Determines isotype (IgM, IgD, etc)

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28
Q

Antibody structure

A
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29
Q

Generation of antibody diversity (antigen independent)

A
  1. Random recombination of VJ (light-chain) or V(D)J (heavy-chain) genes
  2. Random addition of nucleotides to DNA during recombination by terminal

deoxynucleotidyl transferase (TdT)

  1. Random combination of heavy chains with light chains
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30
Q

Generation of antibody specificity (antigen dependent)

A
  1. Somatic hypermutation and affinity maturation (variable region)
  2. Isotype switching (constant region)
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31
Q

Describe three functions of antobodies:

  1. opsonization
  2. neutralization
  3. complement activation
A
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32
Q

What do naive B cells express prior to activation?

A

naive B cells prior to activation express IgM and IgD on their surfaces

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33
Q

What type of cells will naive B cells differentiate into by isotype switching?

A

They may differentiate in germinal centers of lymph nodes by isotype switching (gene rearrangement; induced by cytokines and CD40L) into plasma cells that secrete IgA, IgE, or IgG.

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34
Q

Describe IgG

A

Main antibody in 2 degree response to an antigen. Most abundant isotype in serum. Fixes complement, opsonizes bacteria, neutralizes bacterial toxins and viruses. Only isotype that crosses the placenta (provides infants with passive immunity).

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35
Q

Describe IgA

A

Prevents attachment of bacteria and viruses to mucous membranes; does not fix complement. Monomer (in circulation) or dimer (with J chain when secreted). Crosses epithelial cells by transcytosis. Produced in GI tract (eg, by Peyer patches) and protects against gut infections (eg, Giardia). Most produced antibody overall, but has lower serum concentrations. Released into secretions (tears, saliva, mucus) and breast milk. Picks up secretory component from epithelial cells, which protects the Fc portion from luminal proteases.

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36
Q

Describe IgM

A

Produced in the 1 degree (immediate) response to an antigen. Fixes complement. Cannot cross the placenta. Antigen receptor on the surface of B cells. Monomer on B cell, pentamer with J chain when secreted. Pentamer enables avid binding to antigen while humoral response evolves.

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37
Q

Describe IgD

A

Unclear function. Found on surface of many B cells and in serum.

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38
Q

Describe IgE

A

Binds mast cells and basophils; cross-links when exposed to allergen, mediating immediate (type”I) hypersensitivity through release of in#ammatory mediators such as histamine. Contributes to immunity to parasites by activating eosinophils. Lowest concentration in serum.

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39
Q

Thymus-independent antigens

A

Antigens lacking a peptide component (eg, lipopolysaccharides from gram negative bacteria); cannot be presented by MHC to T cells. Weakly immunogenic; vaccines often require boosters and adjuvants (eg, pneumococcal polysaccharide vaccine).

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40
Q

Thymus-dependent antigens

A

Antigens containing a protein component (eg, diphtheria vaccine). Class switching and immunologic memory occur as a result of direct contact of B cells with Th cells.

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41
Q

Describe complement

A

System of hepatically synthesized plasma proteins that play a role in innate immunity and inflammation. Membrane attack complex (MAC) defends against gram negative bacteria

42
Q

Describe classic complement activation pathway:

A

IgG or IgM mediated.

GM makes classic cars

43
Q

Describe alternative complement activation pathway:

A

microbe surface molecules

44
Q

Describe lectin complement activation pathway:

A

mannose or other sugars on microbe surface.

45
Q

function of c3b

A

opsonization

c3b _b_inds bacteria

46
Q

Function of C3a, C4a, C5a

A

C3a, C4a, C5a—_a_naphylaxis

47
Q

function of c5a

A

anaphylaxis and neutrophil chemotaxis

48
Q

function of c5b-9

A

cytolysis by MAC

49
Q

Opsonins

A

C3b and IgG are the two 1  degree opsonins in bacterial defense; enhance

phagocytosis. C3b also helps clear immune complexes.

50
Q

inhibitors of complement

A

Inhibitors—decay-accelerating factor (DAF, aka CD55) and C1 esterase inhibitor help prevent complement activation on self cells (eg, RBCs).

51
Q

Early complement deficiencies (C1-C4)

A

Increased risk of severe, recurrent pyogenic sinus and respiratory tract infections. Increased risk of SLE.

52
Q

Terminal complement deficiencies (C5–C9)

A

Increased susceptibility to recurrent Neisseria bacteremia.

53
Q

C1 esterase inhibitor deficiency

A

Causes hereditary angioedema due to unregulated activation of kallikrein  = increased bradykinin.

Characterized by decreased C4 levels. ACE inhibitors are contraindicated.

54
Q

Paroxysmal nocturnal hemoglobinuria

A

A defect in the PIGA gene preventing the formation of anchors for complement inhibitors, such as decay-acclerating factor (DAF/CD55) and membrane inhibitor of reactive lysis (MIRL/CD59).

Causes complement-mediated lysis of RBCs.

55
Q

Interleukin

A
56
Q

What interleukins are secreted by macrophages?

A

IL 1

IL 6

IL 8

IL 12

TNF-alpha

57
Q

Interleukin-1

A

Causes fever, acute in#ammation. Activates

endothelium to express adhesion molecules.

Induces chemokine secretion to recruit WBCs.

Also known as osteoclast-activating factor

58
Q

Interleukin-6

A

Causes fever and stimulates production of acute-phase

proteins.

59
Q

Interleukin-8

A

Major chemotactic factor for neutrophils

“Clean up on aisle 8.” Neutrophils are recruited by IL-8 to clear infections

60
Q

Interleukin-12

A

Induces differentiation of T cells into Th1 cells.

Activates NK cells.

61
Q

Tumor necrosis factor-alpha

A

Activates endothelium. Causes WBC

recruitment, vascular leak

Causes cachexia in malignancy.

Maintains granulomas in TB.

IL-1, IL-6, TNF-“ can mediate fever and sepsis

62
Q

What interleukins are secreted by all T Cells?

A
63
Q

What interleukin is secreted by TH1 cells?

A
64
Q

What interleukins are secreted from TH2 cells?

A
65
Q

respiratory burst

A
66
Q

interferon alpha and beta

A
67
Q

Cell surface proteins: T cells

A
68
Q

cell surface proteins: b cells

A
69
Q

cell surface proteins: macrophages

A
70
Q

cell surface proteins: NK cells

A

CD16 and CD56 (marker for NK)

71
Q

cell surface proteins: hematopoietic stem cells

A

CD34

72
Q

anergy

A

State during which a cell cannot become activated by exposure to its antigen. T and B cells become anergic when exposed to their antigen without costimulatory signal (signal 2). Another mechanism of self-tolerance.

73
Q

passive vs active immunity

A
74
Q

Types of vaccination

A
75
Q

Type 1 hypersensitivity

A
76
Q

Type II hypersensitivity

A
77
Q

Type III hypersensitivity

A
78
Q

Type IV hypersensitivity

A
79
Q

How do Marcrophages identify what to engulf?

A

They have a CD14 (TLR) receptor that binds to PAMPs (LPS) and DAMPS (necrotic tissue)

80
Q

Explain macrophage interaction with opsonin

A

FC receptor binds to IgG (opsonin)

C3b receptor binds to C3b (opsonin)

81
Q

Macrophage activity in ACUTE INFLAMMATION

A
  1. infiltrates tissue with 2-3 days
  2. phagocytosis and O2-independent killing
  3. Cytokine secretion
  4. possible abscess formation
82
Q

Macrophage activity during CHRONIC INFLAMMATION

A
  1. local antigen presentation
  2. cytokine secretion
  3. possible granuloma formation
83
Q

Explain Macrophage O2 independent killing

A

following phagocytosis, macrophages use lysozyme to hydrolyze bacterial peptidoglycan to lysis bacteria

84
Q

What cytokines do macrophages and dendritic cells produce?

A

IL-1, TNF, IL-6, IL-8 (NEUTOPHIL CHEMOTAXIS), IL-12 (ACTIVATES NK CELLS AND Th1 cells

85
Q

Macrophages form _________ during acute inflammation and __________ during chronic inflammation.

A

Macrophages form ABSCESS during acute inflammation and GRANULOMA during chronic inflammation.

86
Q

What is the difference in dendritic and macrophage interaction with t cells?

A

dendritic cells activate t cells whereas macrophages restimulate activated T cells

87
Q

What effect does surface protein CD40 (macrophage) and CD40L (t-cell) interaction have on macrophages?

A

macrophage stiumlation -> continued phagocytosis, O2 independent killing, and antigen presentation

88
Q

What surface protein on macrophage is targeted by HIV?

A

CCR5

89
Q

Describe formation of noncaseating granulomas

A

Th1 cells release IFN —–> macrophages become epithelioid cells —> some epitheliloid cells combine to form multi-nucleated giant cells —> epithelioid and giant cells surround infection —-> granuloma surrounded by lymphocytes (Th1 cells)

90
Q

Describe caseating (necrotic) granulomas

A

formation: Th1 cells release IFN —–> macrophages become epithelioid cells —> some epitheliloid cells combine to form multi-nucleated giant cells —> epithelioid and giant cells surround infection —-> granuloma surrounded by lymphocytes (Th1 cells)

91
Q

Describe maintenance and degradation of granulomas

A

maintenance: epithelioid cells (formerly macrophages) secrete TNF –> granuloma remains intact
degradation: TNF inhibitors –> granuloma breakdown –> possible disease dissemination

92
Q

What kind of cells are MHC 1 receptors found on?

A

all nucleated cells

93
Q

What are the two ways a Cytotoxic T-cell can kill infected cells?

A
  1. release perforins and granzymes –> apoptosis
  2. FasL binds to Fas on infected cell –> apoptosis
94
Q

What are the three ways Natural Killer cells recognize what to kill?

A
  1. Lack of MHC I
  2. Presence of foreign surface proteins or carbohydrates
  3. antibody-dependent cell-mediated cytotoxicity (ADCC)
95
Q

How does Natural Killer Cells kill infected cells?

A
  1. Release perforins and granzynes –> apoptosis
  2. FasL on NK cell binds to Fas–> apoptosis
96
Q

What are Natural Killer Cells stimulated by?

A

IFN-alpha, IFN-beta = infected cell (saying kill me)

IL-2 (NK and Th1)

IL-12 (macrophages)

97
Q

What cytokines do Natural Killer Cells secrete?

A

IFN-gamma

IL-2 (keeps its own activity going)

98
Q

What are the surface proteins associated with Natural Killer cells?

A
  1. CD56 (helps identify NK cells)
  2. FasL (binds to Fas)
  3. CD16 (aka FC receptor) (binds to IgG)
99
Q

Describe positive selection

A
  • Occurs in the thymic cortex
  • selction for T cells that bind self MHC
  • Thymic epithelial cells express self MHC
  • If T cells are unable to bind –> apoptosis
  • If T cells successfully bind –> negative selection
  • after positive selection T cells will express either CD4 or CD8
100
Q

Describe negative selection

A
  • occurs in thymic medulla
  • selection against T cells that bind self sntigens with high affinity
  • apoptosis or Treg development
101
Q

Describe autoimmune regulator (AIRE) gene

A
  • responsible for intrathymic expression of self antigens
  • mutations –> impaired negative selection (results in abundance of self-destructive T cells)
  • results in autoimmune endocrine diseases
    • recurrent candida infections
    • hypoparathyroidism
    • adrenal failure

HOST AND DEFENSE (4 decks)

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