Etiology & Pathophysiology 8% Flashcards

1
Q

What are fibrous joints?

A

Bones connected by fibrous connective tissue with little to no motion

e.g. SI joints, sutures of skull

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2
Q

What are cartilaginous joints?

A

Bones connected by cartilage with little to no motion

e.g. intervertebral discs, pubic symphysis, sternomanubrial joints

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3
Q

What are synovial joints?

A

Bones connected by hyaline cartilage and separated by a joint space lined with synovium and filled with synovial fluid, allowing for FREE MOVEMENT

e.g. most joints

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4
Q

What factors contribute to joint stability?

A

Shape of joint
Joint capsule and ligaments prevent hypermobility
Muscles and tendons actively guide and stabilize
Adhesive properties of synovial fluid

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5
Q

What types of cells make up the synovial membrane?

A

Type A synovial membrane cells (20%)
Type B synovial membrane cells (80%)

Synovial membrane is the same thing as synovial lining or synovial intima.

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6
Q

What are Type A synovial membrane cells?

A

Macrophages
20% of synovial membrane cells
Express CD45, MHC class II, CD68 - macrophage cell surface markers
Remove debris from synovial space

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7
Q

What are Type B synovial membrane cells?

A

Fibroblasts
80% of synovial membrane cells
Produce matrix components

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8
Q

What are the principle components and functions of synovial fluid?

A

Synovial fluid is a filtrate of plasma with similar concentrations of small molecules and lower concentrations of large molecules (e.g. proteins)

Functions to lubricate and allow free movement

Does not have any components of coagulation pathway. Doesn’t clot.

Albumin 1.2 g/dL
Total protein 1.7-2.1 g/dL
IgG 13% of serum, igM 5% of serum
Hyaluronic acid 300 mg/dL - provides viscosity

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9
Q

What are the principle components of articular cartilage?

A

Chondrocytes - derived from MESODERM

Extracellular matrix components

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10
Q

How is articular cartilage organized?

A

Into cartilage ZONES

Zone 1: most superficial and contacts synovial lining. Chondrocytes in zone 1 synthesize LUBRICIN. More cellular in zone 1.

Zone 2
Zone 3

Zone 4: separated by zone 3 by “tidemark” a blue line on H&E. Where calcification of matrix starts.

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11
Q

What do chondrocytes of the articular cartilage synthesize?

A

Chondrocytes of the articular cartilage synthesize:

  1. Proteoglycans and collagen of the extracellular matrix
  2. Proteases to degrade ECM components to maintain cartilage regulation
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12
Q

What are the principle components of the extracellular matrix of articular cartilage?

A

Proteoglycans - protein core to which glycosaminoglycans (chondroitin sulfate and keratan sulfate) attach. Primary proteoglycan is aggrecan.

Collagens

  • Type II collagen
  • Type IX, Type X collagen
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13
Q

What are the classifications of bone based on mechanism of ossification?

A

Intramembranous ossification - facial, cranial, clavicular bones

Endochondral ossification - mostly appendicular and axial skeletal bones

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14
Q

What is bone matrix primarily made of?

A

90% Type I collagen

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15
Q

What cells make and degrade bone?

A

Mesenchymal stem cells
Osteoblasts
Osteocytes
Osteoclasts

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16
Q

What is the function of mesenchymal stem cells?

A

Differentiate into cells of bone (osteoblasts, osteocytes, osteoclasts), cartilage (chondrocytes), muscle (myocytes, or fat (adipocytes)

Located in inter-trabecular loose connective tissue next to vascular channels and in the periosteum

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17
Q

What is the function of osteoblasts?

A

Produce organic components of bone, mainly COLLAGEN but also OSTEOCALCIN and OSTEOPONTIN

After becoming entrapped in formed bone, become OSTEOCYTES within lacunae

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18
Q

What is the function of osteocytes?

A

Mineralizes hydroxapatite, bone’s organic matrix

Most abundant bone cell that preserves bone integrity and mediates remodeling in response to mechanical stress

Connected by cytoplasmic tendrils that deliver nutrients and metabolites to keep the osteocytes alive

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19
Q

What is the function of osteoclasts?

A

Bone resorption

Converts trabecular bone to compact bone

Degrade bone by secreting lysosomal enzymes that cause Ca release

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20
Q

What are the differences between cortical (compact) and trabecular (cancellous, spongy) bone?

A

Cortical (compact) bone - outer layer of thick cortical bone

Trabecular (cancellous, spongy) bone - inner layer of interlacing ossified trabeculae. Alignment of trabecular network with long axis of the bone confers maximal tensile strength and compressive tolerance so that less bone mass is required

Bones subject to mostly tensile and compressive forces (e.g. vertebrae) have thin cortical bone and exert their support by their shape and trabecular architecture

Bones subject to torsion, bending, and shearing forces (e.g. bones of the leg) are usually cylindrical with thick collar of cortical bone and a marrow cavity

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21
Q

What type of collagen is bone predominantly made of?

A

Type 1 collagen (bONE)

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22
Q

What type of collagen is articular cartilage predominantly made of?

A

Type 2 collagen (carTWOlage)

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23
Q

What type of collagen is the glomerular basement membrane predominantly made of?

A

Type 4 collagen (basement has a floor = four)

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24
Q

What is a DEXA scan?

Dual Energy X-ray Absorptiometry

A
  • preferred methods for measurement of bone mineral density (BMD)
  • lowest radiation (1/10th of CXR)
  • need to adjust for bone size
  • osteopenia z score -1 to -2.5
  • osteoporosis z score < 2.5
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25
Q

What enzyme is released during osteoblast activity (bone formation)?

A

Alkaline phosphatase

80% of alk phos in children is from bone. The rest is from liver, gut, kidneys.

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26
Q

What protein is secreted into bone extracellular matrix and correlates with bone formation?

A

Osteocalcin

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27
Q

What is a cleavage product of collagen synthesis and correlates with the number of collagen fibrils formed?

A

Procollagen type I carboxy-terminal propeptides

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28
Q

What ratio is increased with bone resorption?

A

Increased urinary Ca:Cr ratio

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29
Q

What enzyme is released during osteoclast activity but is not specific for it?

A

Tartrate-resistant acid phosphatase (TRAP)

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30
Q

What amino acid is present in mature collagen and is released with breakdown of collagen in bone and other connective tissue but is not specific for it?

A

Hydroxyproline

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31
Q

What stabilizes mature collagen and is released during matrix resorption?

A

Collagen crosslinks of pyridoline, deoxypyridinoline-more specific for bone

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32
Q

What are the N-terminal (Ntx) and C-terminal (Ctx) collagen telopeptides?

A

Markers of bone resorption

Ntx more sensitive and measurable in urine

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33
Q

Anaphylaxis, allergic rhinitis, allergic asthma are examples of what type of hypersensitivity reaction?

A

Type I (immediate)

IgE induced mast cell activation
Basophils and mast cells involved

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34
Q

Autoimmune hemolytic anemia, chronic urticaria, Goodpasture syndrome is an example of what type of hypersensitivity reaction?

A

Type II (cytotoxic)

IgG and IgM autoantibodies
Complement activation and complement mediated phagocytosis
NK cells, eosinophils, neutrophils, macrophages

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35
Q

Serum sickness, PSGN, LN are examples of what type of hypersensitivity reaction?

A

Type III (immune complex)

Deposition of antibody-antigen complexes causing tissue damage
Neutrophils involved

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36
Q

Contact dermatitis, RA, MS, Crohn disease are examples of what type of hypersensitivity reaction?

A

Type IV (delayed)

T cell mediated inflammation of cytotoxicity

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37
Q

What increases bone mineral density?

A

weight bearing exercise

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38
Q

What is the structure of collagen?

A

Extracellular structural protein with 3 alpha chains assemble into a triple helix

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39
Q

What amino acids are highly expressed in collagen? There are 3.

A

Has a high proline, hydroxyproline and glycine content which occupies every third amino acid position. Most proline in sequence of Gly-Pro-Xaa (unspecified AA, often alanine or hydroxyproline).

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40
Q

What are endopeptidase enzymes that cleave by hydrolyzing peptide bonds in the middle of molecules are integral to bone and cartilage homeostasis?

A

Proteinases

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41
Q

Which endopeptidases act in neutral pH?

A

Serine and metalloproteinases

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42
Q

What endopeptidases act in acidic pH?

A

Aspartate, cysteine and threonine proteinases

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43
Q

What leads to increased rigidity and decreased tensile strength with age?

A

Increased stable cross-linking of collagen fibers

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44
Q

What factors control the degradation of proteoglycans and hyaluronic acid?

A

Metalloproteinases, adamtss and cysteine proteinases degrade proteoglycans. Fragments are endocytosed and further degraded in lysosomes. Also cathepsin activity.

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45
Q

What enzyme degrades hyaluronic acid?

A

Hyaluronidase

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46
Q

What constituent of the connective tissue is described below:

Lack tensile strength but can stretch. Produced by fibroblasts and by smooth muscle cells.
In ligaments, blood vessels, lungs and skin allowing these to return to original shape after stretch
Degraded by elastase in the pancreas, macrophages, leukocytes and platelets
Is a serine protease
Contribute to aneurysm formation during vasculitis

A

Elastin

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47
Q

What constituent of the connective tissue is described below:

Dimeric glycoprotein that acts as an attachment protein in the ECM. Produced by many cells and binds to collagens, proteoglycans, fibrinogen, actin, cell surfaces and bacteria.
Between basements membranes and cells. In plasma as insoluble matrix through loose conn tissue.
Binds VLA4, an adhesion molecule on inflammatory cells such as activated T cells

A

Fibronectin

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48
Q

What constituent of the connective tissue is described below:

Major constituent of the basement membrane with type IV collagen

A

Laminin

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49
Q

Where does early B cell development occur?

A

Bone marrow

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50
Q

What must occur for pro-B cells to become pre-B cells?

A

VDJ and VJ recombination of heavy and light chains of immunoglobulin

51
Q

What does a pre-B cell express on the cell surface to acquire Ag specificity and become an immature B cell?

A

A unique B cell receptor (BCR)

Surface IgM

52
Q

What are the 3 processes by which a B cell acquires central tolerance?

A

Receptor editing by secondary rearrangement of the IgX allele

Clonal anergy - B cells that react with low acidity to self Ag can migrate into the spleen as anergic cells

Clonal deletion - for cells that fail receptor editing

53
Q

Immature B cells that survive central tolerance turn into ___ that then turn into ___ and ___with Ag engagement.

A

Immature B cells that survive central tolerance turn into naive B cells that then turn into memory or high affinity plasma cells that make Ab with Ag engagement.the plasma cells occur as a result of somatic hyper mutation, clonal expansion, class switching recombination in the germinal center

54
Q

What does the innate immune system recognize?

A

The innate immune system recognizes molecular structures that are produced by microbial pathogens.

PAMPs and DAMPs

55
Q

What are the functions of pattern recognition receptors (PRRs)?

A

Toll-like receptors (TLRs) are a large class of PRRs expressed on plasma membrane and in endosomes

TLR2 - targets are peptidoglycans (gram positive bacteria) and envelope glycoproteins (viruses)
TLR4 - targets LPS (gram negative bacteria), HSP60 (chlamydia pneumonia), RSV fusion protein
TLR 9 - targets unmethylated CG-rich (CpG) oligonucleotides

TLRs recognize pathogenic micro-organisms and activate antimicrobial defenses
The major signal transduction pathway that TLRs engage to activate cells = NF-KB

PRRs recognize PAMPs

PAMPs bind to TLRs -> receptor oligomerization -> downstream cell signaling -> activates inflammatory pathways within cells (ie. NF-kB)

56
Q

What is the function of mannose (lectin) receptors on phagocytes?

A

Phagocytes (neutrophils and macrophages) use surface receptors, including mannose receptors and scavenger receptors, to recognize extracellular bacteria, and they use Fc receptors and complement receptors to recognize bacteria opsonized with antibodies and complement proteins, respectively.

Mannose receptors function mainly to promote phagocytosis of the microbe

Phagocytosis can be enhanced by coating the microbe with IgG antibodies, C3 and other plasma proteins = opsonization

57
Q

What immune cell produces IFN-gamma? What cell of the innate immune system is activated?

A

Th1 cells produces IFN-gamma

IFN-gamma is a potent activator of macrophages

58
Q

What is the immune defect in chronic granulomatous disease?

A

Inherited deficiency of one of the components of phagocyte oxidase. This deficiency compromises the capacity of phagocytes to kill certain bacteria.

59
Q

How do NK cells kill viral-infected cells?

A

Direct action of NK cells: NK cells have granules containing proteins that mediate killing of target cells
When they recognize a virus infected cell and are then activated, they secrete these granules, such as perforin, which puncture the infected cell and release granzymes into the infected cells which cause the cell to undergo apoptosis.

60
Q

What cytokines do NK cells secrete?

A

Mainly TNF-alpha and IFN-gamma

which act on other immune cells like macrophages and DCs to enhance the immune response

Produce high levels of IFN-gamma (a potent stimulator of macrophages), TNF-alpha, GM-CSF, and other cytokines and chemokines

In turn, activated macrophages produce IL-12, a potent inducer of NK cell, IFN-gamma, and cytolytic activity

Additional cytokines secreted include IL-17, IL-22

61
Q

How do NK cells kill target cells?

A

NK cells release cytotoxic granules containing perforin and granzyme, which leads to lysis of the target cell

62
Q

What are the 4 functions of complement proteins?

A

Promote phagocytosis of microbes by opsonization (C3b has the most opsonizing activity)

Complements bind antigen-antibody complexes promoting their solubilization and their clearance by phagocytosis

Stimulation of inflammation - by attracting macrophages and neutrophils

Induction of lysis of microbes

63
Q

What cells produce complement proteins?

A

The liver is the primary source of plasma complements, hepatocytes make most of the proteins and glycoproteins. Tissue macrophages, blood monocytes, and epithelial cells of the GU and GI tract.

64
Q

What inhibits C1r and C1s?

A

C1 inhibitor - serine protease inhibitor.

C1 INH prevents the C1r/C1s complex from starting the proteolytic cascade and causes the complex to dissociate from C1q, creating a time dependent period for C1r/C1s to be activated before being automatically removed

Deficiency of C1 INH leads to hereditary angioedema where you get activation of bradykinin leading to vascular permeability

65
Q

What inhibits C3 and C5 convertase?

A

C3b and C4b, which are found on cell surfaces

66
Q

What inhibits the assembly of MAC complex?

A

CD59 membrane protein

S protein in the blood

67
Q

What chromosome is MHC complex located on?

A

Chromosome 6

68
Q

What are the most common positive acute phase reactants?

A

Procalcitonin, CRP, ferritin, fibrinogen, hepcidin, serum Amyloid A, haptoglobin, complement (C3, C4)

Angiotensinogen, alpha-1-acid glycoprotein, lipopolysaccharide-binding protein (LBP), alpha-1-antitrypsin, vitronectin, ceruloplasmin, alpha-1 macroglobulin

69
Q

What are negative acute phase reactants? (decrease with inflammation)

A

Albumin, prealbumin, transferrin, retinol-binding protein, antithrombin

70
Q

What is a marker for macrophage activation?

A

Neopterin is specifically produced by human monocytes/macrophages when stimulated by IFN-gamma released from activated T cells

Studied in MAS/HLH, AIBD, JDM

71
Q

What part of innate immunity does C-reactive protein activate?

A

C reactive protein is a plasma protein and part of a group of proteins called penntraxins

Penntraxins recognize phospholipids (i.e. phosphorylcholine) found only on bacteria, and bind C1q and initiate the COMPLEMENT CLASSICAL PATHWAY

Interacts with phagocyte C1q receptors and binds directly to the Fc gamma receptors

72
Q

What are the pro-inflammatory cytokines?

A

IL-1alpha, IL-1beta, TNF-alpha, IL-6, IL-17, IL-22

73
Q

What are anti-inflammatory cytokines?

A

IL-10, TGF-beta

74
Q

What cytokines are produced by T helper (Th2) cells?

A

IL-4, IL-5, IL-13

75
Q

What cytokines are produced by Tregs?

A

IL-10 and TGF-beta (anti-inflammatory)

76
Q

What does interferon-alpha do?

A

activates NK cells and increases MHC type 1 presentation, antiviral state, and has multiple other effects (especially in SLE)

77
Q

Which cytokines influence bone destruction?

A

TNF-alpha, IL-1, IL-6, IL-7, and IL-17

In inflammatory bone disorders (JIA, RA), elevated inflammatory cytokines have been implicated in bone destruction through recruitment of osteoclast precursors to the bone environment, where they differentiate into mature osteoclasts

These inflammatory cytokines, such as TNF-alpha, IL-1, IL-6, IL-7, and IL-17, are responsible for the overexpression of RANKL and decreased levels of osteoprotegerin (OPG), a decoy receptor of RANK.

This perturbation leads to an imbalance in the RANKL/OPG ratio, thereby increasing osteoclast differentiation (also known as osteoclastogenesis)

78
Q

What stimulates Type 1 IFN production? What is the function of Type 1 IFN?

A

Type 1 IFN - produced by most cells upon stimulation by a virus (leukocytes, plasmacytoid DCs, Fibroblasts); primary function is to induce viral resistance in cells
Inhibit viral replication, increase the lysis potential of NK cells and expression of MHC class I molecules on viral infected cells, stimulate the development of Th1 cells
IFN-alpha
IFN-beta

79
Q

What size molecules are removed by dialysis? (for Katie)

A

All molecules in plasma > 15 kD

80
Q

What cytokine activates B cells to antibody producing plasma cells and induces Th17 differentiation?

A

IL-6

81
Q

Which interleukins influence fibrosis?

A

Th2-derived cytokines (IL-4, IL-5, IL-6, IL-13, and IL-21) have a distinct role in the regulation of organ fibrosis

Especially IL-6

82
Q

What are the roles of antibodies?

A

Pathogen and toxin neutralization

  • IgG in blood and tissues
  • IgA in gut lumen

Classical complement activation/fixation
- IgG1, IgG3, IgM

Opsonization to promote phagocytosis and pathogen elimination

Antibody-dependent cellular cytotoxicity
- IgG binds infected cell to be killed by NK cells

83
Q

What are the principles of humoral immunity?

A

Humoral immunity encompasses aspects of the immune system mediated by antibodies, complement proteins, and certain antimicrobial proteins (AMPs) found in the extracellular fluid

Humoral immunity refers to antibody production and the coinciding processes that accompany it, including:

  • Th2 activation and cytokine production
  • Activation of specialized antigen-presenting cells leading to…
  • Germinal cell reaction leading to…
  • Generation of long lived plasma cells and memory B cells.
  • Isotype switching of B cells
  • Affinity maturation and memory cell generation
84
Q

What is the germinal center reaction?

A

The GC reaction occurs in response to protein antigen and has several outcomes:

Antibody affinity for antigen increases.
B cells differentiate into long-lived plasma cells that secrete antibodies.
B cells differentiate into memory B cells that can generate more plasma cells.
There is isotype switching at the immunoglobulin genes to create IgA, IgG, or IgE antibodies with the same antigen specificity as the original IgM.

85
Q

What is isotope switching?

A

Generation of different antibody isotypes (IgGAME) that contributes to effective immunity.

B cells undergo isotype switching at the immunoglobulin genes in response to T cell signals in the GC reaction.
There is isotype switching at the immunoglobulin genes to create IgA, IgG, or IgE antibodies with the same antigen specificity as the original IgM.
Isotype switching alters the antibody heavy chain but does not affect antibody affinity for antigen.
Isotype switching involves the cutting and rearranging of DNA.

86
Q

What are the roles of B cells?

A

B cells differentiate into plasma cells that secrete antibodies
B cell affinity maturation so that they make antibodies with higher affinity
B cells differentiate into memory B cells that. can generate more plasma cells

87
Q

What is the structure of IgG?

A

Monomer with 2 heavy chains paired with 2 light chains that create the constant fragment (Fc) and 2 identical variable Ag binding fragments (Fab)

88
Q

What is the function of IgG?

A

Workhorse of humoral immunity
Main Ab of secondary responses

Activates phagocytosis by opsonization - Fc binds to phagocytes
Neutralizes Ag

89
Q

What is the structure of IgA?

A

Dimer

90
Q

What is the function of IgA?

A

Protects mucosal surfaces
Protease-resistant
Functions in the gut as well

91
Q

What is the structure of IgM?

A

Pentamer

92
Q

What is the function of IgM?

A

First Ab produced during an immune response
Activates complement
Low affinity but high avidity
The monomer form of IgM serves as a B cell receptor

93
Q

What is the structure of IgE?

A

Monomer

94
Q

What is the function of IgE?

A

Destroys parasitic worms (extra-cellular parasites)

Involved in allergy and response to helminths (worms)

95
Q

What is the structure of IgD?

A

Monomer

96
Q

What is the function of IgD?

A

B cell receptor

Activation of IgD is an important B cell survival signal

97
Q

What cytokine signal causes proliferating B cell to differentiate into a plasma cell that makes IgG2 or IgG3?

A

IFN-gamma

98
Q

What cytokine signals cause proliferating B cell to differentiate into a plasma cell that makes IgE?

A

IL-4, IL-5

99
Q

What cytokine signal causes proliferating B cells to differentiate into a plasma cell that makes IgA?

A

TGF-beta

100
Q

What cytokine signals causes proliferating B cell to differentiate into a plasma cell that makes IgM?

A

IL-2, IL-4, IL-5

101
Q

What 2 signals/interactions must occur to activate a T helper cell?

A

APC Th cell

  1. MHII-Ag T-cell receptor
  2. B7 CD28
102
Q

What happens when an activated T helper cell secretes cytokines?

A

Class switching

103
Q

What to signals/interactions must occur to activate a B cell to proliferate, differentiate, and secrete Abs?

A

Activated Th cell B cell

  1. T cell receptor MHC II-Ag
  2. CD 40 ligand. CD 40
104
Q

What is somatic mutation in the context of humoral immunity?

A

Somatic hypermutation involves a programmed process of mutation affecting the VARIABLE REGION OF IMMUNOGLOBULIN GENES. Unlike germline mutation, SHM affects only an organism’s individual immune cells, and the mutations are not transmitted to the organism’s offspring. Mistargeted somatic hypermutation is a likely mechanism in the development of B-cell lymphomas and many other cancers.

SHM diversifies B cell receptors used to recognize new Ag and allows the immune system to adapt its response to new threats during the lifetime of an organism.

105
Q

What is affinity maturation?

A

Affinity maturation is a coordinated process with distinct stages including:

migration of B-cells to secondary lymphoid organs where

  • B-cells proliferate in germinal centers to form a colony
  • the B-cell receptor is randomly mutated in different cells

selection of the cells with the highest affinity receptors within the colony by

  • providing a limited number of survival signals
  • allowing mutated B-cells to compete for these signals
  • pruning less effective B-cells through apoptosis
106
Q

What anti-inflammatory cytokines do B regulatory cells (Bregs) release?

A

IL-10, IL-35, and TGF-β

Bregs also interact directly with T cells to encourage differentiation into Tregs

107
Q

Know the general structure, size, and organization of the human genome

A

3.2 billion deoxyribonucleic acid (DNA) base pairs
23 pairs of chromosomes
over 44,000 genes

108
Q

Know how genes are organized (e.g., introns, exons, promoters, and enhancers)

A

Exons: gene segments that encode protein sequences
Introns: do not encode protein sequences

109
Q

How are genes regulated by epigenome?

A

The epigenome is involved in regulating gene expression, development, tissue differentiation, and suppression of transposable elements The epigenome can be dynamically altered by environmental conditions.

110
Q

What is the most predominant isotype of antibody secreted by Plasma B lymphocytes?

A

IgG

Plasma B lymphocytes secrete large quantities of antibodies. The most predominant isotype in the blood and extracellular fluid is IgG.

111
Q

What Isotype are the pathogenic antibodies in lupus patients against double-stranded DNA?

A

IgG

Pathogenic antibodies in lupus patients against double-stranded DNA are mostly of the IgG isotype

112
Q

What cytokines would be used by the body to clear a pinworm infection?

A

IL-4 and IL-5

Pinworms are parasites. Eosinophils are recruited to the sites of infection and inflammation to help clear the worms. Cytokines involved in the parasitic inflammatory response include IL-4 and IL-5. In particular, IL-5, also called eosinophil differentiation factor, is produced in response to a parasitic infection and is mainly responsible for the growth, activation, and differentiation of eosinophils.

113
Q

What type of T cell is needed to protect against intracellular pathogens like mycobacteria or salmonella?

A

Th1 T cells

Th1 T cells produce interferon-γ and induce killing of intracellular pathogens such as mycobacteria or Salmonella.

114
Q

What cells produce INF-gamma to activate macrophages to produce reactive nitrogen species and kill intracellular bacteria and fungi?

A

Th1 CD4+ T cell

115
Q

What cells produce IL 4 and IL 5?

A

Th2 CD4+ T cell

116
Q

Which T cells and interleukins are important for allergy and eosinophils?

A

Th2 CD4+ T cell
IL4 makes IgE
IL 5 activates eosinophils

117
Q

What T cell and interleukin defends against extracellular bacteria and fungi?

A

Th17 CD4+ Tcell

IL 17 induces neutrophil rich inflammation

118
Q

What cells and targets are important for peripheral tolerance?

A

Treg C4+ T cel

expresses CTLA-4 and TGF-betta to suppress auto reactive T cell

119
Q

What cells lyse virus infected cells expressing viral antigens?

A

CD8+ T cell

120
Q

What type of hypersensitivity reaction is described below:

drug-IgE complexes that bind to mast cells and release histamine and inflammatory mediators

A

Type I reactions (IgE-mediated)

Type I reactions (IgE-mediated), such as drug-IgE complexes that bind to mast cells and release histamine and inflammatory mediators

121
Q

What type of hypersensitivity reaction is described below:

specific IgG or IgM antibodies directed at drug hapten-coated cells

A

Type II reactions (cytotoxic)

Type II reactions (cytotoxic), such as specific IgG or IgM antibodies directed at drug hapten-coated cells

122
Q

What type of hypersensitivity reaction is described below:

tissue deposition of drug-antibody immune complexes with activation of complement and inflammation

A

Type III reactions (immune complex), such as tissue deposition of drug-antibody immune complexes with activation of complement and inflammation

123
Q

What type of hypersensitivity reaction is described below:

MHC presentation of drug molecules to T cells with release of cytokines and inflammatory mediators

A

Type IV reactions (delayed, cell-mediated), such as MHC presentation of drug molecules to T cells with release of cytokines and inflammatory mediators