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MLT Semester #1 > 1050 Unit 2 > Flashcards

1050 Unit 2 Flashcards

1
Q

what electrophoretic fraction of serum contains the majority of the immunoglobulins?

A

gamma phase

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2
Q

What are 2 characteristics of an isotype?

A

-located in the same species
-located in constant region of heavy chains

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3
Q

What are 2 characteristics of an alltoype?

A

-same species have allotypes present, some do not
-located in constant regions of the IgG subclasses, one IgA subclasses and the gamma light chain

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4
Q

What are 2 characteristics of an idiotype?

A

-variation in variable regions that give individual antibody molecules specificity
-located in amino acid and terminal region of heavy and light chains

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5
Q

Differentiate between light and heavy chains of immunoglobulins and indicate Greek letter

A

-heavy chain: (y) gamma, 50,000 d molecular weight, unique to IgG molecules

-light chain: 2 types –> (k) kappa and lambda (upside down y). Molecular weight is 22,000 d. found is all subclasses but only one type is present in a single molecule.

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6
Q

Discuss the effects of treating an immunoglobulin with papain

A

One or more peptide bonds in the hinge region are split. Producing 3 fragments -two Fab fragments and on Fc fragments

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7
Q

Discuss the effects of treating an immunoglobulin with pepsin

A
  • cleaves the Ig above the set of disulfide bond that hold together the H chains.
    -F(ab)2 created (contains 2 antigen binding sites)
    -Fc portion (in nonfunctional pieces
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8
Q

Describe characteristics of IgG ( half life, molecular weight, amount, Greek letter)

A
  • most abundant in serum (70-75%)
  • gamma (y)
    -longest half life at 23 days
  • monomer w/ molecular weight of 150,000 d
    -4 subclasses: IgG1 (66%), IgG2 (23%), IgG3 (7%) and IgG4 (4%)
    -increases with second exposure
    -lab testing: precipitation and agglutination
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9
Q

What are the functions of IgG?

A

-neutralizes toxins and bacteria
-binds complement
-binds to receptors on phagocytic cells
-able to cross over to placenta

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10
Q

Describe characteristics of IgM (half life, molecular weight, amount in serum, Greek letter)

A

-muu (u) Greek letter
-“macroglobulin”
-pentamer with 10 antibody-binding sites. can also exist as a monomer
-indicates acute infection
-molecular weight of 900,000 d
-accounts for 5-10%
- half life of 6 days
-contains a J chain (joining). Forms disulfide bonds.

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11
Q

What are the functions of IgM?

A

-neutralizes toxins and bacteria
-primary antibody response
-binds efficiently to complement (complement fixation)
-causes efficient agglutination of antigens

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12
Q

Describe characteristics of IgA

A
  • accounts for 10-15%
    -half life of 5 days
  • alpha (a)
    -molecular weight of 160,000 d
    -monomer in serum, dimer in secretion
    -2 sub classes and secretory IgA
    -present in breast milk
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13
Q

What are the functions of IgA?

A

-pass immunity through breast milk
-protects mucosal surfaces and prevents bacteria adherence.
-neutralizes toxins produced by microorganisms
-acts as opsonin’s
-act as anti-inflammatory (IgA1)

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14
Q

Describe characteristics of IgD

A

-appears second, after IgM
-molecular weight is 180,000 d
-only accounts for 0.001% (rare)
half life of 1-3 days
- sigma (s)
-most susceptible to protelysis
-has extended hinge region

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15
Q

What are the functions of IgD?

A

-present as an antigen receptor on B cells (immunocompetent but unstimulated B-cells)
-role in B cell activation
-identifies mature B cells.
-

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16
Q

Describe characteristics of IgE

A

-half life of 2-3 days
-accounts for 0.005%
molecular weight of 190,000 d
-heavy chain with 4 constant regions
-(E) Greek letter?

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17
Q

What are the functions of IgE?

A

-binds to mast cells, basophils and eosinophils.
-triggers allergic reaction
-role is response to parasites, binding to eosinophils that release enzymes that kill large antigens (parasites)
-2 adjacent IgE molecules on mast cells bind a specific antigen
results in degranulation of mast cells and release of vasoactive amines (histamine and heparin)

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18
Q

what are some characteristics of IgG2, IgG3, and IgG4?

A

-IgG3–>most efficient binding complement. Induced in response to antigen proteins

-IgG2 and IgG4–> poor mediators of complement activation. involved in response to polysaccharides antigen

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19
Q

Describe IgA1 and IgA2

A

-IgA1–> acts as anti-inflammatory by downregulating IgG mediated phagocytosis, chemotaxis, bactericidal activity, and cytokine release

-IgA2–> found is secretion of mucosal surfaces (respiratory, urogenital and intestinal tract)

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20
Q

Describe and give characteristics of Secretory IgA

A

-synthesized by plasma cells
-released as a dimer held together by a J chain
-contains secretory complement (SC) derived from epithelial cells
-neutrophils, macrophages and monocytes posses specific receptors
-binding triggers respiratory burst and degranulation of cells is involved

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21
Q

Describe functions of the J chain and the secretory component and indicate which immunoglobulin class they are found in

A
  • j chain–> joining
    -glycoprotein that holds together monomeric units in IgM, the residue forms disulfide bonds.
    -holds together 2 monomers in IgA. Essential for polymerization and secretion of IgA.
    -Secretory complement–> present in IgA. derived from epithelial cells found in close proximity of plasma cells. serves as specific receptor for IgA
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22
Q

Discuss how IgD is different from the other types

A
  • most susceptible to proteolysis
    -does not provide protection
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23
Q

What type of cells do the IgE bind to in an allergic reaction?

A

-mast cells, basophils, and activated eosinophils

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24
Q

Compare and contrast the primary and secondary antibody response to an antigen

A

-primary –> long lag phase (4-7 days), low antibody titer (lowers in few days), low affinity for antigen

-secondary–> IgM produced, followed by a greater predominance of IgG, higher IgG titer which declines slowly over a long period of time, high affinity for antigen

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25
Q

Describe the genes that code for immunoglobulin proteins, and explain how they combine to code for a unique antibody molecule

A

-heavy chains located on chromosome 14
-light chains (kappa) located on chromosome 2
-light chains (lambda) located on chromosome 22
-Gene rearrangement–> involves cutting and splicing process that removes much of the intervening DNA, resulting in functional genes that code specific antibodies.

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26
Q

Describe class switching in immunoglobulins

A

occurs because of process called switch recombination –> portion of constant region of DNA is deleted and remaining CH genes are placed adjacent to variable region genes. This allows the same VDJ region to be coupled with a different c region to produce antibody of a different class. From IgM to either IgG, IgA, or IgE

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27
Q

Explain how clonal selection hypothesis contributes to antibody specificity

A

antigens bind only to B cells receptors specific for that antigen. Once it does, B cells are stimulated to differentiate into plasma cells that secrete antibody specificity for that antigen

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28
Q

outline the traditional process of mouse monoclonal antibody production.

A

1) mouse immunized
2) spleen cells removed
3) combine spleen cells with myeloma cells in the presence of PEG
4)select fused cells and screen for presence of desired antibody
5) grow positive cells in larger quantities

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29
Q

discuss some clinical and research application of monoclonal antibodies

A

-monoclonal antibody reagents are that they provide decreased lot to lot variations and increased specificity toward single epitope of antigen

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30
Q

what is a structural characteristic of the variable domain of immunoglobulins?

A

they occur on both the heavy chain and light chains

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31
Q

How does the structure of IgE differ from that of IgG

A

IgE has one more constant region that IgG

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32
Q

what does a Fab fragment consist of?

A

One light chain an one-half of a heavy chain

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33
Q

which antibody protects mucosal surfaces?

A

IgA

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34
Q

what does a typical structure of an antibody consist of?

A

A tetrapeptide that has two light chains and two heavy chains.

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35
Q

How do the subclasses of IgG mainly differ?

A

the arrangement of disulfide bonds.

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36
Q

Describe role of SC of IgA?

A

a transport mechanism across the endothelial cells

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37
Q

what is thought to be the main function of IgD?

A

B cell activation

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38
Q

which antibody is best at agglutination and complement fixation?

A

IgM

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39
Q

what is the purpose of HAT medium in the preparation of monoclonal antibody?

A

restricting the growth of myeloma cells

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40
Q

papain digestion of an IgG molecule results in what?

A

Two Fab fragments and one Fc fragment

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41
Q

what are the functions of the carbohydrate portion of Igs?

A

-increases the solubility of antibody
-provides protection against degradation
-Enhances functional activity of the Fc domains

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42
Q

what are 3 functions for complement activation?

A

-enhances the inflammatory response
-uses a positive cycle to promote phagocytosis
-enlists more and more defensive elements

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43
Q

what is neutralization?

A

antibodies bind and block specific sites on viruses/exotoxins which prevents antigens from binding to receptors on tissue cells

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44
Q

what is agglutination?

A

antibodies bind the same determinant on more than one antigen. cell-bound antigens are cross-linked, causing clumping

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45
Q

what is precipitation?

A

soluble molecules ae cross-linked into large insoluble complexes

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46
Q

What produces monoclonal antibodies?

A

hybridoma cells

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47
Q

describe cytokine storm

A

-massive overproduction of cytokines. It leads to shock, multiorgan failure or death.
-also called hypercytokinema

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48
Q

Distinguish between autocrine, paracrine and endocrine effects of cytokines

A

-autocrine–> same cell
-paracrine–> nearby cell
-endocrine–> systemic

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49
Q

Explain functions of interleukin- 1 in mediating response

A

-IL-1alpha and IL-1beta–> proinflammatory cytokines produced by monocytes, macrophages and dendritic cells.
-Fever
-induced by microbial components
-includes IL-1alpha, IL-1beta, and IL-1RA

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50
Q

Explain effects of tumor necrosis factors

A
  • TNF-alpha–>causes vasodilation and increased vasopermeability, activates T cells by inducing expression of the MHC class II molecules, vascular adhesion and molecules. (most prominent cytokine in TNF and secreted by macrophages and monocytes)

-TNF-beta–>cause cell death of many types of cells, plays role in development of lymphoid tissues in the GI tract (produced by lymphocytes)

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51
Q

Discuss how interleukin-6 affects inflammation and other activities of immune response

A

-activates B and T cells
-produced by macrophages, monocytes, lymphocytes and nonlymphoid cells
-stimulate B cells to proliferate and differentiate into plasma cells.
-pleiotropic
-plays role in acute-phase reactions and granulocytes hematopoiesis

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52
Q

Determine the role of chemokines in the chemotaxis of WBC

A

-enhance motility of many types of WBC toward source of the chemokines (chemotaxis)
-modulate adhesion of WBCs endothelial cells lining the blood vessels, facilitating extravasation in the tissues
-classified into 4 families based on the position of N-terminal cytosine residues ( cxc, cc, c, cx3c)
-involved in inflammatory response in many diseases

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53
Q

what are the functions of type 1 interferon (IFNs)?

A

-interfere with viral replication
-activate NK cells
- enhance expressions of MHC class I protein
-IFN-alpha is produced by dendritic cells and macrophages
-IFN-beta is produced by a variety of virus infected cells.
-used for treatment of malignancies and autoimmune diseases

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54
Q

What are the functions of type II interferon?

A

-promote cell-mediated immunity (induce CDBT cells that kill infected host cells, activate macrophages to kill intercellular bacteria)
-cause antigen-activated B cells to produce IgG1 and IgG3 (opsonize pathogens and fix complement)
-includes IFN-gamma and IL-2
-produced in response to infections with viruses and intracellular bacteria
-IFN-gamma –> primary cytokine of Th1 response

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55
Q

Describe actions of interleukin-2 on its target cells

A

-drives proliferation an differentiation of T and B cells
-enhance lytic activity of NK cells
-cause naïve Th to differentiate into Th1 cells
-known as T cell growth factor

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56
Q

What is a general role of hematopoietic growth factor?

A

-stimulate proliferation and differentiation of progenitor cells in the bone marrow
-also known as CNFs

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57
Q

Discuss cytokines involved in differentiation of Th1

A
  • cytokines included –> IL-2 and IFN-alpha
    -IL-2 –> drives proliferation and differentiation of B and T cells , causes naïve Th to differentiate into Th1 helper cells (known as T-cell growth factor)
    -IFN-alpha –> stimulates antigen presentation by class I and II MHC molecules stimulating phagocytosis and killing, regulate actions of CD4+cells, CD8+ cells and NK cells. (influences expression of more than 200 genes
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58
Q

Discuss cytokines involved in differentiation of Th2

A

-cytokines involved –>IL-4 and IL-10
-IL-4 –> promote production and inhibits Th1 cells, drives antibody responses in various diseases
-IL-10 –> inhibits antigen presentation by macrophages and dendritic cells (anti inflammatory and suppressive effects on Th1 cells, down regulate immune response by counter acting IFN-gamma (y)

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59
Q

Discuss cytokines involved in differentiation of Treg Cells

A

-cytokines involved–> TGF-beta and IL-10
-Both –> down regulate immune response to prevent chronic infection, helps establish peripheral tolerance to self-antigens and harmful antigens, may prevent tumor cells from attack by inhibiting cancer-fighting cells

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60
Q

Discuss cytokines involved in differentiation of Th17

A

-cytokines included–> IL-17
-role in host defense against bacterial and fungal infections at mucosal surface
-promote release of antimicrobial peptides
-promote recruitment of neutrophils

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61
Q

Explain the biological role of colony-stimulating factors (CSFs)

A

responsible for inducing differentiation and growth of all WBC types

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62
Q

Describe types of anti-cytokine therapies

A
  • anti-cytokine therapies target chronic inflammation
    -disrupting interaction of between cytokines and their receptors (infliximab)
    -using monoclonal antibodies that function as cytokine antagonist
    -blocking IL-17 function
    -hybrid proteins attached to Ig constant regions to block cytokine activity (etanercept)
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63
Q

describe clinical assays for cytokines

A

-ELISpot assay –> a technique similar to ELISA performed on in vitro-activated peripheral WBCs

-multiplexed ELISAs –> can detect many pro- and anti- inflammatory cytokines in one reaction

-Microbead assay–> allow for the simultaneous detection of multiple cytokines and other biomarkers in a single tube

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64
Q

What is the ability of a single cytokine to alter the expression of several genes called?

A

pleiotropy

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65
Q

what is an effect attributed to IL-3?

A

mediation of innate immune response

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66
Q

what are the precursor target cells for IL-3?

A

-myeloid precursors
-lymphoid precursors
-erythroid precursors

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67
Q

What will happen if there is a lack of IL-4?

A

decreased eosinophil count

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68
Q

which of the following cytokines is also known as T cell growth factor?

A

IL-2

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69
Q

IFN-alpha and IFN-beta differ in which way from IFN-gamma?

A

-IFN-alpha and IFN-beta inhibit viral replication
-IFN-gamma stimulates antigen presentation by class II MHC molecules

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70
Q

A patient in septic shock cause by a gram-negative bacterial infection exhibits high fever, very low BP, and disseminated intravascular coagulation. Which cytokine is most likely contributing to these symptoms?

A

TNF

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71
Q

IL-10 acts as an antagonist to what cytokine?

A

IFN-gamma

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72
Q

Selective destruction of Th cells by the HIV virus contributes to immune suppression by which means?

A

decrease in IL-2

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73
Q

why might a CSF be given to a cancer patient?

A

increase production of certain types of leukocytes

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74
Q

what is the best assay to measure a specific cytokine

A

ELISA testing

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75
Q

What would result from a lack of TNF?

A

decreased ability to fight gram-negative bacterial infections

76
Q

what cytokine acts to promote differentiation of T cells and Th1 subclass?

A

IL-12

77
Q

what is the major function of Treg cells?

A

suppression of the immune response by inducing IL-10

78
Q

TH17 cells affect the innate immune response by inducing production of which cytokines?

A

TNF-alpha and IL-6

79
Q

What are the roles of the complement system?

A

-causes lysis of of foreign cells
-increase vascular permeability
-recruit monocytes and neutrophils to the area of antigen concentration
-Trigger secretion of immunoregulatory molecules that amplify the immune response
-

80
Q

what are the 3 stages of the classical pathway and what are there complements?

A

Recognition –>C1
Activation –> C2, C3, C4
membrane attack complex –> C5-C9

81
Q

What are characteristics of C1 in classical pathway?

A
  • first complement to bind
    -consists of 3 subunits –> C1q, C1r, C1s
    -two globular heads of C1q must be bound to antibody to initiate pathway.
    -stabilized by calcium
    -recognizes the Fc regions of two adjacent antibody molecules
82
Q

what are the steps of the recognition stage of classical pathway?

A

-zygomens C1r and C1s are converted into active enzymes as binding of C1q occurs
-autoactivation of C1r results from a change that takes place as C1q is bound
-when activated, C1r cleaves a thioester bond on C1s, which activates it
-C1s has limited specificity, with its only substances being C2 and C4
-when C1s is activated, the recognition stage ends.

83
Q

what are the steps of the activation stage of classical pathway?

A

-C1 cleaves C4 to create C4b and cleaves C2 to create C2a
-C3 convertase (C4b2a) is formed
-C3b binds to C4b2a to form C5 convertase (C4b2a3b)

84
Q

what are the steps of the membrane attack complex in the classical pathway?

A

-C5 convertase splits C5 into C5a and C5b
-C5b attaches to the cell membrane to initiate formation of the MAC (C5b6789)

85
Q

what are some characteristics of lectin pathway?

A

-activated by carbohydrates on microbial cell walls
- serves as a defense mechanism in infancy in between loss of maternal antibody and development of full antibody response
involves three classes of recognition molecules (lections, ficolin’s, CL-IL)

86
Q

what are the steps of the lectin pathway?

A

-Mannose binding lectin protein binds to mannose on the pathogen, MASP-1 and MASP-2 will bind and cleaves C4 and C2
-C4b2 is convertase C3
- C3 convertase cleaves C3
-C3b binds to pathogen near C3 convertase, creating C5 convertase
-C5 convertase cleaves C5
-C5b joins C6, C7, C8, C9 to form MAC

87
Q

What are some characteristics of the alternative pathway?

A

-acts mainly as an amplification loops for classical or lectin pathway
-can be activated by bacterial or fungal cell walls, viruses, tumor cells, and parasites
-acts as natural defense system
-C1, C2 and C4 are not recognized

88
Q

what are the steps of the alternative pathway?

A

-C3 is hydrolyzed b water to produce C3b, which binds Factor B, and together they attach to target cells surfaces.
-B factor cleaved by Factor D into Ba and Bb. Bb combines with C3b to form C3bBb, enzyme with C3 convertase activity
- More C3 is cleaved, forming more C3bBb. This enzyme is stabilized by properdin and continues to cleave C3
- If C3 molecule remains attached to the C3bBbPenzyme, now can cleave C5. C5 convertase consists of C3bBbP3b
-C5 convertase splits C5 into C5a and C5b
-C5b attaches to the cell membrane to initiate formation of the MAC (C5b6789)

89
Q

How does C3 play a key role in all three pathways of complement activation?

A

-essential for activation complement system
-presence of foreign invaders trigger the C3 protein to be cleaved into two pieces
-C3b interacts with other proteins on surface of cells to trigger the complement system response

90
Q

What are characteristics of DAF? (CD #, ligand, cell type, and function)

A

-CD55
-ligand –> C3b, C4b
- cell type –> RBC. neutrophils, platelets, monocytes, endothelial cells, fibroblast, T cell, B cells, and epithelial cells
-function–> dissociates C2b or Bb from binding sites, preventing formation of C3 convertase

91
Q

What are characteristics of MIRL (CD #, ligand, cell type, and function)

A

-CD59
-ligand –> C8
- cell types –> RBC, neutrophils, platelets, monocytes, endothelial cells, and epithelial cells
-function –> prevents insertion of C9 into cell membrane

92
Q

What are characteristics of MCP (CD #, ligand, cell type, and function)

A

-CD46
-ligand –> C3b, C4b
-cell types–> neutrophils, monocytes, macrophages, platelet, T cells, B cells, endothelial cells
-functions–> co factor for factor I, cleavage of C3b and C4b

93
Q

What are characteristics of CR1 (CD #, ligand, cell type, and function)

A

-CD35
-ligand –> C3b, iC3b, C4b
-cell types –> RBC, neutrophils, monocytes, macrophages, eosinophil, B cells, T cells, follicular dendritic cells
-functions –> co factor for factor I, mediates transport of immune complexes

94
Q

What are characteristics of CR2 (CD #, ligand, cell type, and function)

A

-CD21
-ligand –> C3dg, C3d, iC3b
-cell types –> B cells, follicular dendritic cells, epithelial cells
functions –> B cell co receptors for antigen with CD19

95
Q

What are characteristics of CR3 (CD #, ligand, cell type, and function)

A

-CD11c, CD18
-ligand –> iC3b, C3b
-cell types –> monocytes, macrophages, neutrophils, NK cells
-function –> adhesion and increased activity of phagocytic cells

96
Q

What are characteristics of CR4 (CD #, ligand, cell type, and function)

A

-CD11c, CD18
-ligand –> iC3b, C3b
cell types –>monocytes, macrophages, neutrophils, NK cells, activated T and B cells, dendritic cells

97
Q

C1 deficiencies cause..

A

-lupus-like syndrome
-reoccurring infections

98
Q

C2 deficiencies cause..

A

-lupus-like syndrome
-reoccurring infections
-atherosclerosis

99
Q

C3 deficiencies cause..

A

-severe reoccurring infections
-glomerulonephritis

100
Q

C4 deficiencies cause..

A

-lupus-like syndrome

101
Q

C5-C8 deficiencies cause..

A

-Neisseria infections

102
Q

C9 deficiencies cause..

A

no known disease/disorder

103
Q

C1-INH deficiencies cause..

A

-hereditary angioedema

104
Q

DAF deficiencies cause..

A

-paroxysmal nocturnal hemoglobuneria

105
Q

MIRL deficiencies cause..

A

-paroxysmal nocturnal hemoglobuneria

106
Q

Factor H or I deficiencies cause..

A

-reoccurring pyogenic infections

107
Q

MBL deficiencies cause..

A

-pneumococcal diseases
-sepsis
-Neisseria infections

108
Q

Properdin deficiencies cause..

A

-Neisseria infections

109
Q

MASP-2 deficiencies cause..

A

-pneumococcal diseases

110
Q

Describe potential disease manifestations of improper complement regulation

A

-amplifies inflammatory response (anaphylatoxins–> C5a, C3a)
?

111
Q

How do you measure the components of antigens in serum?

A

-automated nephelometry
-immunoturbidimetry

112
Q

How do you measure functional activity of complement pathways?

A

-Radial immunodiffusion (RiD)

113
Q

what are the 2 processes of complement fixation test?

A

1) test system with antigen and antibody- one of which is known
2) indicator system consisting of sheep RBCs coated with a hemolysis which will lyse in the presence of complement

114
Q

what is the purpose of the complement fixation test?

A

to detect viral, fungal or Ricketts antibodies

115
Q

what are the steps of the complement fixation test?

A

1) Destroy any complement present in patient by heating serum at 56 C for 30 minutes
2) Dilutions of serum are combined with known antigen and a measured amount of Guinea pig complement
3) If patient antibody present, it will bind with the reagent antigen and complement will be bound
4) Add sheep RBCs that are coated with a hemolysis. Will lyse if complement is present
5) Incubate and centrifuge tubes
6) Read for hemolysis
7) present –> no patient antibody- test is negative
not present –> patient antibody bound to complement - test is positive
8) results are expressed aw highest dilution showing no hemolysis
9) controls must be used (positive and negative)
10) more sensitive that agglutination and precipitation

116
Q

what are the errors that can be made when performing the complement fixation test?

A

-amounts of manual manipulations required makes it easy to make technical errors
-lack of standardization
-Numerous controls discouraged use in lab

117
Q

what testing is performed for Classical pathway

A

CH50 - how much paper serum is needed to lyse 50% of sensitized sheep RBCs

118
Q

what testing is performed for alternative pathway?

A

AH50 - screening for complement abnormalities

119
Q

what do therapeutic agents do?

A

can replace specific deficient complement proteins or block proteins or block complement proteins involved in disease pathology

120
Q

what is used to treat HAE?

A

recombinant C1-INH

121
Q

classical pathway is activated by what?

A

antigen-antibody complexes

122
Q

where is complement present in the patient?

A

serum

123
Q

What is the Mannose-binding protein in the lectin pathway?

A

C1q

124
Q

what is the role of properdin?

A

stabilization of C3 convertase

125
Q

best way to characterize MAC?

A

Cq polymerizes to forms the transmembrane channel

126
Q

what diseases are associated with complement deficiencies or improper control?

A

-age-related macular degeneration (AMD)
-paroxysmal nocturnal hemoglobinuria (PNH)
- A typical hemolytic uremic syndrome
-C3 glomerulopathy

127
Q

Factor H acts by competing with what for the binding sites?

A

FactorB

128
Q

what is the role of CR2 on cell membrane?

A

acts as co-receptor on B cells for antigen

129
Q

What tests would be performed on patients who is on complement C5 inhibitor?

A

-AH50
-CH50

130
Q

What best characterizes HUS?

A

it is common cause of renal failure in children

131
Q

A decreased CH50 level and a normal AH50 levels indicate which deficiency?

A

Decrease in components of the classical pathway

132
Q

what is the role of anaphylatoxin?

A

increases permeability of blood vessels

133
Q

what are cofactors of Factor I?

A

-Factor H
-C4-binding
-membrane cofactor protein (MCP, CD46)

134
Q

a lack of C1-INH is associated with what condition?

A

hereditary angioedema

135
Q

if a specimen is left out over night, what would occur?

A

a CH50 level would be falsely low

136
Q

define redundancy

A

when different cytokines activate some of the same pathways and genes

137
Q

define synergistic

A

interactions that complement and enhance each other

138
Q

define macrophage colony stimulating factor (M-CSF)

A

-if activated, the cells become macrophages
-increases phagocytosis, chemotaxis and additional cytokine production in monocytes and macrophages

139
Q

define erythropoietin

A

colony stimulating factor that regulates RBC production in the bone marrow

140
Q

define Pleiotropy

A

single cytokine may have different actions

141
Q

define integrins

A

cell adhesion molecules on leukocytes

142
Q

define endogenous pyrogen

A

induces fever

143
Q

define paracrine activity

A

affecting a target cell in close proximity

144
Q

define hypercytokinemia

A

-also known as cytokine storm
-massive overproduction and dysregulation of cytokines produced hyperstimulation of the immune response

145
Q

define granulocyte-macrophage colony stimulating factor (GM-CSF)

A

cytokine produced by T cells and other cells likes that stimulates an increased supply of granulocytic cells and macrophages

146
Q

define antagonism

A

one cytokine may counteract the action of another cytokine

147
Q

define granulocyte colony stimulating factor (G-CSF)

A

-if activated, cells become neutrophils.
-enhances the function of mature neutrophils and affects the survival, proliferation and differentiation of all cell types in neutrophil lineage

148
Q

DELETE

A

DELETE

149
Q

define adaptive T regulatory I cells (Tr1)

A

CD4+ T cells that are induced from antigen-activated naive T cells in the presence of IL-10

150
Q

define affinity maturation

A

process by which TFH cells activate B cells toproduce antibodies with increased affinity for antigen during the course of immune system. Bind more strongly

151
Q

define allelic expression

A

selection of an allele on one chromosome only

152
Q

define Anamnestic response

A

the memory immune response, secondary response

153
Q

define antibody dependent cellular cytotoxicity (ADCC)

A

process of a destroying antibody-coated target cells by NK cells , monocytes, macrophages, and neutrophils all of which have specific receptors for an antibody

154
Q

define class switching

A

process where activated B cells changes its antibody production from IgM to either IgA, IgG, and IgE depending on functional requirements

155
Q

define clonal selection hypothesis

A

states an individual B cell expresses receptors specific to the distinct antigen, determined before the antibody ever encounters the antigen

156
Q

define constant region

A

carboxyl-terminal segment of antibody molecules (half light chain, 3/4 heavy chains) that consists of polypeptide sequence found in all chains of that type

157
Q

define domains

A

region of antibody molecule that consists of ~110 amino acids

158
Q

define Fab fragments

A

fragment of antibody molecule obtained by papin cleavage that consists of a light chain and one-half of heavy chains held together by the disulfide bonding

159
Q

define F(ab)2 fragment

A

fragment of antibody molecule obtained by pepsin that consists of 2 light chains and 2 heavy chains halves held together by disulfide bonds

160
Q

define Fc fragment

A

fragment of an antibody molecule obtained by papin cleavage that consists of a the carboxyl-terminal halves of two heavy chain and are held together by disulfide bond

161
Q

define heavy chain

A

one of the polypeptide units that make up an antibody molecule. each monomer consists of two heavy chains paired with two light chains

162
Q

define hinge region

A

flexible portion of the heavy chain of antibody that is located between the first and second constant regions This allows molecule to bend to let antigen-binding sites operate independently

163
Q

define hybridoma

A

a cell line resulting from the fusion of myeloma cells and B cells. can produce very specific type of antibody called monoclonal antibody

164
Q

define light chain

A

small chain in an antibody molecule that is bound to larger chain by disulfide bonding

165
Q

define monoclonal antibody

A

very specific antibody derived from a single antibody-producing cell that has been duplicated

166
Q

define opsonization

A

coating of a foreign antigen with antibody or complement to enhance phagocytosis

167
Q

define paratope

A

an antigen-binding site on an antibody molecules

168
Q

define variable regions

A

amino-terminal region of an antibody that has a unique amino acid sequence and is responsible for the antigen specificity of antibody

169
Q

define cascades

A

a series of steps that occur in a progressive manner

170
Q

define ELISpot

A

modified ELISA technique that detects frequency of cultured cells that secrete a particular cytokine

171
Q

define interferons (IFNs)

A

cytokines produced by T cells and other cell line that inhibit viral synthesis or act as immune regulates

172
Q

define interleukins (ILs)

A

group of cytokines produced by leukocytes and other cells that regulate adaptive immune responses and the inflammatory process.

173
Q

define proinflammatory

A

cytokines that are positive mediators of inflammation

174
Q

define transforming growth factor-beta (TGF-beta)

A

cytokines that induces antiproliferation activity in a variety of cell types and down regulation of inflammatory response

175
Q

Define tumor necrosis factor (TNF)

A

family of cytokines that mediate the innate defense against gram-negative bacteria and effect adaptive immune response

176
Q

define atypical hemolytic uremic syndrome (aHUS)

A

a rare genetic disorder associated with defects in complement regulation that cause microvascular thrombosis and affect the kidneys

177
Q

define bystander lysis

A

phenomenon that occurs in complement activation when C3b becomes deposited on host cells, making them a target for destruction by phagocytic cell

178
Q

define C3 glomerulopathies (C3G)

A

disease involving the glomeruli of the kidneys

179
Q

define C4-bining protein

A

(C4BP) protein complement system that serves as a cofactor for factor I in the activation of C4b

180
Q

define factor H

A

a control protein in the complement system. Acts as a cofactor with factor I to breakdown C3b formed during complement activation

181
Q

Define factor I

A

serine protease that cleaves C3b and C4b formed during complement activation. A different cofactor is required for each of these reactions

182
Q

define hereditary angioedema (HAE)

A

disease characterized by swelling of extremities, skin, GI tract, and other mucosal surfaces because of a deficiency in the complement inhibitor CINH

183
Q

define immune adherence

A

ability of phagocytic cells to bind complement-coated particles

184
Q

define membrane cofactor protein (MCP)

A

protein found on all epithelial and endothelial cells that helps to control I component-mediated lysis by acting as a cofactor for Factor I - mediated cleavage of C3b

185
Q

define paroxysmal nocturnal hemoglobinuria (PNH)

A

disease characterized by complement - mediated hemolysis of erythrocytes resulting from deficiency of DAF on RBC

186
Q

define properdin

A

protein that stabilizes the C3 convertase

187
Q

define S protein

A

control protein in the complement cascade that interferes with binding of the C5b67 complex to a cell membrane , this is preventing cell lysis

MLT Semester #1 (15 decks)

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