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IMSE > IMSE I > Flashcards

IMSE I Flashcards

1
Q

C-REACTIVE PROTEIN

–most widely used indicator of _________
–BINDS to [4]
–Effect: [4]

A

Acute Inflammation

small RNA proteins
phospholipids
peptidoglycan
Org. constituents

Opsonization
Complement Activation
Aglutination
Precipitation

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2
Q

C-reactive protein is iNCREASED when there is:

A

Bacterial
Viral

Rheumatic fever
Tuberculosis
Heart attack
Malignant disease

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3
Q

functions by removing cholesterol from cholesterol-filled macrophages @ tissue injury site

contributes to ____ of the area.

A

Serum Amyloid A

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4
Q

Serum Amyloid A is iNCREASED hen there is:

A

Bacterial, Viral infections

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5
Q

________________

acts as____
widely distributed on _______ surfaces throughout the body.

A

Mannose binding Protein/Lectin
[MASP/MBL]

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6
Q

MASP is DECREASED when there is:

A

Recurrent YEAST infection

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7
Q

_____________
a general plasma inhibitor of proteases released from leukocytes, especialy _______.

A

Alpha 1-antitrypsin

elastase

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8
Q

Alpha-1 Antitrypsin is DEFICIENT when there is:

A

Premature emphysema
Smokers
Noxious occupational exposure

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9
Q

Haptoglobin
– bind irreversibly to [bound/free] hemoglobin released by [intravascular/extravascular hemolysis].
– protects the _____ from damage and in [x] loss of ____ by _____ excretion.

A

free

intravascular

kidney

iron
by urinary

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10
Q

PLASMA Haptoglobin is INC. when there is:

A

liver de novo synthesis
no presented release of previously formed from other sites

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11
Q

Haptoglobin is INC. when there is:

A

Inflammation
Stress
Tissue Necrosis

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12
Q

most abundant of the coagulation factors in plasma, and it forms the ______.

A

Fibrinogen

Fibrin clot

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13
Q

principal copper-transporting protein in human plasma.

A

Ceruloplasmin

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14
Q

Ceruloplasmin is DEC. when there is:

A

Wilson’s Disease

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15
Q

Enumerate Acute Phase Reactants

A

C-reactive protein
Serum Amyloid A
Mannose binding protein/lectin
Alpha 1-Antitrypsin
Haptoglobin
Fibrinogen
Ceruloplasmin

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16
Q

Leukocytes percentage in blood

1.Neutrophil
2. Lymphocyte
3. Monocytes
4. Eosinophil
5. Basophil

A
  1. 50-70%
  2. 20-40%
  3. 4-10%
  4. 1-3%
  5. > 1%
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17
Q

Neutrophil
– stages of granules______
– specific granules

Function:
[1]
______: movement through blood vessel wall
–how many percentage are adhered in blood vessel wall and in circulation?
– ______ help make neutrophils sticky and enhance adherence to endothelial cells → that make up the vessel wall.

[2]
______ chemical messengers making cells migrate to a [random/particular] direction.
Examples: [9]

A

primary, secondary, tertiary granules

azurophilic granules

[1]
Diapedesis

50% circulation, 50% blood vessel wall adhesion

Selectins

[2]
Chemotaxins/Chemokines

Complement, Coagulation proteins, Platelet activating factor

Bacteria, Viruses

Mast cells, Macro, Lympho, Neutro

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18
Q

Eosinophils
– INC.: [2]
Function: ______ [less efficient than
neutrophils ← smaller _____ and lack of ______ _______]
– _______ basophil/mast cell products and killing certain ______.

A

allergy, parasitic infections

phagocytosis
numbers
digestive enzymes

neutralizes
parasites

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19
Q

Basophil
– [LARGEST/SMALLEST] of granulocyte
– Maintains [immediate/delayed] _____________.
***looks like ____ cells

A

SMALLEST

immediate
hypersensitivity reactions

mast cells

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20
Q

Monocytes
– _______-shaped nucleus
– ground-glass appearance ← [+] _________ granules.
– BECOME MACROPHAGE: when they go from _______ to _________.

MACROPHAGE
–________ [ less efficient < neutrophils ← __________.

– Life span: range of ______ rather than days.
– Tissue distribution: a [random/specific] phenomenon.

A

Horse-shoe
fine dustlike granules

blood vessel
tissue

phagocytosis
slower motility

months
random

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21
Q

Cells that perform phagocytosis but are less efficient than neutrophils

[Enumerate/Cause of less efficiency]

A

Eosinophil - smaller number, lack digestive enzymes

Macrophages- slower motility

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22
Q

Macrophages in different tissues
enumerate

1.Liver–
2. CNS–
3. Bone—
4. Lung–
5. Connective tissue-
6. Placenta–
7. Spleein–
8. Kidney–
9. Synovial–

A

1.Kupffer cell
2. Microglia
3. Osteoclasts
4. Alveolar macrophage, dust cell
5. Histiocyte
6. Hofbauer cell
7. Littoral cell
8. Mesangial cell
9. Type A lining cell

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23
Q

– common lymphoid precursor.
– differentiated: [3]

A

Lymphocyte

T cell, B cell, NK cell

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24
Q

LYMPHOCYTE TYPES:
1. B lymphocyte/cell: ______. + ____ maturation

  1. T lymphocyte/cell: ______ + ____ maturation
  2. NK lymphocyte/cell: _________

Die in few _____ if not activated by _______.

A

AB production
BM maturation

Regulatory role
Thymus maturation

Innate/Adaptive immuity

thoracic duct

days
foreign antigen

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25
Q

Lymphocyte don’t undergo ______- and ______ to go to the tissue, but rather travel through________.

A

chemotaxis
diapedesis

thoracic duct

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26
Q

product of primary lymphoid organ

product of secondary lymphoid organ

A

Ag-independent

Ag-dependent

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27
Q

Primary lymphoid organ

______- largest tissue in the body. Center for ______________.

______- has cortex and medulla.

A

Bone marrow
Ag-independent lymphopoiesis

Thymus

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28
Q

Secondary lymphoid organ

– Organs [5]

Spleen – filters the [bloodstream/fluid] for ag + removes _______. [smallest/largest] secondary lymphoid organ. [@ upper-[RQ/LQ] of abdomen]

Lymph nodes – filter the [bloodstream/fluid] in the tissue for ag. Generation of ________.

A

Spleen
Lymph nodes
Tonsils
Peyer’s patches
MALT

bloodstream
old RBC
largest
LQ

fluid
b-cell memory

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29
Q

_________
– tells if the lymphocyte is a B, T or NK cell.
– use to name the _____ found in human WBC

Examples
______– T cell
______– NK cell

A

Cluster of differentiation [CD]
protein

CD2/3
CD16/56

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30
Q

Surface Markers/CD on T cells [Elaborate other cells involved]

CDs for:
1. Thymocytes
2. T cells
3. T-helper cell
4. Mature T-cells

  1. Thymocyte subsets
  2. T-cytotoxic
  3. T-cell precursors
  4. Activated T-cell
  5. T-cell subsets
A
  1. CD2 [+NK cells], CD3
  2. CD2 [+NK cells], CD3, CD5- [+B cell subsets]
  3. CD4-[+ mono/macro]
  4. CD5- [+ B cell subsets]
    5.CD8
    6.CD8
    7.CD10-[+ B cell precursors, BM stromal cells]
    8,
    CD25- [+Acitvated B-cell, mono]
  5. CD 56- [+NK cells]
    CD 94- [+NK cells]
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31
Q

B-CELL MATURATION STAGES
[7]

A

Pro-B cell
Pre-B cell
Immature B Cell
Mature B cell
Activated B cell
Plasma B-cell
Memory B-cell

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32
Q

Explain each B-cell stages
1.Pro-B cell
2.Pre-B cell
3.Immature B Cell
4.Mature B cell
5.Activated B cell
6.Plasma B-cell
7.Memory B-cell

A
  1. PRO-B CELL
    Gene rearrangement–> heavy/light chain coding
  2. PRE-B CELL
    Heavy chain starts to synthesize= “u” heavy chain + 2 surrogate light chains
  3. IMMATURE B CELL
    Appearance of Complete IgM molecules [w/ heavy/light chain]
  4. MATURE B-CELL
    Divided: Marginal zone B cell, Folllicular B cell
  5. ACTIVATED B CELL
    Takes place in primary follicles of peripheral lymphoid tissue
  6. PLASMA
    Cytoplasmic Immunoglobulin + little to no Surface Ig.
    AB PRODUCTION.
    [x] blood –> located in germinal centers in peripheral lymphoid organs.
  7. Recirculation
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33
Q

Surface markers for B-cell stages
1.Pro-B cell
2.Pre-B cell
3.Immature B Cell
4.Mature B cell
5.Activated B cell
6.Plasma B-cell
7.Memory B-cell

A
  1. CD19, 24, 43, 45R
  2. CD19, 24, 43
  3. CD21, 40, MHC Class III, IgM
  4. IgM, IgD

5.CD25

  1. Ig in cytoplasm
  2. Surface IgG, IgA, IgE
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34
Q

T-CELL MATURATION STAGES
[4]

A

Double negative
Double Positive
Mature T-cell
Activated

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35
Q

DOUBLE NEGATIVE
— These large double-negative thymocytes actively proliferate in the ________ under the influence of ____.
— Coding for ___ chain starts here

A

outer cortex

IL-7

beta

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36
Q

DOUBLE POSITIVE

-– Coding for ____ chain starts here

–[POSITIVE selection] allows only double-positive cells: ___ and ____ + functional ___________ to survive.
T cells must “[weakly/intermediately/strongly’ recognize foreign antigen [+]_______

Afterwards → A [2nd selection process] _________, takes place among the surviving double-positive T cells.

**Weak/Strong reactions with MHC Class I/II [Positive selection] / self-peptides [Negative selection]→ ________.

A

alpha chain

CD4/CD8+
Functional TCR receptors
Class I/II MHC

Negative selection

apoptosis, programmed cell death

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37
Q

MATURE T-CELL
CD4+: T ____/___ cell [1/3 or 2/3 of T cell]

— Th1: [3]
[protect cells against _____ infections]

— Th2: [4]
[help __ cells produce ___ against [intracellular/extracellular _____ and ____]

— Th17: [2]
[protection against [intracellular/extracellular ____ and ______]

CD8+: T ______ cell [1/3 or 2/3 of T cell]

CD4+ and CD___+: T _____
– [stimulating/suppressing] the immune response to self-antigens

A

helper/inducer
2/3

IFN-y, IL-2, TNF-B
intracellular infections

IL4, 5, 10, 13
extracellular parasites/allergen

IL17, 1L22
extracellular bacteria/fungi

cytotoxic
1/3

CD25
regulator
suppressing

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38
Q

ACTIVATED T CELL

—resting T cell→ activated =
_______ cell [3] OR _____ cell.

A

Effector
Helper, Cytotoxic, Regulator

T Memory cell

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39
Q

NK CELL MATURATION
– [X/+] PROTEIN MARKERS [CD]
–______ unique to express them
– [+] ________ for identification.
– ____ shaped nuclei
– % of the circulating lymphocytes in the blood @[#] ____, peripheral blood.
– ability to mediate _____ reactions and kill target cells [WITH/WITHOUT] PRIOR EXPOSURE to them.

A

X
Surface Ag
Specific combination of Ag

Kidney-shaped
5 to 10%
spleen

cytolytic
WITHOUT

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40
Q

T-cells

Develop in _____
% in blood _____ @ [2]
Identified by _______ w/ _____

End products ______
Located ____ region of lymph nodes.

A

Thymus

60-80% @ Thoracic fluid, lymph nodes

Rosette formation
SRBCs

cytokines
paracortical region of lymph nodes.

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41
Q

B-cells

Develop in _____
@ [3]
Identified by _____________

End products ______
Located ____ region of lymph nodes.

A

Bone marrow

Bone marrow, spleen, lymph nodes

surface immunoglobulin

Antibody
cortical region of lymph nodes.

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42
Q

Of all the lymphocytes, again, how do we know what kind of lymphocyte it is?

[3]

+can use _______ but unaccurate because od [warm/cold] acting antibody.

A
  1. Ficoll-Hypaque - isolation through density gradient centrifugation
  2. Flow cytometer- lymphocyte seperation into diffl subsets
  3. CD marker detection

rosette technique
cold antibody

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43
Q

MOST POTENT PHAGOCYTIC CELL in the tissue.

A

Dendritic cell

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44
Q

MAIN FUNCTION: phagocytose antigen and present it to T-helper.

A

Dendritic cell

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45
Q

Dendritic cell’s Classification/Naming: accdg. to _____ .

A

location

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46
Q

PHAGOCYTOSIS

general process

  1. Physical contact
  2. Cytoplasm outflowing 3. Phagosome
  3. Phagolysosome
    → DIGESTION
  4. Digestion
  5. Excretion
A

INITIATION → CHEMOTAXIS →ENGULFMENT→ DIGESTION

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47
Q

What specifically happens in engulfment process of phagocytosis?

A
  1. Physical contact
  2. Cytoplasm outflowing
  3. Phagosome
  4. Phagolysosome
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48
Q

What specifically happens in digestion process of phagocytosis?

A

5.Digestion
6. Excretion

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49
Q

glycoproteins found on the serum portion of blood.

A

Antibody

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50
Q

Each Ab is made up of a basic [#] chain polypeptide unit that consists [2]. Ab can be cleaved by ____ or ____.

A

4

2 large HEAVY CHAINS
2 smaller LIGHT CHAINS

papain
pepsin

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51
Q

Pepsin digestion

Trimmed at [before/after] hinge region.

End products:
Fab are [monovalent/divalent]

A

after

F[ab]2 + Fc
monovalent

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52
Q

Papain digestion

Trimmed at [before/after] hinge region.

End products:
Fab are [monovalent/divalent]

A

before

2 Fab + Fc
divalent

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53
Q

ANTIGENS

– substances that react with __.

–_______ are antigens → TRIGGERS immune response.
All ______ are antigens but NOT ALL AG ARE ________.

_________ – recognized part of antigen by B [readily/delayed] and T cell [Ag should be processed first by ____ to be recognized]

______ – nonimmunogenic materials that, when combined with a carrier, create new antigenic determinants.

A

Ab

Immunogens
immunogens
immunogens

Epitope/Determinant site
B-readily
T-APC

Haptens

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54
Q

_______ – increase the power of immunogens to create immune response.
– works by attracting the ______ to the site of _______.
– _________ is the only approved adjuvant in the US.

A

Adjuvants
lymphocyte
administration

Aluminum salts

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55
Q

_______ – antigens that belong to the host
________- other members of the host’s species
________- from other species **_____ antigens

A

Autoantigens
Alloantigens

Heteroantigens
Heterophile antigens

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56
Q

IDEAL ANTIGENS to stimulate an immune response:
1. macromolecular size: should be m/w]
2. chemical composition and molecular complexity.
protein → poly > carbs > nylon > Teflon
3. foreignness
4. ability to be processed and presented with MHC molecules

A
  1. macromolecular size [10k m/w, best: 100k
  2. chemical composition/ molecular complexity [protein > poly > carbs> nylon >teflon]
  3. foreignness
  4. ability to be processed/presented w/ MHC molecules.
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57
Q

MHC
— Genes that controls the expression of ____.
— ___= MHC molecules.
— @ all [annucleated/nucleated] cell of the body.

MAIN ROLE:

A

HLA
HLA

nucleated

bind peptides/antigen WITHIN/ON cells> Present to t-cell

58
Q

CLASS 1
– [+] all [nucleated/annucleated] cell
– [#/few on] lymphocyte
– [LOW/UNDETECTED:]
– Binds to [exogenous/endogenous antigen]

A

-nucleated
-#
-hepatocytes, neural cells, muscle cells, sperm cells
–endogenous antigen

59
Q

CLASS 2
– [+] _____
– @ [4]
– Binds Ag found on _______.

A

APC

B lympho, mono, macro, dendritic cells

cell’s surface

60
Q

CLASS 1
Presents antigen to ______
Chain structure _____
Locus/Ag: HLA- _____

NONCLASSICAL CLASS I
HLA-______

A

CD8
a-chain b2-microglobulin
HLA-A,B,C

HLA-E,F,G

61
Q

CLASS 2
Presents antigen to ______
Chain structure _____
Locus/Ag: HLA- _____

NONCLASSICAL CLASS I
HLA-______

A

CD4
a-chain b-chain
HLA-DP,DQ,DR

62
Q

CYTOKINES
— Effect: [3] activity
— Individual cytokines [ACT/DO NOT ACT] ALONE
— produced by different type of cells

A

autocrine, paracrine, systemic/endocrine

DO NOT ACT ALONE

63
Q

TUMOR NECROSIS FACTOR
–[orig. TNF] because it induces ____ of TUMOR cells

  1. TNF - α [also called as] – [least/most] prominent member;
    –FUNCTIONS: [4]
  2. TNF – β [also called as] – produced by ______ & _____ cells.
A

lysis

CACHECTIN
most
Vasodilation, vasopermeability, T-cell/Mono/Macro activation

LYMPHOTOXIN
CD4/8

64
Q

interfere w/ VIRAL REPLICATION

A

Interferon

65
Q
  1. IFN-a
    Other name _______
    Secreted by _______
    Features [2]
  2. IFN-b
    Other name _______
    Secreted by _______
    Features [2]
  3. IFN-y
    Other name _______
    Secreted by _______
    Features [2]
A
  1. Leukocyte IFN
    Leukocytes
    INC. MHC Class 1/2 replication
    [X] Viral replication
  2. Fibroblast/Epithelial cell IFN
    Fibroblasts
    INC. MHC Class 1/2 replication
    [X] Viral replication

3.
immune IFN
TH1, NK
INC. MHC CLASS 1/2 replication
ACTIVATE MACROPHAGE

66
Q

INTERLEUKINS
IL- __ – simulate T cells
IL-__ – inducer of hot body temperature
IL- __ – stimulates bone marrow >= T and B cells
IL- __– stimulates IgE prod.
IL- __ – stimulates IgA prod.
IL- __ - stimulates acute phase reactants production.

A

IL-2
IL-1
IL-3
IL-4
IL-5
IL-6

67
Q

IL1
Induced by:[3]
Released by: [2]

A

microbial pathogens, bacterial lipopolysaccharide, other cytokines

mano/macro

68
Q

IL6
Released in response to ________

A

lipopolysaccharides

69
Q
  1. IL-1α – [intra/extracellularly.]
    [Released] ________.
    Once released, it attracts the ______ cells.
  2. IL-1β –
    [Secreted] by _____.
    [Induces] : [3]
  3. IL-1__ – ANTAGONIST to the rest of IL-1members by competing with receptor.
A
  1. intracellularly
    inflammatory cells
  2. monocytes
    fever, phagocytes, acute phase reactants production
  3. RA
70
Q

CHEMOKINES
– production is by [3]

A

TNF-a, IL-6, many cytokines

71
Q

[NORM] random movement [ABN] chemotaxis

A

Job syndrome

72
Q

[ABN] random movement + chemotaxis

A

Lazy Leukocyte Syndrome

73
Q

receptor of HIV in CD4+ cells

A

CXCR4/CCR5

74
Q

– responsible for the ANTIPROLIFERATIVE activity in a wide variety of cell types.

A

Transforming Growth Factor

75
Q

Transforming Growth Factor Isoforms

A

TGF B1
TGF B2
TGF B3

76
Q

– FAMILY of different GROWTH FACTOR.

A

Colony Stimulating Factor

77
Q

Colony stimulating factors types:

A

IL-3
EPO

GCSF
M-CSF
GM-CSF

78
Q

Promotes opsonization
LYSIS of foreign cells, immune complexes

A

COMPLEMENT

79
Q

Most plasma complement proteins are synthesized in the ___ [EXCEPT C1 components from _______ + Factor D from_____]

A

liver
intestinal epithelial cell
adipose tissue

80
Q

EFFECTOR MOLECULES OR THE COMPLEMENTS that causes an effect on the cell

A

Anaphylatoxins
Chemotazins
Opsonins

81
Q

ANAPHYLATOXINS
– CAUSE: [3]
–COMPLEMENT PROTEINS:
(most to least effective)

A

inc. vascular permeability
smooth muscle contraction
histamine release from baso/mast cell

C5a, C3a, C4a

82
Q

–movement of cells toward the source of chemotaxins

A

Chemotaxins

83
Q

Complement protein of Chemotaxins

A

C5a

84
Q

facilitates PHAGOCYTOSIS and CLEARANCE OF FOREIGN SUBSTANCES

A

Opsonins

85
Q

Complement protein of Opsonins

A

C4b, C3b, iC3b

86
Q

— provide LINK between innate & acquired immune response.

A

CLASSICAL PATHWAY

87
Q

CLASSICAL PATHWAY
Activated by: [9]

A

IgM, IgG3, IgG1, IgG2 [most-least]

Gram [-] Bacteria-E-coli, Viral,

Protozoa, C-reactive protein, Mycoplasma

88
Q

part of INNATE NATURAL IMMUNITY

A

ALTERNATIVE PATHWAY

89
Q

no need need Ab-Ag complex → activates as soon as organism is detected.

A

ALTERNATIVE PATHWAY

90
Q

Activated by: [6]

A

Bacteria [Lipopolysaccharide], Viral, Parasites [Trypanosomes], Yeast, Fungal

Tumor cell lines

91
Q

– proteins that BIND TO CARBOHYDRATES

– RECOGNITION OF CARBS
common constituents of [=]_______+ [≠]________

A

LECTIN PATHWAY

microbial cell walls

human cell surfaces

92
Q

– Provides an ADDT’L LINK between the innate and acquired immune response

A

LECTIN PATHWAY

93
Q

_____: Acute phase reactant

KEY FACTOR:
Mannose-binding or Mannan-binding lectin
that BINDS Mannose or related sugars in the _____of ________.

A

MBL

Carbohydrates
Bacteria, Viral, Parasites, Yeasts

94
Q

Associated disease of
1.C1
2.C2
3.C3
4.C4
5. Factor H/I

A

1.Lupuslike syndrome, recurrent infections
2. Lupuslike syndrome, recurrent infections; Atherosclerosis
3. Severe recurrent infections, Glomerulonephritis
4. Lupuslike syndrome
5. Recurrent pyogenic infections

95
Q

Associated disease of
1.C5-8
2. Properdin
3. MBL
4. MASP-2

A
  1. Neisseria infections
  2. Neisseria infections,
  3. Pneumococcal diseases, Neisseria infections
  4. Pneumococcal diseases
96
Q

Associated disease of
1.DAF
2.MIRL

A
  1. Paroxysmal nocturnal hemoglobinuria
  2. Parozysmal nocturnal hemoglobinuria
97
Q

Associated disease of
1. C9
2. C1INH

A
  1. no known disease
  2. Hereditary angioedema
98
Q

CLASSICAL - LECTIN
REGULATORS

A
  1. C1INH
  2. [C4b-binding protein]/ C4BP
  3. [Complement receptor type 1]/CR1
  4. [Membrane cofactor protein]/ MCP
  5. [Delay Accelerating Factor] DAF
99
Q

inactivates C1; MASP-2
–by binding to the active site of C1r and C1s. → separates them from C1q. C1q remains bound to antigen but all the proceeding processes halt – binding to the MBL-MASP-2 complex.

A

C1-INH

100
Q

– [X] C3 convertase formation
– by disassociating them every time it forms.
– [+] on [SELF/FOREIGN] CELLS
– [absent/present] FOREGIN cells/particles. This is how the body knows what to lyse and what not to.

A

DAF

SELF
ABSENT

101
Q

ALTERNATIVE PATHWAY
REGULATORS

A

Factor H

102
Q

binding to C3b, thus preventing the binding of factor B. [C3bBb/C3 convertase]

A

Factor H

103
Q

ALL PATHWAY [MEMBRANE ATTACK COMPLEX]
REGULATORS

A

S protein/Vitronectin

104
Q

S PROTEIN/VITRONECTIN
– Interacts with the ____ complex
– as it forms in the ______ and prevents it from binding to cell membranes to prevent lysis.

A

C5b67

fluid phase

105
Q

ability of cells to bind complement coated particles.

A

Immune adherence

106
Q

COMPLEMENT CAN BE HARMFUL IF:
[1] ACTIVATED
a. on a [small/large] scale [example]
b. ____ necrosis [example]

[2] ____ LYSIS occurs

A

large
gram [-] septicemia

tissue [MI]

RBC

107
Q

COMPLEMENT’S DEC. LEVELS: [3]

o Clot tube [should be SPUN DOWN]
w/o serum-seperator
o Serum: frozen/dry ice if not tested within 1 to 2 hours

A

– decreased production
– consumption
– in vitro consumption

108
Q

COMPLEMENT LAB DIAGNOSIS:

Type of tube
Tube should be SPUN [up/down]
[With/Without] Serum seperator

Serum, if not tested w/in 1-2 hrs should be at what temp? + placed on a ?

A

Clot tube
down
without

Frozen
Dry ice

109
Q

Immunologic Assays of INDIVIDUAL COMPONENTS

A
  1. Radial Immunodiffusion
  2. Nephelometry
110
Q

Assay for CLASSICAL PATHWAY

A
  1. Hemolytic titration Assay [CH50]
  2. Radial hemolysis
  3. ELISA
111
Q

measures the px serum amount required to lyse 50%
of standardized conc of antibody- sensitized [human/sheep] erythrocytes.

A

[CH50] Hemolytic Titration Assay

112
Q

Assay for ALTERNATIVE PATHWAY

A
  1. AH50
  2. ELISA
113
Q

75-80 % Serum Antibody LARGEST

A

IgG

114
Q

largest to smallest hinge region of IgG

A

IgG3
IgG1
IgG2
IgG4

115
Q

IgG that cannot transfer placenta

A

IgG2

116
Q

Maternal immunity is actively/passively transferred across placenta to fetus> imparts passive protection to newborn

A

IgG

117
Q

Ab type functions:
opsonization
complement fixation
neutralization of toxins/viruses
agglutination & precipitation

A

IgG

118
Q

star-shaped w/ ten functional binding sites

has pentamer: @[2]
monomer: @[1]

A

IgM

secretions, body fluids [saliva,blood]

B-cell surface

119
Q

5-10% Serum Ab

10 days half life

A

IgM

120
Q

First/Most effective in complement fixation

Cannot transfer placenta but FIRST to appear in maturing _____.

A

IgM

infant

121
Q

First to appear in infection/Primary Response. Short-lived response because it is only synthesized as long as Ag is present since there are no memory cells here.

A

IgM

122
Q

Most potent powerful agglutinator
Most effective complement fixation
Opsonization
Neutralization of toxins

A

IgM

123
Q

a dimer joined by J chain

2 types:
[w/ its corresponding Ig subtype]

A

IgA

Serum IgA- IgA1
Secretory IgA- IgA2

124
Q

Found in serum, but # in MALT

A

IgA

125
Q

Cannot activate complement system since it is anti_______

A

IgA

inflammatory

126
Q

Patrol mucosal surfaces
First line of defense of natural immunity
Prevent adherence of organism on mucosal surfaces
Neutralizes toxins

A

IgA

127
Q

abundant on the membrane of many circulating naive b-markers or immunocompetent B lymphocytes & unstimulated B cells

A

IgD

128
Q

one of the heat-labile in Ig class

2 days half-life

A

IgD

129
Q

Cannot activate complement
Cannot transfer placenta
Cannot bind to neutro/acro

Second to appear after IgM on infection ONSET
Play a role in antigen-triggered lymphocyte differentiation/B-cell siurface initate immune response [B-MEMORY CELL activation/maturation/diff]

A

IgD

130
Q

MOST HEAT LABILE

2 days half-life too.
w/ LEAST ABUNDANT % Serum Ab: 0.0005%

A

IgE

131
Q

Cannot activate complement
Cannot transfer placenta

Cannot perform opsonization
Cannot perform agglutination

A

IgE

132
Q

Role in hypersensitivity/parasitic infections [large antigens]

A

IgE

133
Q

Certain cells has had specific surface receptors for antigen that were present before contact with antigen occurred.
○ Once antigens was introduced, it would select the cell with proper receptors, combination would take place and then receptors will break off & enter the circulation as ab molecules. New receptors will be formed in place of those broken off

A

Erlich’s Side Chain Theory

134
Q

Individual lymphocytes are gentically pre-programmed to produce one type of immunoglobulin, and that specific antigen finds or selects those particular cells capable of responding to it, causing these to proliferate

A

Clonal selection theory

135
Q

Clonal selection theory is proposed by

A

Niels Jerne
MacFarlane Burnet

136
Q

pioneering DNA experiments > discovered that CHROMOSOMES contain [x] intact Ig genes, ONLY BUILDING BLOCKS.

A

Susumu Tonegawa

137
Q

a technique to ab production arising from a single b cell> fuses an ACTIVATED B CELL + MYELOMA CELL that can be GROWN INDEFINITELY, which has revolutionized serological testing.

A

Hybridoma technology

138
Q

Year proposed and people behind Hybridoma technology

A

1975
Georges Kohler
Cesar Milstein

139
Q

Ig class w/ 7s sedimentation coefficient

A

IgG
Serum IgA
IgD

140
Q

Ig class w/ 8s sedimentation coefficient

A

IgE

141
Q

Ig class w/ 19s sedimentation coefficient

A

IgM

IMSE (3 decks)

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