IMSE I Flashcards
C-REACTIVE PROTEIN
–most widely used indicator of _________
–BINDS to [4]
–Effect: [4]
Acute Inflammation
small RNA proteins
phospholipids
peptidoglycan
Org. constituents
Opsonization
Complement Activation
Aglutination
Precipitation
C-reactive protein is iNCREASED when there is:
Bacterial
Viral
Rheumatic fever
Tuberculosis
Heart attack
Malignant disease
functions by removing cholesterol from cholesterol-filled macrophages @ tissue injury site
contributes to ____ of the area.
Serum Amyloid A
Serum Amyloid A is iNCREASED hen there is:
Bacterial, Viral infections
________________
acts as____
widely distributed on _______ surfaces throughout the body.
Mannose binding Protein/Lectin
[MASP/MBL]
MASP is DECREASED when there is:
Recurrent YEAST infection
_____________
a general plasma inhibitor of proteases released from leukocytes, especialy _______.
Alpha 1-antitrypsin
elastase
Alpha-1 Antitrypsin is DEFICIENT when there is:
Premature emphysema
Smokers
Noxious occupational exposure
Haptoglobin
– bind irreversibly to [bound/free] hemoglobin released by [intravascular/extravascular hemolysis].
– protects the _____ from damage and in [x] loss of ____ by _____ excretion.
free
intravascular
kidney
iron
by urinary
PLASMA Haptoglobin is INC. when there is:
liver de novo synthesis
no presented release of previously formed from other sites
Haptoglobin is INC. when there is:
Inflammation
Stress
Tissue Necrosis
most abundant of the coagulation factors in plasma, and it forms the ______.
Fibrinogen
Fibrin clot
principal copper-transporting protein in human plasma.
Ceruloplasmin
Ceruloplasmin is DEC. when there is:
Wilson’s Disease
Enumerate Acute Phase Reactants
C-reactive protein
Serum Amyloid A
Mannose binding protein/lectin
Alpha 1-Antitrypsin
Haptoglobin
Fibrinogen
Ceruloplasmin
Leukocytes percentage in blood
1.Neutrophil
2. Lymphocyte
3. Monocytes
4. Eosinophil
5. Basophil
- 50-70%
- 20-40%
- 4-10%
- 1-3%
- > 1%
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]
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
Eosinophils
– INC.: [2]
Function: ______ [less efficient than
neutrophils ← smaller _____ and lack of ______ _______]
– _______ basophil/mast cell products and killing certain ______.
allergy, parasitic infections
phagocytosis
numbers
digestive enzymes
neutralizes
parasites
Basophil
– [LARGEST/SMALLEST] of granulocyte
– Maintains [immediate/delayed] _____________.
***looks like ____ cells
SMALLEST
immediate
hypersensitivity reactions
mast cells
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.
Horse-shoe
fine dustlike granules
blood vessel
tissue
phagocytosis
slower motility
months
random
Cells that perform phagocytosis but are less efficient than neutrophils
[Enumerate/Cause of less efficiency]
Eosinophil - smaller number, lack digestive enzymes
Macrophages- slower motility
Macrophages in different tissues
enumerate
1.Liver–
2. CNS–
3. Bone—
4. Lung–
5. Connective tissue-
6. Placenta–
7. Spleein–
8. Kidney–
9. Synovial–
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
– common lymphoid precursor.
– differentiated: [3]
Lymphocyte
T cell, B cell, NK cell
LYMPHOCYTE TYPES:
1. B lymphocyte/cell: ______. + ____ maturation
- T lymphocyte/cell: ______ + ____ maturation
- NK lymphocyte/cell: _________
Die in few _____ if not activated by _______.
AB production
BM maturation
Regulatory role
Thymus maturation
Innate/Adaptive immuity
thoracic duct
days
foreign antigen
Lymphocyte don’t undergo ______- and ______ to go to the tissue, but rather travel through________.
chemotaxis
diapedesis
thoracic duct
product of primary lymphoid organ
product of secondary lymphoid organ
Ag-independent
Ag-dependent
Primary lymphoid organ
______- largest tissue in the body. Center for ______________.
______- has cortex and medulla.
Bone marrow
Ag-independent lymphopoiesis
Thymus
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 ________.
Spleen
Lymph nodes
Tonsils
Peyer’s patches
MALT
bloodstream
old RBC
largest
LQ
fluid
b-cell memory
_________
– tells if the lymphocyte is a B, T or NK cell.
– use to name the _____ found in human WBC
Examples
______– T cell
______– NK cell
Cluster of differentiation [CD]
protein
CD2/3
CD16/56
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
- Thymocyte subsets
- T-cytotoxic
- T-cell precursors
- Activated T-cell
- T-cell subsets
- CD2 [+NK cells], CD3
- CD2 [+NK cells], CD3, CD5- [+B cell subsets]
- CD4-[+ mono/macro]
- CD5- [+ B cell subsets]
5.CD8
6.CD8
7.CD10-[+ B cell precursors, BM stromal cells]
8,
CD25- [+Acitvated B-cell, mono] - CD 56- [+NK cells]
CD 94- [+NK cells]
B-CELL MATURATION STAGES
[7]
Pro-B cell
Pre-B cell
Immature B Cell
Mature B cell
Activated B cell
Plasma B-cell
Memory B-cell
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
- PRO-B CELL
Gene rearrangement–> heavy/light chain coding - PRE-B CELL
Heavy chain starts to synthesize= “u” heavy chain + 2 surrogate light chains - IMMATURE B CELL
Appearance of Complete IgM molecules [w/ heavy/light chain] - MATURE B-CELL
Divided: Marginal zone B cell, Folllicular B cell - ACTIVATED B CELL
Takes place in primary follicles of peripheral lymphoid tissue - PLASMA
Cytoplasmic Immunoglobulin + little to no Surface Ig.
AB PRODUCTION.
[x] blood –> located in germinal centers in peripheral lymphoid organs. - Recirculation
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
- CD19, 24, 43, 45R
- CD19, 24, 43
- CD21, 40, MHC Class III, IgM
- IgM, IgD
5.CD25
- Ig in cytoplasm
- Surface IgG, IgA, IgE
T-CELL MATURATION STAGES
[4]
Double negative
Double Positive
Mature T-cell
Activated
DOUBLE NEGATIVE
— These large double-negative thymocytes actively proliferate in the ________ under the influence of ____.
— Coding for ___ chain starts here
outer cortex
IL-7
beta
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]→ ________.
alpha chain
CD4/CD8+
Functional TCR receptors
Class I/II MHC
Negative selection
apoptosis, programmed cell death
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
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
ACTIVATED T CELL
—resting T cell→ activated =
_______ cell [3] OR _____ cell.
Effector
Helper, Cytotoxic, Regulator
T Memory cell
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.
X
Surface Ag
Specific combination of Ag
Kidney-shaped
5 to 10%
spleen
cytolytic
WITHOUT
T-cells
Develop in _____
% in blood _____ @ [2]
Identified by _______ w/ _____
End products ______
Located ____ region of lymph nodes.
Thymus
60-80% @ Thoracic fluid, lymph nodes
Rosette formation
SRBCs
cytokines
paracortical region of lymph nodes.
B-cells
Develop in _____
@ [3]
Identified by _____________
End products ______
Located ____ region of lymph nodes.
Bone marrow
Bone marrow, spleen, lymph nodes
surface immunoglobulin
Antibody
cortical region of lymph nodes.
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.
- Ficoll-Hypaque - isolation through density gradient centrifugation
- Flow cytometer- lymphocyte seperation into diffl subsets
- CD marker detection
rosette technique
cold antibody
MOST POTENT PHAGOCYTIC CELL in the tissue.
Dendritic cell
MAIN FUNCTION: phagocytose antigen and present it to T-helper.
Dendritic cell
Dendritic cell’s Classification/Naming: accdg. to _____ .
location
PHAGOCYTOSIS
general process
- Physical contact
- Cytoplasm outflowing 3. Phagosome
- Phagolysosome
→ DIGESTION - Digestion
- Excretion
INITIATION → CHEMOTAXIS →ENGULFMENT→ DIGESTION
What specifically happens in engulfment process of phagocytosis?
- Physical contact
- Cytoplasm outflowing
- Phagosome
- Phagolysosome
What specifically happens in digestion process of phagocytosis?
5.Digestion
6. Excretion
glycoproteins found on the serum portion of blood.
Antibody
Each Ab is made up of a basic [#] chain polypeptide unit that consists [2]. Ab can be cleaved by ____ or ____.
4
2 large HEAVY CHAINS
2 smaller LIGHT CHAINS
papain
pepsin
Pepsin digestion
Trimmed at [before/after] hinge region.
End products:
Fab are [monovalent/divalent]
after
F[ab]2 + Fc
monovalent
Papain digestion
Trimmed at [before/after] hinge region.
End products:
Fab are [monovalent/divalent]
before
2 Fab + Fc
divalent
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.
Ab
Immunogens
immunogens
immunogens
Epitope/Determinant site
B-readily
T-APC
Haptens
_______ – 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.
Adjuvants
lymphocyte
administration
Aluminum salts
_______ – antigens that belong to the host
________- other members of the host’s species
________- from other species **_____ antigens
Autoantigens
Alloantigens
Heteroantigens
Heterophile antigens
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
- macromolecular size [10k m/w, best: 100k
- chemical composition/ molecular complexity [protein > poly > carbs> nylon >teflon]
- foreignness
- ability to be processed/presented w/ MHC molecules.
MHC
— Genes that controls the expression of ____.
— ___= MHC molecules.
— @ all [annucleated/nucleated] cell of the body.
MAIN ROLE:
HLA
HLA
nucleated
bind peptides/antigen WITHIN/ON cells> Present to t-cell
CLASS 1
– [+] all [nucleated/annucleated] cell
– [#/few on] lymphocyte
– [LOW/UNDETECTED:]
– Binds to [exogenous/endogenous antigen]
-nucleated
-#
-hepatocytes, neural cells, muscle cells, sperm cells
–endogenous antigen
CLASS 2
– [+] _____
– @ [4]
– Binds Ag found on _______.
APC
B lympho, mono, macro, dendritic cells
cell’s surface
CLASS 1
Presents antigen to ______
Chain structure _____
Locus/Ag: HLA- _____
NONCLASSICAL CLASS I
HLA-______
CD8
a-chain b2-microglobulin
HLA-A,B,C
HLA-E,F,G
CLASS 2
Presents antigen to ______
Chain structure _____
Locus/Ag: HLA- _____
NONCLASSICAL CLASS I
HLA-______
CD4
a-chain b-chain
HLA-DP,DQ,DR
CYTOKINES
— Effect: [3] activity
— Individual cytokines [ACT/DO NOT ACT] ALONE
— produced by different type of cells
autocrine, paracrine, systemic/endocrine
DO NOT ACT ALONE
TUMOR NECROSIS FACTOR
–[orig. TNF] because it induces ____ of TUMOR cells
- TNF - α [also called as] – [least/most] prominent member;
–FUNCTIONS: [4] - TNF – β [also called as] – produced by ______ & _____ cells.
lysis
CACHECTIN
most
Vasodilation, vasopermeability, T-cell/Mono/Macro activation
LYMPHOTOXIN
CD4/8
interfere w/ VIRAL REPLICATION
Interferon
- IFN-a
Other name _______
Secreted by _______
Features [2] - IFN-b
Other name _______
Secreted by _______
Features [2] - IFN-y
Other name _______
Secreted by _______
Features [2]
- Leukocyte IFN
Leukocytes
INC. MHC Class 1/2 replication
[X] Viral replication - 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
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.
IL-2
IL-1
IL-3
IL-4
IL-5
IL-6
IL1
Induced by:[3]
Released by: [2]
microbial pathogens, bacterial lipopolysaccharide, other cytokines
mano/macro
IL6
Released in response to ________
lipopolysaccharides
- IL-1α – [intra/extracellularly.]
[Released] ________.
Once released, it attracts the ______ cells. - IL-1β –
[Secreted] by _____.
[Induces] : [3] - IL-1__ – ANTAGONIST to the rest of IL-1members by competing with receptor.
- intracellularly
inflammatory cells - monocytes
fever, phagocytes, acute phase reactants production - RA
CHEMOKINES
– production is by [3]
TNF-a, IL-6, many cytokines
[NORM] random movement [ABN] chemotaxis
Job syndrome
[ABN] random movement + chemotaxis
Lazy Leukocyte Syndrome
receptor of HIV in CD4+ cells
CXCR4/CCR5
– responsible for the ANTIPROLIFERATIVE activity in a wide variety of cell types.
Transforming Growth Factor
Transforming Growth Factor Isoforms
TGF B1
TGF B2
TGF B3
– FAMILY of different GROWTH FACTOR.
Colony Stimulating Factor
Colony stimulating factors types:
IL-3
EPO
GCSF
M-CSF
GM-CSF
Promotes opsonization
LYSIS of foreign cells, immune complexes
COMPLEMENT
Most plasma complement proteins are synthesized in the ___ [EXCEPT C1 components from _______ + Factor D from_____]
liver
intestinal epithelial cell
adipose tissue
EFFECTOR MOLECULES OR THE COMPLEMENTS that causes an effect on the cell
Anaphylatoxins
Chemotazins
Opsonins
ANAPHYLATOXINS
– CAUSE: [3]
–COMPLEMENT PROTEINS:
(most to least effective)
inc. vascular permeability
smooth muscle contraction
histamine release from baso/mast cell
C5a, C3a, C4a
–movement of cells toward the source of chemotaxins
Chemotaxins
Complement protein of Chemotaxins
C5a
facilitates PHAGOCYTOSIS and CLEARANCE OF FOREIGN SUBSTANCES
Opsonins
Complement protein of Opsonins
C4b, C3b, iC3b
— provide LINK between innate & acquired immune response.
CLASSICAL PATHWAY
CLASSICAL PATHWAY
Activated by: [9]
IgM, IgG3, IgG1, IgG2 [most-least]
Gram [-] Bacteria-E-coli, Viral,
Protozoa, C-reactive protein, Mycoplasma
part of INNATE NATURAL IMMUNITY
ALTERNATIVE PATHWAY
no need need Ab-Ag complex → activates as soon as organism is detected.
ALTERNATIVE PATHWAY
Activated by: [6]
Bacteria [Lipopolysaccharide], Viral, Parasites [Trypanosomes], Yeast, Fungal
Tumor cell lines
– proteins that BIND TO CARBOHYDRATES
– RECOGNITION OF CARBS
common constituents of [=]_______+ [≠]________
LECTIN PATHWAY
microbial cell walls
human cell surfaces
– Provides an ADDT’L LINK between the innate and acquired immune response
LECTIN PATHWAY
_____: Acute phase reactant
KEY FACTOR:
Mannose-binding or Mannan-binding lectin
that BINDS Mannose or related sugars in the _____of ________.
MBL
Carbohydrates
Bacteria, Viral, Parasites, Yeasts
Associated disease of
1.C1
2.C2
3.C3
4.C4
5. Factor H/I
1.Lupuslike syndrome, recurrent infections
2. Lupuslike syndrome, recurrent infections; Atherosclerosis
3. Severe recurrent infections, Glomerulonephritis
4. Lupuslike syndrome
5. Recurrent pyogenic infections
Associated disease of
1.C5-8
2. Properdin
3. MBL
4. MASP-2
- Neisseria infections
- Neisseria infections,
- Pneumococcal diseases, Neisseria infections
- Pneumococcal diseases
Associated disease of
1.DAF
2.MIRL
- Paroxysmal nocturnal hemoglobinuria
- Parozysmal nocturnal hemoglobinuria
Associated disease of
1. C9
2. C1INH
- no known disease
- Hereditary angioedema
CLASSICAL - LECTIN
REGULATORS
- C1INH
- [C4b-binding protein]/ C4BP
- [Complement receptor type 1]/CR1
- [Membrane cofactor protein]/ MCP
- [Delay Accelerating Factor] DAF
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.
C1-INH
– [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.
DAF
SELF
ABSENT
ALTERNATIVE PATHWAY
REGULATORS
Factor H
binding to C3b, thus preventing the binding of factor B. [C3bBb/C3 convertase]
Factor H
ALL PATHWAY [MEMBRANE ATTACK COMPLEX]
REGULATORS
S protein/Vitronectin
S PROTEIN/VITRONECTIN
– Interacts with the ____ complex
– as it forms in the ______ and prevents it from binding to cell membranes to prevent lysis.
C5b67
fluid phase
ability of cells to bind complement coated particles.
Immune adherence
COMPLEMENT CAN BE HARMFUL IF:
[1] ACTIVATED
a. on a [small/large] scale [example]
b. ____ necrosis [example]
[2] ____ LYSIS occurs
large
gram [-] septicemia
tissue [MI]
RBC
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
– decreased production
– consumption
– in vitro consumption
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 ?
Clot tube
down
without
Frozen
Dry ice
Immunologic Assays of INDIVIDUAL COMPONENTS
- Radial Immunodiffusion
- Nephelometry
Assay for CLASSICAL PATHWAY
- Hemolytic titration Assay [CH50]
- Radial hemolysis
- ELISA
measures the px serum amount required to lyse 50%
of standardized conc of antibody- sensitized [human/sheep] erythrocytes.
[CH50] Hemolytic Titration Assay
Assay for ALTERNATIVE PATHWAY
- AH50
- ELISA
75-80 % Serum Antibody LARGEST
IgG
largest to smallest hinge region of IgG
IgG3
IgG1
IgG2
IgG4
IgG that cannot transfer placenta
IgG2
Maternal immunity is actively/passively transferred across placenta to fetus> imparts passive protection to newborn
IgG
Ab type functions:
opsonization
complement fixation
neutralization of toxins/viruses
agglutination & precipitation
IgG
star-shaped w/ ten functional binding sites
has pentamer: @[2]
monomer: @[1]
IgM
secretions, body fluids [saliva,blood]
B-cell surface
5-10% Serum Ab
10 days half life
IgM
First/Most effective in complement fixation
Cannot transfer placenta but FIRST to appear in maturing _____.
IgM
infant
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.
IgM
Most potent powerful agglutinator
Most effective complement fixation
Opsonization
Neutralization of toxins
IgM
a dimer joined by J chain
2 types:
[w/ its corresponding Ig subtype]
IgA
Serum IgA- IgA1
Secretory IgA- IgA2
Found in serum, but # in MALT
IgA
Cannot activate complement system since it is anti_______
IgA
inflammatory
Patrol mucosal surfaces
First line of defense of natural immunity
Prevent adherence of organism on mucosal surfaces
Neutralizes toxins
IgA
abundant on the membrane of many circulating naive b-markers or immunocompetent B lymphocytes & unstimulated B cells
IgD
one of the heat-labile in Ig class
2 days half-life
IgD
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]
IgD
MOST HEAT LABILE
2 days half-life too.
w/ LEAST ABUNDANT % Serum Ab: 0.0005%
IgE
Cannot activate complement
Cannot transfer placenta
Cannot perform opsonization
Cannot perform agglutination
IgE
Role in hypersensitivity/parasitic infections [large antigens]
IgE
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
Erlich’s Side Chain Theory
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
Clonal selection theory
Clonal selection theory is proposed by
Niels Jerne
MacFarlane Burnet
pioneering DNA experiments > discovered that CHROMOSOMES contain [x] intact Ig genes, ONLY BUILDING BLOCKS.
Susumu Tonegawa
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.
Hybridoma technology
Year proposed and people behind Hybridoma technology
1975
Georges Kohler
Cesar Milstein
Ig class w/ 7s sedimentation coefficient
IgG
Serum IgA
IgD
Ig class w/ 8s sedimentation coefficient
IgE
Ig class w/ 19s sedimentation coefficient
IgM
