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152 Cards in this Set

  • Front
  • Back
Structure of Ig
4 polypeptide chains
2 heavy
2 light
Arms: FAB and Fc
Where does Antigen bind to Ig
Binds to FAB, antigen binding site
High concentration (75-80 %) in circulation at all times
a. Formed after IgM
b. Neutralizes toxins by interfering with the protein binding sites, attachment, tissue damaging enzymes – very good
c. Inactivates viruses – when viruses are extracelluar
d. Acts as a great opsonin: bridges MO and macrophage surfaces
e. The only antibody that crosses the placenta to provide newborns with passive immunity – Natural Acquired Passive Immunity – all the immunity of the mother – provides protection for several months after birth
f. IgG immune response could last for years. Their presence persists over time
g. A whole bunch (2,000) can activate the classical compliment pathway
10% of Ig in circulation
a. First Immunoglobulin made in immune response. Use that fact diagnostically – can look for IgMs in blood for a specific disease.
b. Forms a pentamer (5) of the Y shaped structures linked together at Fc ends so have 10 exposed Fab ends – large molecule
c. Neutralize infectivity by interfering with the protein binding sites (attachment)
i. neutralizes toxins (binding to it interferes with toxins’ functions)
d. Inactivates viruses – when they are extracelluar
e. When the antigen binds to the variable regions, the Fc region undergoes a conformational change and which allows it to bind to PMN’s and macrophages which assists phagocytosis. – not an opsonin
f. Good activator of the classical compliment pathway – only need 1 pentamer to bind to the target to get C1q to bind.
g. Presence indicates the acute inflammation phase of an illness – don’t have a lot just floating around in blood in normal times
fxn= as antigen receptor
very little in circulation, but important in secretions (saliva, tears, breast milk, mucus: intestinal urinary etc.)
a. In blood it forms a monomer: Y
b. In circulation the monomer doesn’t last very long, ~ a few months
c. Consists of 10% of IgAs
d. Functions as a weak opsonin
e. In secretions, it forms a dimer: >=J=< (2 Ys with the stems joined by “J” chain)
f. As the dimer passes thru epithelial cells, a secretory component is added before the IgA is secreted as sIgA
g. Secretory unit is there to transport it
h. sIgA interferes with attachment of foreign materials to mucosal linings - neutralizes infectivity
i. Does not activate the classical pathway
j. So even if we have a secretory response that is very good, we will continue to have to re-develop it, if exposed after a few months.
k. Breast fed infants are passively immunized as they breast feed due to sIgA – Natural Acquired Passive Immunity
In secretions, it forms a dimer: >=J=< (2 Ys with the stems joined by “J” chain)
f. As the dimer passes thru epithelial cells, a secretory component is added before the IgA is secreted as sIgA
g. Secretory unit is there to transport it
h. sIgA interferes with attachment of foreign materials to mucosal linings - neutralizes infectivity
i. Does not activate the classical pathway
j. So even if we have a secretory response that is very good, we will continue to have to re-develop it, if exposed after a few months.
k. Breast fed infants are passively immunized as they breast feed due to sIgA – Natural Acquired Passive Immunity
-neutralizes toxins
Almost no free IgE; all of it binds to cell surfaces – cytophilic
a. IgE’s tail (Fc) binds to surface of mast cells and basophils - receptor for antigens
b. Thousands of IgEs attach to the cell’s surface, presenting a wide variety of antigen binding specificities – gets acute inflammation up and running
c. If an antigen binds to IgE on a Mast cell, the tail of the IgE undergoes a conformational change that stimulates the Mast cell to release its stored vasoactive substances
ii. The more IgE on the surface, the more histamine can be released. Allergies are the excessive production of IgE and a proportional excessive release of vasoactive substances in response to a normally innocuous substance/antigen
iii. Allergies are the result of:
• To many IgE receptors on Mast cells
• Host produces too many of a particular IgE
• You CAN’T have an allergic reaction the first time (it could take several exposures before allergic rxn) stings before
not free circulating
a. Bound to mature/immunocompetent B-cells on the surface
b. Serves as a receptor (along with IgM) for antigen on B cells
c. A conformational change in the tail triggers B cell activation
d. One B-cell recognizes a single antigenic determinant
innate or natural immunity is
1.nonspecific host resitance, 2.not acquired, 3.first line of defense
innate or natural immunity characteristics
1. not acquired, pre-existing, always available, 2. not specific=not directed at a particular agent
acquired immunity results from
results from interaction b/t cells of the imm system&components of inf or non inf Ag
acquired immunity products
Abs and sensitized lymphocytes
acquired immunity characteristics
1. highly specific, 2. requires previous exposure, 3. involves the recog'n of Ag by Ab or sensitized lymphocytes
passive immunity is
nonsusceptibility due lack of approp receptors
nonspec host resistance-mechanical and chemical factors (external)
skin, muc membr, leuk in/on muc memb, nasal hair, ciliated cells, coughing, fever, lysozyme, fa on skin, flusing of urin, saliva, terars, acidity and mobility of dg tract
nonspec host resistance-normal microflora (external)
presence/balance is a dynamic equilibrium, bact living on/in us are impt for competition w/pathogens for space, nutrients; normal prod'n metabolic wastes-->inhibit some pathogens
nonspec host resistance-internal
blood, mast cells, lymphatic system, reticuloendothelial system/mononuclear phagocyte system, other soluble factors (defensins, cathelicidins)
nonspec host resistance-formed elements(internal)
neutrophils/PMNs, monocytes, basophils, eosinophils, NK cells, platelets
nonspec host resistance-plasma(internal)
interferon, alternative complement pthwy, classical complement pthwy, acute phase proteins
nonspec host resistance-phagocytosis (internal)
PMNs, macrophages
antibiotics and normal microflora
antibiotics can kill normal flora, enabling resistant pathogens to fluorish i.e. thrush, vaginal yeast infections
neutrophils or PMNs
first cellular responders in acute inflamm'n, multilobular nucleus, most numerous, phagocytes
phagocytic cells that migrate into tissues (not as quick as PMNs); in tissues are called macrophages, impt in transition from nonspecific defenses to acquired immunity
contain histamine, overresponse leads to allergic rxn w/body-wide vasodilation, decr in bp, decr bldflow to major organs, stasis, incr clotting, mobile
effective against parasitic inf, can respond in allergic rxns
NK cells
kill malignant cells, viral-inf'd cells, nonspecifically recog target due to abnormal cell surface (low MHC-I on surface)
nec for bld clotting, source of vasoactive substances and fibroblast growth factors which make collagen to promote healing
vasodilator, bronchioconstrictive; produced by mast cells and basophils
prot found in plasma that is synth'd by viral inf'd cells that inhibits viral inf in other cells, non-spec for infec agent, species specific (cannot use IF from other animals)
complex of serum proteins that act in a seq toenhance and amplify phagocytosis, acute inflamm'n and lysis of MOs
acute phase protein
prot prod by hepatocytes and found in the plasma that grtly increases in [ ] in resp to early alarm mediators (i.e. complement reactive proteins CRP); APP binds MO and enhances binding of complement to MO
complement reactive protein
CRP facilitate the complement binding to MO and activation of the alternative pthwy
soluble mediator of inflamm'n (i.e.C3a,C5a)-> induce contrx of sm m and incr vasc permeability
why more infections in winter?
dry->reduces mucous thickness which normally traps Mos and prevents them from contacting underlying epithelium
purpose of the alternative complement pathway (3)
non-specific pathway whose purpose is to generate molecules that enhace and amplify: 1. phagocytosis, 2. acute inflammation, 3. lysis of MO
purpose of the classical complement pathway
specific pthwy in response to reinfection - Abs bind to spec Ags
mast cells
non-motile, typically found in sub-cu tissue and mucosa, *critical in establishing the def supply line by releasing vasoactive substances
lymphatic system-purpose in the imm response
contain a lg # of macrophages and lymphocytes; where acquired imm resp begins
reticuloendothelial system-purpose
participant in initiation of acute inflammation
reticuloendothelial system-players
sm bld vessels, Kupffer cells from liver and spleen, alveolar macrophages, serosal macrophages, microglia, osteoblasts, lymph nodes (=mononuclear phagocyte system)
phagocytosis-cell types
PMNs, macrophages, monocytes
same as opsonization->phago+target must make physical contact (i.e. Ig&C3b bridge)
phagocytosis-vacuole formation
phagosome(phagocytosed target)+lysosome(preexisting-nec for degrad'n and killing) = phagolysosome (fusion of the 2)->where killing and degrad'n takes place
phagocytosis-nonoxidative killing and digestion
lysozyme, defensin, Fe depriv'n, membr damage, proteolytic degrad'n
phagocytosis-oxidative killing
occurs in phagolysozome, much more lethal, requires inducement (i.e. C3a,C5a), phagocytes exhibit incr in ox consumption to produce an oxygen burst, highly reactive H and O intermediates needed to KILL MO but still need degrad'n Es to degrade MO
intermediates for oxidative killing
HClO-, O2-, H2O2, 1O2, NO
secretion by phagocytes
if phago has difficulty killig MO, frustration, secretes mediators of oxid and nonox killing ->tissue damage (i.e. TB tissue damage is caused by frustrated phagos)
intracellular survival of some MOs
i.e.TB interferes w/phagolysosome form'n, phago still senses presence TB -> secretes mediators of non-oxid killing -> tissue damage (walls off TB in a granuloma)
death of PMNs - advantages
NAs in exudate makes it thick so it contains foreign MOs better
acute inflamm'n - purpose
containment, destruction and removal of foreign material
acute inflamm'n - order of events
1.increased vascular permeability, 2.edema, 3.leukocytosis=chemotaxis, 4.exudate, 5.pus, 6.abcess form'n, 7.healing
acute inflamm'n - increased vascular permeability
release of histamine by mast cells results in vasodilation, followed by constriction of endothelial cells
acute inflamm'n - edema
fluid movement through spaces in capillaries out into tissues
acute inflamm'n - leukocytosis
PMNs bind ICAMs produces by endothelial cells, bind and then moves out of blood into the tissues (chemotaxis toward C3a, C5a)
acute inflamm'n - exudate
extravascular accumulation of fluid + cells to maintain viscous state and further contain defensive supply line and MOs
acute inflamm'n - pus
exudate+dead cells
acute inflamm'n - abcess form'n
large accum'n of pus which is further contained w/fibroblast and conn tissue
chronic inflamm'n - purpose
nonspecific containment, destruction and removal of persistent foreign material
chronic inflamm'n - players
T-lymphocytes, macrophages, fibroblasts
features of acquired immunity
1.high degree of specificity, 2.can disting b/t self and non-self, 3.involves humoral immun(Igs/Abs), 4.displays immunologic memory
Ags - do what, best kind
provoke Ab prod'n, lg complex prots are best, then polysaccs (lipids, NAs no good)
first form of immunization in China - inf'd people w/minor form of vareola to prevent inf w/more dangerous, deadly form
will react w/Ab,but must bind to larger molecule first to be seen(i.e. some Abiotix)
often used w/vaccines to make the Ag bigger, more complex/foreign -> enhances immunogenicity
B-/T-lymphocytes come from
B from lymphoid tissue in bone marrow, T from lymphoid tissue in the thymus
number of variable peptides in the Fab region of the heavy chain
3 variable pp, each w/difft possible alleles; 200X4X12
number of variable peptides in the Fab region of the light chain
2 variable pp, each w/difft possible alleles; 200X5
management of self-reactive Abs
clonal deletion, anergy(arnd but inactive)
heavy chain switch
switch in the Fc region of the heavy chains - results in change in Ab type but not in specificity
alternative pthwy - anaphylotoxins
C3a and C5a
alternative pthwy - key enzymes
C3bBb and C3bC3bBbPr
alternative pthwy - opsonins
C3b enhances phagocytosis
alternative pthwy - results
1.enhance accute inflamm'n, 2.enhance phagocytosis, 3.cause lysis of the MO
classical pthwy - anaphylotoxins
C2b, C3a, C4a
classical pthwy - key enzymes
C1qrs, C2aC4b, C2aC4bC3b
classical pthwy - opsonins
classical pthwy - results
1.enhance accute inflamm'n, 2.enhance phagocytosis, 3.cause lysis of the MO
approx# of difft Fab's
10 million (200X5X200X4X12 = 9,600,000)
how is autoimmunity prevented by the body?
clonal deletion, anergy(arnd but inactive)
assist macrophages in cell-mediated response
assist B cells in the humoral response to extracellular pathogens
primary target is virally infected cells, 2nd is malignant cells; involved in rejection of organ transplants
primary target is virally infected cells, 2nd is malignant cells
type of TH1
NK cells
kill malignant cells, viral-inf'd cells, nonspecifically recog target due to abnormal cell surface (low MHC-I on surface)
C3b stabilized by
binding of CRP to MO, binding of C3b to polysacc on the MO
cell-mediated immunity
memory T cells respons
antigen-presenting cells
monocytes, macrophages, B cells, dendritic cell
immunocompetent B and T cells
B and T cells become immunocompetent when they have been exposed to and are able to recognize a specific Ag and participate in an immune response
plasma cells
Ab synthesizing B cells that participate in the humoral response
first Ig made in an immune response, best initiator of the classical pthwy (C1q binds to IgM), pentamer with 5 Fab's, monomeric IgM is found on the surface of B cells, opsonin?, inhibits infectivity by 1.binding extracellular pathogen which prevents the pathogen from binding, 2.binds a toxin preventing its action, 3.damage enzymes
best opsonin, most abundant Ig and is found in the blood at all times, can cross the placents, activates the classical pthwy, inhibits infectity by 1.binding toxins, 2.binding tissue damaging enzymes
weak opsonin, predominant Ig in external secretions, found in breast milk and secretions of allergic rxns even tho not inv'd, two forms 1.monomeric IgA in low amts in the blood, 2.dimeric sIgA in secretion (tears, saliva, breastmilk, RS and GI tracts), glandular epith'cells make the secretory component -> internalize IgA and then secrete it with the secretory component
all IgE is bound to the surface of mast cells and basophils (not free) which est the def supply line and do this by the release of histamine (degranulation) in response to binding of Ag to IgE on the surface
major membrane-bound Ig, along with IgM on mature B cells
allergic response is a result of
too many IgE receptors on mast cells (first exposure does not produce an allergic response -> may take several exposures)
clonal selection
proliferation of T and B cells specific to an Ag
malignant cells and target for NK
malignant cells do mot produce sufficient amounts of MHC-I which marks them for death by the NK cells
C3b and Ig's (G and A, M?) enhance phagocytosis
body-wide anaphylaxis, Ag is usually injected (i.e. bee sting) resulting in body-wide release of histamine resulting in body-wide dilation of blood vessels causing sig drop in bp (shock) along with bronchoconstriction resulting in suffocation
major histocompatibility complex - primary Agenic determinant that differs from person to person
cells that deal w/extracellular pthgn
Ag-presenting cells, Th2, B-cells/plasma cells
problems the immune system must deal with (4)
1.extracellular pathogens(Mos on mucosal surfaces or introduced due to wound), 2.intracellular pathogens(TB or chlamydial persistance inside a phagosome w/in the mphage), 3.virus-inf'd host cells (inf'd host cells is killed as a result), 4.cancer cells (surface continuously examined by imm cells for dev'ns from norm)
humoral immune response - cells involved
macrophages or other APC, Th0, Th2, B-cells, plasma cells
seq to deal w/extracellular MO: T-cell side of the humoral response
phagocytosis of MO by Ag-presenting cell(macrophage) -> APC kills, degrades MO and presents parts on its surface in conjunction w/MHC-II -> approp Th0 recog and binds both the MH-II and foreign Ag -> binding of Th0 causes APC ro secrete IL4 -> IL4 causes Th0 to difftiate into Th2(now committed to participate in the humoral imm response altho some Th1 will still be produced) -> APC now secretes IL1 which causes Th2 to make and release IL2 receptors and IL2 (autocrine=self-stimulatory) -> binding of IL2 to IL2 receptors on Th2 causes clonal expansion of Th2 -> Th2s synth a lot of IL4,5,6,10 which act on selected B-cell clones -> drives clonal expansion of B-cells and difftiation of B-cells into Ab-secreting plasma cells and formation of memory B cells -> plasma cells secrete IgM then IgG, A and E
seq to deal w/extracellular MO: B-cell side of the humoral response
phagocytosis of MO by Ag-presenting cell(macrophage) -> APC kills, degrades MO and presents parts on its surface in conjunction w/MHC-II -> approp B cell binds Ag only w/IgM or IgD (not MHC-II like the Th0) -> B-cells makes receptors for IL4,5,6,10 -> IL4,5,6,10 from APC and Th2 induces B-cell clonal expansion -> after 4-5 days, B-cells difftiate into plasma cells which synth and rls IgM's -> get heavy chain switch to go from IgM (first) to IgG,A,E -> memory B-cells formed
seq to deal w/intracellular MO: T-cell side of cell-mediated immunity
intracellular pathogen(i.e.TB) making high amt of endogenous Ag's, therefore presented in high conc on the APC in assoc'n w/MHC-II (like phagocyt'd extracell MO) -> Th0 binds Ag+MHC-II -> APC secretes IL12 -> drives difftiation of Th0 to Th1 (still get some Th2) -> APC+Th1 causes the APC to release IL1 and make gamma-IF receptors -> IL1 causes Th1 to make IL2 receptors and rls IL2 (autocrine) -> clonal expansion of Th1s which then make gamma-IF which attacts and activate mphages -> gamma-IF cont to stim and attact mphages pushing them to RS burst and making them cap of ox killing (better killers), TB is an example
seq to deal w/intracellular MO: B-cell side of cell-mediated immunity
B-cells are not needed/involved
seq to deal w/viral infection
viral and host proteins are synt'd and presented in conjuct'n with MHC-I -> Tctl=Tk binds Ag+MHC-1 -> Tctl makes IL2 receptors and releases IL2 (autocrine response) and makes more perforins and granzymes -> clonal expansion of Tctl -> Tctl releases perforins (like MAC) and granzymes (contain hydrolytic enzymes in cytoplasmic granules) onto the surface of the target -> lysis of the target = example of cell-mediated immunity (no B-cell involvement), Tctl's also respond to gamma-IF and IL2 from Th1 which are created as a result of ingested cellular debris created by killing by Tctl action
presentation of processed vs synthesised Ag's
processed Ag's are presented in conjunction w/MHC-II (difft'n to Th1 vsTh2 depends on the density of presentation), synthesized Ag's are presented in conjunction w/MHC-1
virally inf'd cells are taken care of by
NK cells and Tctl cells - activity of both is enhanced by gamma IF and IL2
seq to deal w/cancer cells
malignant cells do not produce sufficient amounts of MHC-I -> attract attention of NK cells which survey cells -> release of perforins and granzymes (Tctl cells can also kill malignant cells, but are not the major line of defense) -> NK cells also respond to IL2 and can culture NK cells with human tumor tissue w/high [IL2] to make them more targeted to the tissue when injected into the pt
Tctl vs NK cells
Tctl cells are the primary defense against viral infections, and NK cells are the primary defense against malignant cells
naturally acquired active immunity
immune response
naturally acquired passive immunity
IgG crossing the placenta, sIgA in mother's milk
artificially acquired active immunity
artificially acquired passive immunity
Ig's from someone else
killed vaccine
pathogen is killed by heat or highly purified Ag -> vaccine contains nothing infectious, only Ag -> host response yields Ab only (i.e.Salk)
attenuated vaccine
use a mutant inf agent that cannot cause disease, but will still infect -> yields both Ab and cell-mediated immunity (i.e.Sabin)
hybrid vaccine
can take vaccinia virus and add genes for other organisms that code for immunogenic proteins -> yields both Ab and cell-mediated immunity
primary immunodeficiency
secondary immunodeficiency - natural causes
are acquired (HIV, malignancy of B,T and plasma cells, severe malnutrition, uncontrolled diabetes, pregnancy, stress, aging)
secondary immunodeficiency - other causes
immunosuppressants, chemotherapy, splenectomy, irradiation, severe burns, steroids
primary B cell immunodeficiency
Infantile X-linked agammaglobulinemia
primary T cell immunodeficiency
DiGeorge Syndrome (congenital thymic aplasia)
primary B and Tcell immunodeficiency
SCID = severe combined immunodeficiency
excessive or inappropriate reactivity resulting in tissue damage - i.e. allergies
type I hypersensitivity
mediated by IgE, mast cells and basophils
type II hypersensitivity
mediated by IgM, IgG, complement, PMN & Mθ
type III hypersensitivity
mediated by IgM, IgG, complement, PMN & Mθ
type IV hypersensitivity
Th1 (Tdth) lymphocytes & Mθ (i.e. TB)
for which Ig classes do phagocytes have receptors?
IgA, IgG and IgM
Ig class most directly assoc's w/dil'n of capillaries
which Ig's are found on the surface of mature, immunocomp B cells
IgD and IgM
Ig's likely to be responsible for neutralizing infectivity of extracellular virus
IgM, IgG and IgA
Ig most responsible for est the def supply line
site of Ig synthesis
most Ig synthesis takes place in the lymph nodes, away from the site of infection
Ig's most likely to activate the alternative complement pthwy
fetus acquires which Ig
breast milk contains which Ig
Ig class first formed in an imm resp
Ig class that greatly increases w/subsequent exposure
anamnestic imm response occurs when w/immunizations
injections after the first
types of Ag's in immunization
large, complex prots and polysaccharides
on switch cell of the imm response
ac inflamm: edema serves to deliver
Ig's, components of the complement system, fibrinogen, plasminogen
antigenic stimulation in the gut results in sec'n of sIgA where?
gut, upper Rs tract, saliva, genito-urinary tract
what do platelets do?
release vasoactive substances, clot formation, promote healing, release fibroblast growth factors