Fate of the Immunogen Clearance after 1 o exposure Equilibrium phase Catabolic decay phase Immune...
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Transcript of Fate of the Immunogen Clearance after 1 o exposure Equilibrium phase Catabolic decay phase Immune...
Fate of the Immunogen
Clearance after 1o exposureEquilibrium phaseCatabolic decay phaseImmune elimination phase
• Clearance after 2o exposure
– More rapid onset of immune elimination phase
Immune Elimination
Phase
Days after Injection2 4 6 8 1210
Am
oun
t of
Cir
cula
tin
g A
g (%
)
25
75
100
50
Equilibrium Phase
Catabolic Decay Phase
Kinetics of the Ab ResponseT-dependent Ag; 1o Response
• Lag phase
• Log phase
• Plateau phase
• Decline phase Ag
D a y s A f t e r I m m u n i z a t i o n
A b
T i
t e
r
LAG LOG DECLINEPLATEAU
Kinetics of the Ab ResponseT-dependent Ag; 2o Response
* Specificity
• Lag phase
• Log phase
• Plateau phase
• Decline phase
1o Ag 2o Ag
D a y s A f t e r I m m u n i z a t i o n
A b
T i
t e
r
Kinetics of Ab Response toT-independent Ags
4 PhasesIgM
antibodyNo
secondary response
1o Ag 2o Ag
D a y s A f t e r I m m u n i z a t i o n
A b
T i
t e
r
IgM Ab
1500BC Turks introduce
variolation
1885AD Pasteur discovers rabies
attenuated vaccine
3000BCEvidence of sniffing powdered small pox crust in Egypt
2000BCSniffing of small pox crust in China
1700ADIntroduction of variolation in England and later in the US
1780ADEdward Jenner discovers small pox vaccine
Edward Jenner
Discovery of small pox vaccine
1920s
Diphtheria and Tetanus
1934
Pertussis
1955
Salk polio
1960s
Mumps measles and rubella virus
Sabin polio
1990s
Hepatitis and varicella
1985
Haemophilus
Different modes of acquiring immunityDifferent modes of acquiring immunity
Innate
A r ti f ic ia l N a tu ra l
P ass ive
A r ti f ic ia l N a tu ra l
A ctive
Acuired
Im m unity
Innate
A r ti f ic ia l N a tu ra l
P ass ive
A r ti f ic ia l N a tu ra l
A ctive
Acuired
Im m unity
Natural Artificial
Colostral transfer of IgA
Placental transfer of IgG
Antibodies or immunoglobulins
Immune cells
Passive ImmunityPassive Immunity
disease indicationantibody source
Passive ImmunizationPassive Immunization
human, horsediphtheria, tetanus prophylaxis, therapy
vericella zoster human immunodeficiencies
gas gangrene, botulism, snake bite, scorpion sting
horse post-exposure
rabies, human post-exposure
hypogamma-globulinemia
human prophylaxis
Active ImmunizationActive Immunization
Natural Artificial
exposure to sub-clinical infections
Attenuated organisms
killed organisms
sub-cellular fragments
toxins
others
tuberculosisnot used in this country
polio*not used in std. schedule
measles, mumps & rubella yellow fever
Military and travelersVaricella zoster
children with no history of chicken pox
hepatitis A
not required in SC
Live Attenuated VaccinesLive Attenuated Vaccines
Recommended Childhood Immunization Schedule (2002)
Complement
Discovered in 1894 by Bordet
It represents lytic activity of fresh serum
Its lytic activity destroyed when heated at 56C for 30 min
Complement functions
Host benefit:opsonization to enhance phagocytosisphagocyte attraction and activationlysis of bacteria and infected cellsregulation of antibody responsesclearance of immune complexesclearance of apoptic cells
Host detriment:Inflammation, anaphylaxis
CLASSICALPATHWAY
ALTERNATINEPATHWAY
activationof C5
LYTIC ATTACKPATHWAY
antibodydependent
LECTINPATHWAY
antibodyindependent
A damage to host mediated by preexisting immunity to self or foreign antigen
Types of hypersensitivity reactionsTypes of hypersensitivity reactions
Type I: anaphylactic or immediateType II: cytotoxicType III: Immune complexType IV: cell mediated or delayed
Type I: anaphylactic or immediateType II: cytotoxicType III: Immune complexType IV: cell mediated or delayed
Type-I hypersensitivityType-I hypersensitivity
The common allergy
B cell
Histamine, tryptase, kininegenase, ECFA
Leukotriene-B4, C4, D4, prostaglandin D, PAF
Newly
synthesized mediators
TH1
Complement mediated
lysis
ADCCfrustrated
phagocytosis
B cell
Histamine, tryptase, kininegenase, ECFA
Leukotriene-B4, C4, D4, prostaglandin D, PAF
Newly
synthesized mediators
TH1
Type III hypersensitivityType III hypersensitivity
Serum sicknessmediated by immune complexes
Type III hypersensitivitythe role of immune complex size
Type III hypersensitivitythe role of immune complex size
Type IV hypersensitivityType IV hypersensitivity
Delayed reaction 36 to 48 hours Characterized by
induration and erythema Also known as cell
mediated hypersensitivity
Tuberculin test is the most common example
Delayed reaction 36 to 48 hours Characterized by
induration and erythema Also known as cell
mediated hypersensitivity
Tuberculin test is the most common example
persistent antigen stimulus, chronic infection
M, giant cells, epitheloid cells, fibroblasts
hardening21-28 days
granuloma
intradermal: tuberculin, lepromin, etc.
lymphocytes, monocytes
local induration
48-72 hourstuberculin
epidermal: heavy metals, poison ivy, rubber, latex
T cells, later macrophageseczema
48-72 hours
contactdermatitis
antigen and sitehistologyclinical appearance
time of reaction
type
APC
IL2, TNF , IFN
TH1
IL2 TNF , IFN /
N O 2
NK
M M
LAK
preTc
Tc
Type-IVType-IIIType-IIType-Icharacteristic
Comparison of hypersensitivity reactionsComparison of hypersensitivity reactions
TB test, poison ivy, granuloma
farmers’ lung, SLE
pemphigus, Goodpasture
hay fever, asthma
examples
antibody IgE IgG, IgM IgG, IgM none
antigen Exogenous cell surface cellularsoluble
response time
15-30 min. Min.-hrs 3-8 hours 48-72 hoursor longer
appearance Weal & flare Lysis & necrosis
Erythema & edema
Erythema & induration
baso- and eosinophils
Ab and complement
histology PMN andcomplement
Monocytes & lymphocytes
T-cellsantibodyantibodyantibodytransfer with
Two major types of immunodeficiency diseasesTwo major types of immunodeficiency diseases
Secondary immunodeficiencies immunodeficiency resulting from
infections and other diseases immunodeficiency resulting from
iatrogenic causes immunodeficiency due to aging or
malnutritionPrimary immunodeficiency
Inherited immunodeficiencies
Secondary immunodeficiencies immunodeficiency resulting from
infections and other diseases immunodeficiency resulting from
iatrogenic causes immunodeficiency due to aging or
malnutritionPrimary immunodeficiency
Inherited immunodeficiencies
ImmunodeficiencyImmunodeficiency
Immunologic defects caused by HIV infectionImmunologic defects caused by HIV infection
Cellular abnormalitiesdecrease in CD4 T cells (reversal of
CD4/CD8 ratio)
Functional abnormalities increased susceptibility to infections
particularly intracellular pathogens
decrease in cell mediated immunity
decrease in the NK cell functions
Cellular abnormalitiesdecrease in CD4 T cells (reversal of
CD4/CD8 ratio)
Functional abnormalities increased susceptibility to infections
particularly intracellular pathogens
decrease in cell mediated immunity
decrease in the NK cell functions
Primary immunodeficiency diseasesPrimary immunodeficiency diseasesStem cell defect
Reticular dysgenesisT and B cell defect
severe combined immunodeficiency X-linked
IL2 receptor -chain autosomal
adenosine deaminase (ADA) purine nucleoside phosphorylase (PNP)
Stem cell defectReticular dysgenesis
T and B cell defectsevere combined immunodeficiency
X-linked IL2 receptor -chain
autosomal adenosine deaminase (ADA) purine nucleoside phosphorylase (PNP)