1. Ab formation

2. Immune Elimination Phase Amount of Circulating Ag (%)
Fate of the Immunogen
Clearance after 1o exposure
Equilibrium phase
Catabolic decay phase
Immune elimination phase
Immune Elimination Phase
Days after Injection 2 4 6 8 12 10
Amount of Circulating Ag (%) 25 75
100 50
Equilibrium Phase
Catabolic Decay Phase
Clearance after 2o exposure
More rapid onset of immune elimination phase

3. Kinetics of the Ab Response T-dependent Ag; 1o Response
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
DECLINE
PLATEAU
Lag phase
Log phase
Plateau phase
Decline phase

4. Kinetics of the Ab Response T-dependent Ag; 2o 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
Lag phase
Log phase
Plateau phase
Decline phase
* Specificity

5. Kinetics of Ab Response to T-independent Ags
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
4 Phases
IgM antibody
No secondary response

6. Milestones in immunization
3000BC
Evidence of sniffing powdered small pox crust in Egypt
1700AD
Introduction of variolation in England and later in the US
2000BC
Sniffing of small pox crust in China
1780AD
Edward Jenner discovers small pox vaccine
1500BC
Turks introduce variolation
1885AD
Pasteur discovers rabies attenuated vaccine

7. Discovery of small pox vaccine
Edward Jenner
In 1798, Jenner introduced 1st vaccination (vacca: cow) following his experimentation with isolates of cow pox virus from ‘Blossom’.
Discovery of small pox vaccine

8. Modern era of the vaccine
1920s
Diphtheria and Tetanus
1960s
Mumps measles and rubella virus
Sabin polio
1934
Pertussis
1985
Haemophilus
1955
Salk polio
1990s
Hepatitis and varicella

9. Different modes of acquiring immunity
Immunization is the means of providing specific protection against most common and damaging pathogens. Specific immunity can be acquired either by passive or by active immunization and both modes of immunization can occur by natural or artificial means (Figure 1).

10. Passive Immunity Natural Artificial Placental transfer of IgG
Antibodies or immunoglobulins
Colostral transfer of IgA
Immune cells

11. Passive Immunization disease indication antibody source human, horse
diphtheria, tetanus
prophylaxis, therapy
vericella zoster
human
immunodeficiencies
gas gangrene, botulism, snake bite, scorpion sting
horse
post-exposure
Artificially acquired passive immunity: Immunity is often artificially transferred by injection with gamma‑globulins from other individuals or gamma‑globulin from an immune animal. Passive transfer of immunity with immune globulins or gamma‑globulins is practiced in numerous acute situations of poisoning (insects, reptiles, botulism), infections (tetanus, measles, rabies, etc.) and as a prophylactic measure hypo-gamma-globulinemia). In these situations, gamma‑globulins of human origin are preferable although specific antibodies raised in other species are effective and used in some cases (acute poisoning and tetanus and diphtheria infections.
Passive transfer of cell mediated immunity can also be accomplished in certain diseases (cancer, immunodeficiency). The donor cells must be histocompatible.
rabies,
human
post-exposure
hypogamma-globulinemia
human
prophylaxis

12. Active Immunization Artificial Natural Attenuated organisms
killed organisms
exposure to sub-clinical infections
sub-cellular fragments
This refers to immunity produced by the body in consequence of exposure to antigens.
Naturally acquired active immunity: Exposure to different pathogens leads to sub-clinical or clinical infections which result in a protective immune response against these pathogens.
toxins
others

13. Live Attenuated Vaccines
hepatitis A
not required in SC
polio*
not used in std. schedule
measles, mumps & rubella
yellow fever
Military and travelers
Varicella zoster
children with no history of chicken pox
tuberculosis
not used in this country

14. Recommended Childhood Immunization Schedule (2002)

15. Complement Discovered in 1894 by Bordet
It represents lytic activity of fresh serum
Its lytic activity destroyed when heated at 56C for 30 min

16. Complement functions Host benefit: Host detriment:
opsonization to enhance phagocytosis
phagocyte attraction and activation
lysis of bacteria and infected cells
regulation of antibody responses
clearance of immune complexes
clearance of apoptic cells
Host detriment:
Inflammation, anaphylaxis

17. Pathways of complement activation
CLASSICAL
PATHWAY
LECTIN
PATHWAY
ALTERNATINE
PATHWAY
antibody
dependent
antibody
independent
Activation of C3 and
generation of C5 convertase
activation
of C5
LYTIC ATTACK
PATHWAY

18. HYPERSENSITIVITY
A damage to host mediated by preexisting immunity to self or foreign antigen

19. Types of hypersensitivity reactions
Type I: anaphylactic or immediate Type II: cytotoxic Type III: Immune complex Type IV: cell mediated or delayed

20. Anaphylaxis can be fatal
Type-I hypersensitivity
The common allergy
Anaphylaxis can be fatal

21. Sensitization against allergens
B cell
TH1
Histamine, tryptase, kininegenase, ECFA
Leukotriene-B4, C4, D4, prostaglandin D, PAF
Newly
synthesized mediators

22. Type II hypersensitivity role of neutrophils
Complement mediated lysis
frustrated phagocytosis
ADCC

23. Type II hypersensitivity role of neutrophils
B cell
TH1
Histamine, tryptase, kininegenase, ECFA
Leukotriene-B4, C4, D4, prostaglandin D, PAF
Newly
synthesized mediators

24. Type III hypersensitivity
Serum sickness mediated by immune complexes

25. Type III hypersensitivity mechanism

26. Type III hypersensitivity mechanism

27. Type III hypersensitivity the role of immune complex size

28. Type 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

29. Delayed hypersensitivity reactions
epidermal: heavy metals, poison ivy, rubber, latex
T cells, later macrophages
eczema
48-72 hours
contact
dermatitis
antigen and site
histology
clinical appearance
time of reaction
type
intradermal: tuberculin, lepromin, etc.
lymphocytes, monocytes
local induration
48-72 hours
tuberculin
granuloma
persistent antigen stimulus, chronic infection
M, giant cells, epitheloid cells, fibroblasts
hardening
21-28 days

30. Mechanism of damage in contact hypersensitivity
APC
TH1
LAK NK
preTc Tc

31. Comparison of hypersensitivity reactions
Type-IV
Type-III
Type-II
Type-I
characteristic
antibody
IgE
IgG, IgM
none
antigen
Exogenous
cell surface
cellular
soluble
response time
15-30 min.
Min.-hrs
3-8 hours
48-72 hours
or longer
appearance
Weal & flare
Lysis & necrosis
Erythema & edema
Erythema & induration
baso- and eosinophils
Ab and complement
histology
PMN and
complement
Monocytes & lymphocytes
T-cells
antibody
transfer with
TB test, poison ivy, granuloma
farmers’ lung, SLE
pemphigus, Goodpasture
hay fever, asthma
examples

32. Two major types of immunodeficiency diseases
Secondary immunodeficiencies
immunodeficiency resulting from infections and other diseases
immunodeficiency resulting from iatrogenic causes
immunodeficiency due to aging or malnutrition
Primary immunodeficiency
Inherited immunodeficiencies

33. Immunologic defects caused by HIV infection
Cellular abnormalities
decrease 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

34. Primary immunodeficiency diseases
Stem cell defect
Reticular dysgenesis
T and B cell defect
severe combined immunodeficiency
X-linked
IL2 receptor -chain
autosomal
adenosine deaminase (ADA)
purine nucleoside phosphorylase (PNP)