immunity and its applied

1. 1

3. 3
CONTENTS
1) INTRODUCTION
2) ANTIGEN
3) ANTIBODY
4) ANTIGEN – ANTIBODY REACTIONS
5) IMMUNE RESPONSE
6) HYPERSENSITIVITY
7) AUTOIMMUNITY
8) IMMUNODEFICIENCY
9) GRAFT REJECTION
10) CONCLUSION
11) REFERENCES

4. • The term immunity refers to the resistance
exhibited by the host towards injury caused
by microorganisms and their products.
• The immune system produces antibodies or
cells that can deactivate pathogens.
• Fungi, protozoans, bacteria and viruses are
all potential pathogens.
4
IMMUNITY

5. Complex organisation of cells, consisting of
lymphoreticular components distributed widely
in organs or tissues and is responsible for
immunity.
5
IMMUNE SYSTEM

6. 6
IMMUNOLOGY
Study of development and
function of both cellular and
humoral components of
immune system by which the
body reacts to expel, destroy
or neutralize foreign substance
including pathogenic
microorganisms.

7. ANTIGEN/IMMUNOGEN
Any substance
capable of
provoking
lymphoid tissues
of animals to
respond by a
reaction
specifically
directed against
inducing
substance.
7

8. 1. A Complete Antigen:- Substances which can
induce antibody formation by themselves and
can react specifically with these antibodies.
2. Haptens:- Substances unable to induce
antibody formation on its own but can become
immunogenic (capable of inducing antibodies)
when linked to proteins called carrier proteins.
8
CLASSIFICATION OF ANTIGEN

9. 9
Haptens
Haptens are of 2 types :
1. Complete Hapten:- can combine with specific
antibodies to form precipitates.
2. Simple Hapten:-Combine with specific
antibodies but no precipitate is produced.

10. EPITOPE
 Smallest unit of antigenicity against which all
immune activity is directed
 Each antibody recognizes one epitope rather
than the whole antigen
10

11. • Antigens derived from
extracellular sources are
presented by antigen
presenting cells with MHC class
II molecules. The 3 main
professional APC are
Peripheral dendritic cells
Monocyte derivatives
B-cells
11

12. • Immunoglobins which are formed in the
serum and tissue fluids in response to
an antigen and react with that antigen
specifically.
12
ANTIBODIES/IMMUNOGLOBULINS

13. • Antibodies have 2 roles to play
(a) To bind antigen
(B) To interact with host tissues
and effector systems to remove
the antigen
13

14. STRUCTURE OF ANTIBODIES
• Both L and H chains
consist of 2 proteins
each having :
 A variable region at
amino terminal.
 A constant region at
carboxy terminal .
• Antigens combine at the
amino terminal.
14

15. Five Classes[subclasses]
of Immunoglobulins:
1. IgG [subclass IgG1,
IgG2, IgG3, IgG4]
2. IgA [subclass IgA1,
IgA2]
3. IgM
4. IgD
5. IgE
IMMUNOGLOBULIN
CLASSES
15

16. • Major serum (Constitute 70-75% of
total immunoglobulin pool)
• IgG molecules are synthesized and
secreted by Plasma B cells.
• Normal serum concentration : 8 to
16 mg/ml (Molecular wt 150,000)
• Half life 23 days
• Transported through placenta
provides the neonate with humoral
immunity before its own immunity
developes.
IgG
16

17. Protects body surfaces
• Normal serum conc. 0.6 – 4.2 mg/ml (Half life
6-8 days)
• Mol wt 1,60,000
• 2 forms
•
• Structure: Dimer formed by 2 monomer units
joined together by a glycoprotein named J
chain.
IgA
SECRETORY IgA
( mol wt 160,000) .
Found on mucosal
surfaces
SERUM Ig A ( mol wt
400,000)
present in secretions
such as milk, saliva,
tears etc
17

18. Protects blood stream
• 5 -8 % of serum Igs
• Serum conc. 0.5 – 2 mg/ml
• Half life 5 days
• Present on the surface of immature B
cells.
• Earliest Ig formed by foetus
• Structure: pentamer ( J chain joining
the basic 5 monomer units)
• Appears early in response to infection
before IgG. Hence its presence in
serum indicates recent infection.
• Cannot cross placenta
IgM
18

19. • Serum conc. 3mg per 100 ml
• Mostly intravascularly present
• Mol wt 1,80,000
• Half life 3 days
• Present on the surface of B cells
• Structure similar to Ig G
IgD
19

20. Mediates Reaginic
Hypersensitivity
• Only Ig which is heat labile
• Serum contains only traces
• Mostly distributed extravascularly
• Mol wt 190,000
• Half life 2-3 days
• Structure resembles Ig G
• Mainly produced in the linings of
respiratory and intestinal tracts
• Mediates type 1 anaphylactic
hypersensitivity reaction via mast
cells sensitization
• Cannot cross placental barrier
IgE
20

21. 21

22. 22
ANTIGEN ANTIBODY REACTIONS
Antigen combines with its specific antibody in an observable
manner
Uses
 In the Body (In vivo)
Forms the basis of immunity against infectious diseases.
 In the laboratory ( in vitro)
For diagnosis of infections
Detection and quantitation of antigens or antibodies.

23. TYPES OF ANTIGEN ANTIBODY
REACTIONS
1. Precipitation
2. Agglutination
3. Complement-Fixation Test (CFT)
4. Neutralization Test
5. Immunofluorescence
6. Radioimmunoassay (RIA)
7. Enzyme linked Immunosorbent Assay
(ELISA)
23

24. 24
1. PRECIPITATION REACTION
• When a soluble antigen reacts with its antibody in the
presence of electrolytes (NaCI) at an optimal temperature
and pH, the antigen antibody complex forms an insoluble
precipitate and it is called as precipitation.
• The precipitate usually sediments at the bottom of the
tube.

25. APPLIED
 Identification of Bacteria
 Detection of antibody for
diagnostic purposes.
 Example -VDRL in syphilis.
 Forensic application in
identification of human blood and
seminal stains.
25

26. 2.AGGLUTINATION REACTION
APPLIED
 Blood grouping and cross matching
 Antibody detection in diagnosis of typhoid (Widal
test) 26
It is an antigen antibody reaction in which a
particulate antigen combines with its antibody in the
presence of electrolytes at an optimal temperature
and pH, resulting in visible clumping of particles.

27. 3.COMPLEMENT FIXATION TEST
(CFT)
• The antigen antibody
complexes have the ability
to fix complement.
• This reaction has no
visible effect. To detect
the fixation of
complement, an indicator
system consisting of sheep
erythrocytes coated with
amboceptor (rabbit
antibody to sheep
erythrocytes) is used.
• Complement can lyses
these erythrocytes coated
with antibodies.
27

28. Positive complement Fixation Text:
If complement is fixed and utilized in the antigen
antibody reaction, there is no free complement to
act on the indicator system and hence no lyses of
erythrocytes.
Negative Complement fixation Test:
Lyses of erythrocytes indicates that complement
was not fixed in the l step and therefore the serum
is negative for Antibodies.
28

29. APPLIED
 CFT for kala azar
 CFT for filaria
 Wassermann test for diagnosis of syphilis.
 Gonococcal CFT
 CFT for many viral Infection
29

30. 4. NEUTRALISATION TEST
• Bacterial exotoxins are
capable of producing
neutralizing antibodies
(antitoxins) which protects
against diseases such as
diphtheria and tetanus.
• Viruses may also be
neutralized by their
antibodies and they are
named as VIRUS
NEUTRALISATION TESTS.
30

31. APPLIED
IN VIVO TESTS:
(1) It is done for detection of toxin of
Corynebacterium diphtheria
(2) Shick Test
IN VITRO TESTS:
(1) Antistreptolysin ‘0’ (ASO) Test
(2) Virus Neutralisation Test
31

32. 5.IMMUNOFLUORESCENCE
• Fluorescence is the property of certain dyes which
absorb rays of one particular wavelength (Ultra
violet light) and emit rays with a different
wavelength (visible light)
• Commonly used fluorescent dyes are
Fluorescin isothiocyanate- exhibit blue green
fluorescence.
Lissamine rhodamine -exhibit orange red
fluorescence.
32

33. TYPES
I. Direct- Immunofluorscence test
II. Indirect-Immunofluorscence test
33

34. Direct Immunofluorescence Test
Principle
 The specific antibodies tagged with fluorescent
dye (i.e.- labeled antibodies) are used for
detection of unknown antigen in a specimen.
 If antigen is present, it reacts with labeled
antibodies and fluorescence can be observed
under ultraviolet light of fluorescent microscope
34

35. APPLIED:
For detection of bacteria, viruses or other antigens
in blood, CSF, tissues and other specimens
Sensitive method to diagnose rabies
DISADVANTAGE:
Separate specific fluorescent antibody has to be
prepared against each antigen to be tested
35

36. Indirect Immunofluorescence Test
It is employed for detection of antibodies in serum
or other body fluids
PRINCIPLE:
A known antigen is fixed on a slide.
The unknown antibody (serum) is applied to the slide
If antibody (globulin) is present in the serum, it attaches
to known antigen on the slide.
For detection of this antigen antibody reaction,
fluorescein tagged antibody to human globulin is added-
in positive test, fluorescence occurs under ultraviolet
light
36

37. 6.RADIOIMMUNOASSAY (RIA)
• Based on competition for
fixed amounts of specific
antibody between a
known radiolabelled
antigen & unknown
unlabelled (test) antigen.
•
Competition
determined
level of the test antigen
present in reacting system
37

38. 7.ENZYME LINKED IMMUNOSORBENT
ASSAY(ELISA)
• It is simple and nearly as
sensitive as RIA
• Requires only microlitres
quantities of test reagents
PRINCIPLE:
 Same as that of
immunofluorescence except
that an enzyme is used
instead of fluorescent dye.
 The enzyme acts on
substrate to produce a color
in a positive test.
 ELISA can be used for the
detection of antigen and
antibody 38

39. TYPES
1. SANDWICH ELISA
2. INDIRECT ELISA
3. COMPETITIVE ELISA
APPLIED
HIV antibodies in serum
Mycobacterial antibodies in tuberculosis
Hepatitis B markers in serum
39

40. 40

41. TYPES
INNATE
Specific
Non
specific
ACQUIRED
Active
Cell
mediated
Humoral
Passive
Artificial Natural
41

42. • The resistance to infection, which individual possesses by
virtue of his genetic and constitutional make up.
2 TYPES:
– Non specific
Resistance to infection in general
– Specific
Resistance to a particular pathogen
42
INNATE IMMUNITY

43. • SPECIES
refers to the resistance to a pathogen shown by all the
members of a particular species.
Eg :B anthracis infects human beings but not chickens
• RACIAL
Within a species, different races show differences in
susceptibility or resistance to infection.
Such racial differences are known to be genetic in origin
Eg :Genetic resistance to Plasmodium falciparum malaria.
Africa and the Mediterranean coast.
Sickle cell anemia prevalent in this area confers immunity
43
INNATE IMMUNITY AT DIFFERENT LEVELS

44. 1. Anatomic barrier
2. Physiologic barrier
3. Phagocytic barrier
4. Inflammatory barrier
44
DEFENSIVE BARRIERS OF INNATE
IMMUNITY

45. The first line of defense:
I. Skin - acts as barrier to microorganisms.
II. Mucous membrane- nasal mucosa entraps foreign
microorganisms and cilia propel microorganisms
out of the body
III. Mucous secretions- Saliva, tears and other mucous
secretion act to wash away potential invaders and
also contain antibacterial or antiviral substances
45
1. ANATOMIC BARRIER

46. I. Temperature - fever destroys the infecting organisms and
stimulates the production of interferons which help in
recovery from viral infections
II. pH - Acidic pH destroys microorganisms
III. Various body secretions -prevent growth of many
microorganisms
 lysozyme
 interferon
46
2. PHYSIOLOGIC BARRIERS

47. Ingestion of extracellular macromolecules and
particles.
47
3.PHAGOCYTIC BARRIERS
PHAGOCYTIC CELLS
Neutrophils
Tissue Macrophages

48. Is a complex sequence of events due to tissue damage.
Cardinal signs of inflammation
• RUBOR (redness)
• TUMOR (swelling)
• COLOR (heat)
• DOLOR (pain)
• LOSS OF FUNCTION
(functio laesa)
48
4.INFLAMMATORY RESPONSE

49. TYPES
INNATE
Specific
Non
specific
ACQUIRED
Active
Cell
mediated
Humoral
Passive
Artificial Natural
49

50.  Is the resistance that an individual acquires during life.
 It is triggered when a pathogen evades the innate
immune system and generates a threshold level of
antigen.
 Capable of recognizing and selectively eliminating
specific microorganisms. 50
ACQUIRED IMMUNITY

51.  SPECIFICITY: ability to distinguish differences among
various foreign molecules
 DIVERSITY: recognize a vast variety of foreign molecules
 DISCRIMINATION BETWEEN SELF AND NON-SELF: to recognize and
respond to molecules that are foreign or non-self
 MEMORY: Once the immune system has responded to an
antigen, it exhibits memory and the second encounter
with the same antigen induces a heightened state of
immune response
51
CHARACTERISTICS

52. 52

53. 53
Active immunity
(According to mechanism of action)
Cell Mediated
(T –cell)
– through formation of
large number of
activated T lymphocytes
– specifically designed to
destroy the foreign
agent.
Humoral
(B-cell)
– Body develops circulating
antibodies which are globulin
molecules in the blood
– capable of attacking the
invading agents.

54.  Resistance is transmitted to a recipient as readymade pre-
formed antibodies
 No antigenic stimulus
 Protection is transient & less effective
2 types
 Natural: transferred from mother to fetus or infant.
 Artificial: through administration of antibodies example
antisera.
54
PASSIVE IMMUNITY

55. Acute inflammation :
 Cells :
- Polymorphonuclear leukocytes
- Mast cells
- Platelets.
 Mediators : - Lysosomal enzymes (such as
collagenase, β-glucoronidase and neutrophil elatase)
- Complement components
- Vasoactive amines
- Arachidonic acid metabolites (such as
prostaglandin E2 and leukotriene B4). 55
INNATE IMMUNITY

56. II) Humoral immunity :
Cells :
B lymphocytes, which give rise to plasma cells.
Mediators :
5 antibody isotypes (IgG, Ig M, IgA, IgD & IgE).
III) Cellular immunity :
Cells :
T lymphocytes, monocytes/macrophages
Mediators:
Interleukin/cytokines (Such as IL-1α, IL-1β, IL-6, IL-8 and
tumor necrosis factor α).
56
SPECIFIC IMMUNITY

57. 57

58. HYPERSENSITIVITY
Condition in which immune response
results in excessive reactions leading
to tissue damage, disease or even
death in the sensitized host.
58

59. Classification of hypersensitivity
(Coomb and Gel)
TYPE I ANAPHYLACTIC
TYPE II CYTOTOXIC
TYPE III IMMUNE COMPLEX
TYPE IV DELAYED OR CELL MEDIATED
TYPE V (STIMULATORY TYPE) REACTION
59

60. Immediate type
(Type I II III V )
Delayed type
(Type IV)
Onset and
duration
Appears and recedes rapidly Appears slowly in 24-72
hours and lasts longer
Immune
response
Antibody mediated
(B-Lymphocytes)
Cell mediated
(T-lymphocytes)
Passive
transfer
Possible with serum Cannot be transferred with
serum but possible with
lymphocytes
Desensitizat
ion
Easy but short lived Difficult but long lasting
Induction Antigens
- by any route
Antigen
-injected intradermally
-skin contact
60

61. TYPE I (ANAPHYLACTIC)
REACTION
 occur in two forms –
1. ANAPHYLAXIS- the
acute potentially fatal,
systemic form
2. ATOPY -recurrent
non-fatal localized form
61

62. A). PRIMARY MEDIATORS
(i) Histamine
causes vasodilatation, increased capillary permeability and
contraction of smooth muscle.
(ii) Serotonin
causes vasoconstriction, increased capillary permeability
and smooth muscle contraction
(iii) Eosinophil chemotactic factor of anaphylaxis (ECFA)
contribute to the eosinophilia associated with many
hypersensitivity conditions.
62

63. B. SECONDARY MEDIATORS
(i) Slow reaction substance of anaphylaxis
(SRSA)
cause sustained contraction of smooth muscles.
(ii) Prostaglandins and thromboxane
bronchoconstrictors
(iii) Platelet activation factor (PAF)
causes aggregation of platelets
(iv) Other mediators of anaphylaxis
bradykinin
63

64. Features of Anaphylaxis
 Occurs within a few seconds to few minutes
following shocking dose of antigen.
 Antibody responsible- IgE
 Lung - principal shock organ in humans
 Bronchospasm, laryngeal edema, respiratory
distress, shock and death may occur.
64

65. Atopy (coca )
 Naturally occurring familial hypersensitivities
of human beings.
 Antigens involved - pollens, house dust and
foods.
 Atopens induce IgE antibodies formerly
termed as ‘Reagin Antibody’
65

66. TREATMENT
TYPE I
 Skin rash – Antihistamines
 Anaphylactic shock –
adrenalin (1:1000) .2-0.5mg (i.m)
oxygen
ancillary agents - antihistamines, bronchodialators
glucocorticoids – hydrocortisone sod.succinate 100-200mg
resuscitative measures
 Bronchospasm- adrenalin + glucocorticoids
66

67. TYPE II (CYTOTOXIC) REACTION
 reaction is mediated by IgG
 antibodies bind to an
antigen on the cell surface
and cause (i) phagocytosis
of the cell
(ii) lysis through
activation of complement
system.
 Example
1. Autoimmune anaemias and
haemolytic disease of the
newborn
2. Drug reactions
3. Erythroblastosis fetalis
67

68. TYPE III (IMMUNE
COMPLEX) REACTION
 Characterized by deposition of antigen-
antibody complexes in tissues
 Activation of complement and infiltration of
polymorphonuclear leucocytes leading to
tissue damage
 TYPE:
1. Arthus reaction(localised) –due to relative
antibody excess
2. Serum sickness(generalised)- due to relative
antigen excess 68

69. TYPE IV (DELAYED OR CELL
MEDIATED) REACTION
 Mediated by sensitized T-lymphocytes
which, on contact with specific antigen,
release lymphokines
 Hypersensitivity occur within 24 -72 hours
 Not antibody mediated ,but due to antigen
challenge
 TYPES
1. Tuberculin (infection) type
2. Contact dermatitis type
69

70. TYPE V (STIMULATORY
TYPE) REACTION
 Modification of type II Hypersensitivity
reaction
 Antigen antibody reaction leads to cell
proliferation and differentiation instead of
inhibition or killing
 Example- Grave’s disease in which thyroid
hormones are in excess
70

71. OTHER APPLIED ASPECT
1. AUTOIMMUNITY
2. IMMUNODEFICIENCY
3. GRAFT REJECTION
71

72. 1.AUTOIMMUNITY
Condition when the body
produces auto-antibodies and
immunologically competent T
lymphocytes against its own
tissues leading to structural or
functional damage of tissues.
Eg.
• Systemic lupus erythematosus
• Pemphigus vulgaris
• Bullous pemphigoid
72

73. MECHANISM
1. Failure of Tolerance:
a. Breakdown of T-cell energy
b. Failure of T-cell mediated suppression
c. Molecular mimicry
d. Failure of activation-induced cell death
73

74. 2. Genetic factors
Familial clustering of several human
autoimmune diseases. Eg.: SLE,
Autoimmune hemolytic anemia
HLA-B27 gene- strongly associated
with ankylosing spondylitis.
74

75. 3. Microbial factors
Streptococci & Klebsiella sp.- share
cross reacting epitopes with self
antigens
 Viruses like EBV & some bacterial
products are nonspecific polyclonal B-
or T- cell mitogens- thus may induce
formation of autoantibodies
75

76. Condition where the defense mechanisms of
the body are impaired leading to
• repeated microbial infections
• of varying severity
• sometimes enhanced susceptibility to
malignancies
76
2. IMMUNNODEFICIENCY

77. 1 PRIMARY IMMUNODEFICIENCY
Result from abnormalities in the development of the
immune mechanisms
A. Disorders of specific immunity
• Humoral immunodeficiency (B cell defect)
• Cellular immunodeficiency (T cell defect)
• Combined immunodeficiency ( B &T cell defect)
B. Disorders of complement
C. Disorders of phagocytes
77
CLASSIFICATION OF IMMUNODEFICIENCY

78. 2. SECONDARY IMMUNODEFICIENCY
Consequences of
• Disease
• Drugs
• Nutritional inadequacies
• Other process that interfere with the proper
functioning of the immune system
78

79. • PREVENTION - Chances of local infection should be
minimized
• Before instituting antibiotic therapy-
culture and sensitivity for bacteria and fungi
• Prior to dental treatment the gamma globulin
level should be 200 mg/dl
• Monthly therapy with concentrated human
gamma globulin
79
DENTAL MANAGEMENT OF IMMUNOCOMPROMISED
PATIENTS

80. In case of oral surgery- administration of extra dose of
gamma globulin 1 day before surgery (dose- 100-200
mg/kg body weight)
80

81. GRAFT
IMMUNOLOGICAL CONSIDERATION:
immune response (antigen-antibody reaction)
of the body plays an active role in graft
rejection procedures
• 3 types of surface antigens provoke rejection:
1. the major Histocompatibility complex (MHC)
2. the minor Histocompatibility antigens
3. the blood group antigens
81

82. 1. Major Histocompatibility
complex (MHC)
antigen
• MHC- The site within the genome
having genes important in provoking
graft rejection function- recognition
and elimination of foreign cells and
antigens that enter the body.
2. Minor Histocompatibility
antigens
• antigens causing Cell mediated graft rejection
3.The blood group antigens
• carbohydrates and glycoproteins present on the surface
of red blood cells
• unusual as they develop without prior exposure to foreign
blood cells
82

83. 83
Skin graft applied and initially accepted
First 2-3 days – graft is vascularized – morphologically and
functionally healthy
4th day -- inflammation becomes evident
Graft invaded by lymphocytes and macrophages , blood
vessels occluded , vascularity diminishes , necrosis occurs.
When necrosis extended – scar like appearance and sloughing
takes place – 10th day
1st set of response

84. 84
2nd set of response
Another graft from the same donor applied – rejection in an
accelerated fashion takes place.
Vascularisation soon interrupted by inflammatory response,
Necrosis sets in early –graft sloughs in on 6th day .

85. CLASSIFICATION OF GRAFT REJECTION
1. HYPERACUTE REJECTION
• immediate rejection (min to 1-2 Days) after restoration of the
blood supply to the transplanted organ.
• preformed circulating antibody fixes to antigens in the graft
vascular bed
Avoidance
• By cross match
• Testing potential recipients for the existence of preformed
antibodies
• Allowing selection of those donors whose cells did not manifest
any antigen against which the recipient had already formed
antibodies
85

86. 2. ACUTE REJECTION
• occurs within a few days of transplantation or after
cessation of immunosuppressive therapy
• Mechanism involved- Cellular and humoral
TREATMENT -Immunosuppressive drugs
3. CHRONIC REJECTION
• Occurs over months to years
• Characterized by progressive organ dysfunction
• Dense fibrosis in arterioles- leading to ischemic injury
• It is the end stage of recurrent acute infection 86

87. 87
APPLICATIONS

88. 1. Diagnosis of disease
2. Therapeutic response
3. Prevention and treatment of diseases
4. Blood transfusion serology
5. Tissue typing & Histocompatibility
testing
6. Forensic Medicine
88
Applications of Immunology

89. 1. DIAGNOSIS OF DISEASE-
Antigen antibody reactions- used for the purpose
of diagnosis of many diseases
a) VDRL - syphilis - precipitation test
b) WIDAL - typhoid
- agglutination test
c) ELISA - HIV,TB
89

90. 2. THERAPEUTIC RESPONSE
• To check for increasing or decreasing
Ag-Ab titre
• Test repeated in a week or 10 days
• Example- VDRL (syphilis)
Widal (typhoid)
90

91. 3. PREVENTION AND TREATMENT
OF DISEASES-
• Active and Passive immunization against
many diseases by vaccines &
immunoglobulins
91

92. 92
VACCINES

93. • Preparations of live or killed
microorganisms or their products used
for immunization
• Induces Artificial Active Immunity
93

94. TYPES
a. Killed-Vaccines containing killed microbes –
previously virulent -killed with chemicals or
heat. Eg.: vaccines against :
 Cholera
 Polio
 Hepatitis A
94

95. b.Attenuated- Vaccines containing
live, attenuated microorganisms. They
typically provoke more durable
immunological responses and are the
preferred type for healthy adults.
Eg.: vaccines against :
- Measles
- Rubella
- Mumps
95

96. c.Toxoid- Inactivated toxic compounds in cases
where these (rather than the micro-organism
itself) cause illness.
Eg.: Tetanus & Diptheria vaccines
d.Subunit- Protein subunit – rather than
introducing an inactivated or attenuated
micro-organism to an immune system a
fragment of it can induce immune response.
Eg.: Vaccine against Hepatitis B & HPV
96

97. e.Conjugate- Certain bacteria
have polysaccharide outer coats that are
poorly immunogenic. By linking these outer
coats to proteins (e.g. toxins), the immune
system can be led to recognize the
polysaccharide as if it were a protein antigen.
Eg.: Haemophilus influenzae type B vaccine
97

98. 98
 Birth BCG OPV -0 Hep B -1st
 6wks OPV 1st DPT 1st Hep B 2nd Hib 1st
 10 wks OPV 2st, DPT 2nd,Hib conj 2nd
 14 wks OPV 3rd, DPT 3rd Hep B 3rd Hib conj 3rd
 9mths Measles
 12-15 mths MMR
 16-18 mths OPV 4th DPT 1st booster Hib conj booster
 2yrs Typhoid vaccine
 4-6 yrs OPV 5th DPT 2nd booster
 10 yrs TT booster
 16 yrs TT booster
OPTIONAL VACCINES
 >1yr Varicella vaccine
 >2yrs Hep A
VACCINATION SCHEDULE

99. MECHANISM OF ACTION OF VACCINE
VACCINE
PRIMARY RESPONSE
B &T LYMPHOCYTE STIMULATION
MEMORY CELLS
SECONDARY RESPONSE AS A RESULT OF
EXPOSURE TO ANTIGEN
99

100. CARIES VACCINE

101. PRINCIPLE
• Production of enzyme inhibiting antibodies
• Prevention of bacterial accumulation on teeth
Best time – age of one
(after teeth have emerged but before colonization of
streptococcus mutans)
101

102. 102
 TOPICAL APPLICATION HAS BEEN
SUGGESTED: Mouthrinse or Painting tooth
with antibodies.
 IF ANTIBODIES ARE TO BE EFFECTIVE,
THEY HAVE TO HOST GENERATED TO
ENSURE A CONTINUOUS SUPPLY.
ROUTE OF ADMINISTRATION

103. 103
 ORAL VACCINE HAS BEEN SUGGESTED TO
BE SAFER THAN AN INJECTED VACCINE.
 ENCAPSULATED PILL WHOSE CONTENT IS
NOT RELEASED UNTIL IT REACHES
PEYER’S PATCHES > ANTIBODY RESPONSE

104. TARGETTING MICROORGANISMS
• Streptococcus mutans (serotype c,d)
• Streptococcus sobrinus
TARGETTED IMMUNE SYSTEM
• IgA
• IgG
• IgM
104

105. 3.BLOOD TRANSFUSION SEROLOGY-
Grouping, typing and cross matching in transfusion.
105

106. BLOOD TRANSFUSION
• Recipient plasma should
not contain Ab which
damage donors
erythrocyte
• Donor plasma should not
contain Ab which damage
recipients erythrocyte
• Donors red cell should not
contain Ag which lacks in
the recipient
If transfused cells posses a
foreign Ag –stimulates
immune response in the
recipient
106

107. Rh COMPATIBILITY
• Hemolytic disease of the newborn (HDN) results from Rh
incompatibility between an Rh- mother and Rh+ fetus.
• Rh+ blood from the fetus enters the mother's system during
birth, producing Rh antibodies.
• The first child is usually not affected
• Subsequent Rh+ fetuses cause a massive secondary reaction of
the maternal immune system.
• To prevent HDN, Rh- mothers are given an Rh antibody during
the first pregnancy with an Rh+ fetus and all subsequent Rh+
fetuses.
107

108. 5. TISSUE TYPING &
HISTOCOMPATIBILITY
TESTING
Necessary for successful
transplantations
108

109. 6. FORENSIC
MEDICINE-
• Paternity testing
• Stain identification
(of blood or semen)
109

110. CONCLUSION
• It is the immune system that determines the
level of resistance an individual possess to an
external stimuli.
• The immune system is like a double edged
sword. It renders an individual ineffective to any
disease or infection, on the other hand a
compromised or exaggerated immune response
would lead to fatal results.
110

111. REFERENCES
 Textbook Of Physiology By Prof A.K. Jain
 Review Of Medical Physiology By William F. Ganong
 Textbook Of Medical Physiology By Guyton And Hall
 Robbins- Textbook Of Pathology
 Textbook Of Microbiology By C.P. Baveja
 Textbook Of Pathology By Harsh Mohan
 Clinical Periodontology By Newman Takei Carranza
 Jan Lindhe-clinical Periodontology & Implantology

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