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CONTENTS

1) INTRODUCTION2) ANTIGEN3) ANTIBODY4) ANTIGEN – ANTIBODY REACTIONS5) IMMUNE RESPONSE6) HYPERSENSITIVITY7) AUTOIMMUNITY8) IMMUNODEFICIENCY9) GRAFT REJECTION10) CONCLUSION11) REFERENCES

• The term immunity refers to the resistanceexhibited by the host towards injury causedby microorganisms and their products.

• The immune system produces antibodies orcells that can deactivate pathogens.

• Fungi, protozoans, bacteria and viruses areall potential pathogens.

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IMMUNITY

Complex organisation of cells, consisting of lymphoreticular components distributed widely

in organs or tissues and is responsible for immunity.

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IMMUNE SYSTEM

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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.

ANTIGEN/IMMUNOGEN

Any substance capable of provoking

lymphoid tissues of animals to respond by a

reaction specifically

directed against inducing

substance.

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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.

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CLASSIFICATION OF ANTIGEN

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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.

EPITOPE

Smallest unit of antigenicity against which all immune activity is directed

Each antibody recognizes one epitope rather than the whole antigen

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• 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

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• Immunoglobins which are formed in the serum and tissue fluids in response to an antigen and react with that antigen

specifically.

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ANTIBODIES/IMMUNOGLOBULINS

• Antibodies have 2 roles to play

(a) To bind antigen

(B) To interact with host tissuesand effector systems to removethe antigen

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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.

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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

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• 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 humoralimmunity before its own immunity developes.

IgG

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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.

IgASECRETORY 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

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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

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• 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

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Mediates ReaginicHypersensitivity

• 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

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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.

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)

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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.

APPLIED

Identification of Bacteria

Detection of antibody for

diagnostic purposes.

Example -VDRL in syphilis.

Forensic application in

identification of human blood and

seminal stains.

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2.AGGLUTINATION REACTION

APPLIED

Blood grouping and cross matching

Antibody detection in diagnosis of typhoid (Widaltest)

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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.

3.COMPLEMENT FIXATION TEST (CFT)

• The antigen antibodycomplexes have the abilityto fix complement.

• This reaction has novisible effect. To detectthe fixation ofcomplement, an indicatorsystem consisting of sheeperythrocytes coated withamboceptor (rabbitantibody to sheeperythrocytes) is used.

• Complement can lysesthese erythrocytes coatedwith antibodies.

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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.

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APPLIED

CFT for kala azar

CFT for filaria

Wassermann test for diagnosis of syphilis.

Gonococcal CFT

CFT for many viral Infection

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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.

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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

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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.

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TYPES

I. Direct- Immunofluorscence test

II. Indirect-Immunofluorscence test

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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

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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

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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

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6.RADIOIMMUNOASSAY (RIA)

• Based on competition for fixed amounts of specific antibody between a known radiolabelledantigen & unknown unlabelled (test) antigen.

•Competition

determined

level of the test antigen present in reacting system

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7.ENZYME LINKED IMMUNOSORBENT ASSAY(ELISA)

• It is simple and nearly as sensitive as RIA

• Requires only microlitresquantities of test reagentsPRINCIPLE:

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

TYPES

1. SANDWICH ELISA

2. INDIRECT ELISA

3. COMPETITIVE ELISA

APPLIED

HIV antibodies in serum

Mycobacterial antibodies in tuberculosis

Hepatitis B markers in serum

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TYPES

INNATE

SpecificNon

specific

ACQUIRED

Active

Cell mediated

Humoral

Passive

Artificial Natural

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• 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

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INNATE IMMUNITY

• SPECIESrefers to the resistance to a pathogen shown by all themembers of a particular species.

Eg :B anthracis infects human beings but not chickens

• RACIALWithin a species, different races show differences insusceptibility 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

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INNATE IMMUNITY AT DIFFERENT LEVELS

1. Anatomic barrier

2. Physiologic barrier

3. Phagocytic barrier

4. Inflammatory barrier

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DEFENSIVE BARRIERS OF INNATE IMMUNITY

The first line of defense:

I. Skin - acts as barrier to microorganisms.

II. Mucous membrane- nasal mucosa entraps foreignmicroorganisms and cilia propel microorganismsout of the body

III. Mucous secretions- Saliva, tears and other mucoussecretion act to wash away potential invaders andalso contain antibacterial or antiviral substances

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1. ANATOMIC BARRIER

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

interferon46

2. PHYSIOLOGIC BARRIERS

Ingestion of extracellular macromolecules and particles.

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3.PHAGOCYTIC BARRIERS

PHAGOCYTIC CELLS

Neutrophils

Tissue Macrophages

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

TYPES

INNATE

SpecificNon

specific

ACQUIRED

Active

Cell mediated

Humoral

Passive

Artificial Natural

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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

SPECIFICITY: ability to distinguish differences amongvarious foreign molecules

DIVERSITY: recognize a vast variety of foreign molecules

DISCRIMINATION BETWEEN SELF AND NON-SELF: to recognize andrespond to molecules that are foreign or non-self

MEMORY: Once the immune system has responded to anantigen, it exhibits memory and the second encounterwith the same antigen induces a heightened state ofimmune response

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CHARACTERISTICS

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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.

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

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

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).

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SPECIFIC IMMUNITY

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HYPERSENSITIVITY

Condition in which immune response

results in excessive reactions leading

to tissue damage, disease or even

death in the sensitized host.

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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) REACTION59

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

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TYPE I (ANAPHYLACTIC)

REACTION

occur in two forms –

1. ANAPHYLAXIS- the

acute potentially fatal,

systemic form

2. ATOPY -recurrent

non-fatal localized form

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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.

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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

bradykinin63

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.

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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’

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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

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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

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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

TYPE IV (DELAYED OR CELL

MEDIATED) REACTION

Mediated by sensitized T-lymphocyteswhich, 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

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

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OTHER APPLIED ASPECT

1. AUTOIMMUNITY

2. IMMUNODEFICIENCY

3. GRAFT REJECTION

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1.AUTOIMMUNITY

Condition when the bodyproduces auto-antibodies andimmunologically competent Tlymphocytes against its owntissues leading to structural orfunctional damage of tissues.Eg.

• Systemic lupus erythematosus

• Pemphigus vulgaris

• Bullous pemphigoid

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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

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2. Genetic factors

Familial clustering of several humanautoimmune diseases. Eg.: SLE,Autoimmune hemolytic anemia

HLA-B27 gene- strongly associatedwith ankylosing spondylitis.

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3. Microbial factors

Streptococci & Klebsiella sp.- sharecross reacting epitopes with selfantigens

Viruses like EBV & some bacterialproducts are nonspecific polyclonal B-or T- cell mitogens- thus may induceformation of autoantibodies

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Condition where the defense mechanisms of the body are impaired leading to

• repeated microbial infections

• of varying severity

• sometimes enhanced susceptibility to malignancies

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2. IMMUNNODEFICIENCY

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 phagocytes77

CLASSIFICATION OF IMMUNODEFICIENCY

2. SECONDARY IMMUNODEFICIENCY

Consequences of

• Disease

• Drugs

• Nutritional inadequacies

• Other process that interfere with the proper functioning of the immune system

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• 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

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DENTAL MANAGEMENT OF IMMUNOCOMPROMISED PATIENTS

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

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GRAFTIMMUNOLOGICAL 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

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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

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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

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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 .

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

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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

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APPLICATIONS

1. Diagnosis of disease2. Therapeutic response3. Prevention and treatment of diseases4. Blood transfusion serology5. Tissue typing & Histocompatibility

testing6. Forensic Medicine

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Applications of Immunology

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,TB89

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

3. PREVENTION AND TREATMENT

OF DISEASES-

• Active and Passive immunization against

many diseases by vaccines &

immunoglobulins

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VACCINES

• Preparations of live or killed microorganisms or their products used for immunization

• Induces Artificial Active Immunity

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TYPES

a. Killed-Vaccines containing killed microbes –previously virulent -killed with chemicals orheat. Eg.: vaccines against :

Cholera

Polio

Hepatitis A

94

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

c.Toxoid- Inactivated toxic compounds in caseswhere these (rather than the micro-organismitself) cause illness.

Eg.: Tetanus & Diptheria vaccines

d.Subunit- Protein subunit – rather thanintroducing an inactivated or attenuatedmicro-organism to an immune system afragment of it can induce immune response.

Eg.: Vaccine against Hepatitis B & HPV

96

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

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

MECHANISM OF ACTION OF VACCINE

VACCINE

PRIMARY RESPONSE

B &T LYMPHOCYTE STIMULATION

MEMORY CELLS

SECONDARY RESPONSE AS A RESULT OF EXPOSURE TO ANTIGEN

99

CARIES VACCINE

PRINCIPLE

• Production of enzyme inhibiting antibodies

• Prevention of bacterial accumulation on teeth

Best time – age of one

(after teeth have emerged but before colonization ofstreptococcus mutans)

101

102

TOPICAL APPLICATION HAS BEEN SUGGESTED: Mouthrinse or Painting toothwith antibodies.

IF ANTIBODIES ARE TO BE EFFECTIVE, THEY HAVE TO HOST GENERATED TO ENSURE A CONTINUOUS SUPPLY.

ROUTE OF ADMINISTRATION

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

TARGETTING MICROORGANISMS

• Streptococcus mutans (serotype c,d)

• Streptococcus sobrinus

TARGETTED IMMUNE SYSTEM

• IgA

• IgG

• IgM104

3.BLOOD TRANSFUSION SEROLOGY-

Grouping, typing and cross matching in transfusion.

105

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

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

5. TISSUE TYPING & HISTOCOMPATIBILITY TESTING

Necessary for successful transplantations

108

6. FORENSIC MEDICINE-

• Paternity testing

• Stain identification (of blood or semen)

109

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

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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