immunity and its applied aspect
TRANSCRIPT
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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
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 .
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
93
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
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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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