Immunity - The basic concept

By -
Dr. Sudeep M. Chaudhari
MDS 2nd Year
Dept. of Paedodontics & Preventive Dentistry
Immunity – The Basic Concept

2
Contents
 Introduction
 Types of immunity
 Innate Immunity
 Acquired Immunity
 Clinical considerations
 Conclusion
 References

3
Introduction
 The Latin term “IMMUNIS” means EXEMPT, referring to
protection against foreign agents.
 Immune system is a biological structures and processes
within an organism that protects against disease by
identifying and killing pathogens and tumour cells. It detects
a wide variety of agents, from viruses to parasitic worms,
and needs to distinguish them from the organism's own
healthy cells and tissues in order to function properly.

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Types of immunity
Innate
Immunity
Acquired
Immunity
Special Immunity
Individual Immunity
Racial Immunity
Natural
Active
Artificial
Passive Active Passive

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Types of immunity
Innate
Immunity
Acquired
Immunity
Natural
Active
Artificial

6
1) Innate immunity
 It is also called natural or native immunity.
 It refers to nonspecific defense mechanisms that come into
play immediately or within hours of an antigen's appearance
in the body. These mechanisms include physical barriers
such as skin, chemicals in the blood and immune system
cells that attack foreign cells in the body.

7
Types of innate immunity-
Species
immunity
It is the total
immunity
shown by all
members of a
species
against
pathogen; e.g.
birds immune
to tetanus.
Racial
immunity
It is that in
which various
races show
marked
difference in
their resistance
to certain
infectious
disease.
Individual
immunity
It is very
specific for
each and every
individual
despite having
same racial
background
and opportunity
for exposure.

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It comprises four types of defense barriers
(1)Anatomical barriers
(2)Phagocytic barriers
(3)Blood proteins and
(4)Cytokines.

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1)Anatomical barriers
a)Skin
It acts as a mechanical barrier to microorganisms and
provide bactericidal secretions.
Resident microflora of skin and mucous membrane suface
help to prevent colonisation by pathogens.
Mechanism of innate immunity

10
b)Resiratory tract:
 Inhaled particals are arrested in the nasal passage on the
moist mucous membrane surface.
 Mucous membrane acts as a trapping mechanism. It has
hair like cilia that propels the particals towards pharynx
where its swallowed or coughed out.
 Cough reflex acts as a defence mechanism.

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c)Intestinal tract:
 Mouth possesses saliva which has a inhibitory effect on
many micro-organisms some bacteria are destroyed by
acidic pH of gastric juices.
 Normal bacterial flora of intestine exerts a protective
colonisation of pathogenic bacteria.

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d)Conjunctiva:
 Tears (contain lysosyme which has anti bacterial property)
helps in flusing away bacteria and other dust particals.
e)Genitourinary tract:
 Flusing action of urine eliminates bacteria from uretar.

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2)Antibacterial substances in blood & tissues:
 Complement system:
 The complement system is a complex system composed of a
large number of proteins that acts in a sequential cascade.
Many of these proteins are pro-enzymes that require
proteolytic cleavage in order to become active. Since
complement acts non-specifically, regulation of the cascade is
crucial. This is achieved by a number of regulatory
components such as inhibitors.
 Able to augment the effects of other components of the
immune system
 Three main effects:
 1. Lysis of cells (bacteria, allografts, tumor cells)

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 Interferons
 are natural proteins produced by the cells of the immune
system of most vertebrates in response to challenges by
foreign agents such as viruses, parasites and tumor cells.
Interferons belong to the large class of glycoproteins
known as cytokines.

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3)Cellular factors:
 Pathogens invading blood & tissue are destroyed by
phagocytic cells
 Types-
 Phagocytes
 Microphages are polymorphonuclear leucocytes
 Macrophages are wandering amoeboid cells in tissues,
reticuloendothelial cells & monocytes in blood.

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 Phagocytes
 The white blood cells that protect the body by ingesting
(phagocytosing) harmful foreign particles, bacteria and
dead or dying cells.
 Phagocytic Cells: Macrophages (Monocytes), Neutrophils &
Eosinophils (Macrophages)

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 Professional phagocytes
 have receptors on their surfaces
 can detect harmful objects
 Non-professional phagocytes
 Phagocytosis is not their principal function

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 Professional Phagocytes-
Location Variety of phenotypes
Blood Neutrophils, monocytes
Bone marrow Macrophages, monocytes
Gut & intestine Macrophages
Skin Dendric cells, conventional
macrophages, mast cells

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Location Variety of phenotypes
Blood, lymph nodes Lymphocytes
Skin Epithelial cells
Connective tissue Fibroblast
Blood Erythrocytes
 Non- professional Phagocytes-

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 Phagocytic action of phagocytes is divided in 4 stages:
i. Chemotaxis:
Phagocytic cells attracted by chemotactic substances →
reach site of inflammation
ii.Attachment:
Infective agent gets attached to phagocytic membrane
iii.Ingestion:
 Bacteria are engulfed by phagocytes
 Membrane of phagosome fuses with lysosome to form
phagolysosome

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iv.Intracellular killing:
 Lytic enzymes in phagolysosome destroy bacteria
 Some bacteria (mycobacteria) resist such killing & can
multiply within phagolysosome
 A class of lymphocyts called Natural killer (NK) cells play
important role in non-specific defence against viral
infections & tumor

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 Natural Killer Cells
 All nucleated cells in body have membrane major
histocompatibility complex (MCH) i.e. tissue typing
antigens.
 In virus-infected cells, MHC is reduced in amount or
contains virus peptides.
 NK cells recognize this altered MHC and kill virus-infected
cells (also tumor cells).

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Role of Natural killer Cells
Natural killer cells (or NK cells) are a type of cytotoxic
lymphocyte that constitute a major component of the innate
immune system. NK cells play a major role in the rejection of
tumours and cells infected by viruses. The cells kill by releasing
small cytoplasmic granules of proteins called perforin and
granzyme that cause the target cell to die by apoptosis.

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4)Inflammation:
 Entry of pathogens causes tissue injury & irritation which
leads to inflammation
 Inflammation leads to vasodilation, increased vascular
permiability & cellular infiltration
 Arterioles at the site of infection constrict initially & then
dilate leading to increased blood flow → leucocytes escape
into tissues by diapedesis → accumulate in large numbers
→ attracted by chemotactic substances at site of injury →
phagocytose microbes.

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Inflammation is characterised by:
1)Pain (Dolor)
2)Redness (Rubor)
3)Heat (Calor)
4)Swelling (Tumor)
5)Loss of function.

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5)Fever:
 Rise in temperature after infection: helps to accelerate
physiological processes
 Fever stimulates production of interferons & helps in
recovery from viral infections
6)Acute phase proteins:
 Infection or injury leads to sudden increase in concentration
of certain proteins: called Acute phase proteins
 Eg: C ractive protein (CRP), alpha-1-acid glycoprotein,
mannose binding protein

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Factors affecting individual innate immunity
1)Age:
 Very young & very old: more susceptible to infectious disease.
 Fetus in uterus is protected from maternal infection by
placental barrier. But some pathogens cross the barrier
causing overwhelming infection resulting in fetal death.
 Some infections are more severe in adults than in young
children due to hypersensitivity.
 Old persons are highly susceptible to infections due to
declined immune responses.

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2)Hormonal influence:
 Endocrine disorders (diabetes, hypothyroidism, adrenal
dysfunction) are associated with enhanced sensitivity to
infections.
 High incidence of staphylococcal sepsis in diabetes is due to
increased level of carbohydrates in tissues.
 Corticosteroid hormones have anti-inflammatory & anti-
phagocytic effect which depress host’s resistance.
 Elevated steroid level during pregnancy results in increase
susceptibility to many infections.

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3)Nutrition:
 Malnutrition which causes reduced cell mediated & humoral
immunity.
 Cell mediated immune responses decrease in severe protein
deficiency.

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Types of immunity
Innate
Immunity
Acquired
Immunity
Special Immunity
Individual Immunity
Racial Immunity
Natural
Active
Artificial

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Acquired immunity
 It is the second line of defence which is based upon
resistance acquired during life. It relies on genetic events
and cellular growth.
 Responds slowly, over few days
 It is specific
 each cell responds to a single epitope on an antigen
 Has anamnestic memory
 repeated exposure leads to faster, stronger response
 Leads to clonal expansion

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Types of immunity
Innate
Immunity
Acquired
Immunity
Special Immunity
Individual Immunity
Racial Immunity
Active
Natural
Passive
Artificial Natural Artificial

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1)Active immunity:
 Resistance developed by individual as a result of antigenic
stimulus.
 Involves active functioning of host’s immune apparatus to
produce antibodies & immunologically active cells. Active
immunity sets in after a latent period.
 During its development, there is often a negative phase
(immunity lower than it was before antigenic stimulus):
because antigen combines with pre-existing Ab in circulation
 Once developed, it is long-lasting. When actively immunised
individual encounters subsequent attack of same antigen,
immune response occurs more quickly (called as secondary
response)

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a)Natural active immunity:
 Results from either clinical or inapparent infection by a
microbe.
 Eg: person recovered from attack of measles develops
natural active immunity.
 Such immunity is usually long-lasting but duration varies with
types of pathogen
 Immunity is lifelong following many viral diseases
 Immunity following bacterial infection is generally less
permanent

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b)Artificial active immunity:
 Resistance induced by vaccine
 Examples of vaccines:
 Bacterial vaccines:
 Live (BCG for tuberculosis)
 Killed (Cholera vaccine)
 Subunit (Typhoid VI antigen)
 Bacterial products (Tetanus toxoid)
 Viral vaccines:
 Live (Oral polio vaccine- Sabin)

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 Live vaccines initiate an infection without causing any injury
or disease
 Immunity following live vaccine administration resembles that
following natural infection
 Immunity lasts for several years but booster doses may be
required
 Live vaccines can be administered orally or parenterally
 Killed vaccines are less immunogenic than live vaccines, &
protection lasts for short period.
 Thus, administered repeatedly

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2)Passive immunity:
 Resistance transmitted passively to recipient in a readymade
form
 Recipient’s immune system plays no active role
 There is no antigenic stimulus; instead, preformed antibodies
are administered
 No latent period
 No negative phase
 Immunity is transient lasting for days or weeks

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 No secondary type response occurs in this immunity.
 When antibodies are administered 2nd
time, they are
eliminated more rapidly
 Passive immunisation is less effective
 Employed when instant immunity is desired

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a)Natural passive immunity:
 Resistance passively transferred from mother to baby
 In human infants, maternal antibodies are transmitted
predominantly through placenta
 In animals such as pigs, antibodies are transmitted through
colostrum
 Human fetus acquires ability to produce antibodies from 20th
week of life. Till then, maternal antibodies give passive
protection against infectious diseases

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b)Artificial passive immunity:
 Resistance passively transferred to recipient by
administration of antibodies
 Agents used for this purpose:
 Hyperimmune sera of animal or human origin
 Convalescent sera
 Pooled human gammaglobulin
 These are used for prophylaxis & therapy

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Hyperimmune sera:
 Antitetanus serum prepared form hyperimmune horses
 Give temporary protection
 Disadvantage: hypersensitivity & immune elimination
 Human hyperimmune globulin: more lasting protection
Convalescent sera:
 Sera of patients recovering from disease
 Contains high levels of specific antibodies

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Pooled human gammaglobulin:
 Gammaglobulin from pooled sera of healthy individuals
 Contains Ab against all common pathogens prevalent in the
region

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 Mechanism of Acquired Immunity
 Cell-mediated immune response (CMIR)
 T-lymphocytes
 eliminate intracellular microbes that survive within
phagocytes or other infected cells
 Humoral immune response (HIR)
 B-lymphocytes
 mediated by antibodies
 eliminate extra-cellular microbes and their toxins

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Cell-mediated immune response
 T-cell
 recognizes peptide antigen on macrophage in association
with major histocompatibility complex (MHC) class
 identifies molecules on cell surfaces
 helps body to distinguish between self from non-self
 T-cell goes into effectors cells stage that is able to kill
infected cells

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 Primary response
 production of specific clones of effector T cells and
memory clones
 develops in several days
 does not limit the infection
 Secondary response
 more pronounced, faster
 more effective at limiting the infection
 Example - cytotoxic reactions against intracellular parasites,
delayed hypersensitivity (e.g., Tuberculin test) and allograft
rejection

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Humoral immune response
1. B lymphocytes recognize specific antigens
- proliferate and differentiate into antibody-secreting plasma
cells
2. Antibodies bind to specific antigens on microbes; destroy
microbes via specific mechanisms
3. Some B lymphocytes evolve into the resting state
- memory cells

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ANTIGEN
 An antigen is a molecule that induces an immune response
in the body .

50
Origin of antigen
 Exogenous antigen
 Antigens that have entered the body from the outside.
 E.g. By inhalation, ingestion or injection.

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 Endogenous antigens
 Antigens that have been generated within previously normal
cells as a result of normal cell metabolism or because of viral
or intracellular bacterial infection.
 An autoantigen is usually a normal protein or complex of
proteins (and sometimes DNA or RNA) that is recognized by
the immune system of patients suffering from a specific
autoimmune disease.
 These antigens should, under normal conditions, not be the
target of the immune system, but, due to mainly genetic and
environmental factors, the normal immunological tolerance
for such an antigen has been lost in these patients.

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Antibody : immunoglobulin
 Immunoglobulin is a glycoprotein that is made in response to
an antigen and can recognize and bind to the antigen that
caused its production.
 They are gamma globulins
 Synthesized by plasma cells
 Constitute 25-30 % of total serum proteins
 Antibodies are present in serum, tissue fluids and mucosal
surfaces.
 All antibodies are immunoglobulins, but all immunoglobulins
may not be antibodies.

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ANTIBODY STRUCTURE
 It’s a large Y-shape protein produced by B cells that is used
by the immune system to identify and neutralize foreign
objects such as bacteria and viruses.
 The antibody recognizes a unique part of the foreign target,
called an antigen.

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Basic structure
 Composed of 4 polypeptide chains.
 2 identical light and 2 identical heavy chains
 Linked by disulphide bonds
 Light chains similar in all immunoglobulins
 Light chains occur in 2 varieties kappa and lambda
 Light and Heavy chains are subdivided into variable and
constant region.
 Each heavy and light chain contains amino terminal in variable
region, carboxyl terminal in constant region

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 Heavy chains are structurally and antigenically distinct for
each class
 Each immunoglobulin peptide chain has intra chain
disulphide bonds- form loops
 Each loop is compactly folded to form a globular structure-
domain
 Light chain contains a single variable domain (VL) and a
single constant domain (CL).
 Heavy chain contains one variable domain (VH) and 3
constant domains (CH1, CH2, CH3)
 Hinge region is the segment in heavy chain -between CH1,
CH2

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 Each tip of the "Y" of an antibody contains a paratope that is
specific for one particular epitope on an antigen, allowing
these two structures to bind together with precision.
 Using this binding mechanism, an antibody can tag a
microbe or an infected cell for attack by other parts of the
immune system, or can neutralize its target directly.
 The production of antibodies is the main function of the
humoral immune system.
 Antibodies are secreted by a type of white blood cell called a
plasma cell.

57
 Antibodies can occur in two physical forms
1. Soluble form that is secreted from the cell,
2. Membrane-bound form
 That is attached to the surface of a B cell and is referred to
as the B cell receptor (BCR).
 Facilitates the activation of these cells and their subsequent
differentiation into either antibody factories called plasma
cells or memory B cells
 That will survive in the body and remember that same
antigen so the B cells can respond faster upon future
exposure.
 The BCR is only found on the surface of B cells

58
 Based on structure and antigenic nature of H chain the
immunoglobulins are classified into 5 classes.
1)Ig G- (gamma)
2)Ig A- (alpha)
3)Ig M- (mu)
4)Ig D- (delta)
5)Ig E - (epsilon)

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Functions of Different Antibodies
1. IgA plays a role in localized defense mechanism in external
secretions like tear
2. IgD is involved in recognition of the antigen by B lymphocytes
3. IgE is involved in allergic reactions
4. IgG is responsible for complement fixation
5. IgM is also responsible for complement fixation.

61
Immunodeficiency disorders
 A state in which the immune system's ability to fight
infectious disease is compromised or entirely absent.
 It may be 2 types
 Primary: Usually congenital, resulting from genetic
defects in some components of the immune system.
 Secondary (Acquired): as a result of other diseases or
conditions such as HIV infection, malnutrition,
immunosuppression

62
Primary Immunodeficiency Disease
 Myeloid lineage
– Congenital agranulocytosis
– Leukocyte-adhesion deficiency
• Lymphoid lineage
– Severe combined immunodeficiency (SCID)
– B cells
• Disorder of Phagocytosis : chronic granulomatous disease

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 Agammaglobulinemia
• Hypogammaglobulinemia
• Specific Ig Deficiencies
– T cells
• DiGeorge Syndrome
• Wiskott Aldrich Syndrome
• Complement system deficiency

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 Aetiology associated with
 Genetic defects of missing enzymes.
 Specific development impairment (pre-B cell failure).
 Infections, malnutrition and drugs

65
Symptoms
 Recurrent respiratory infections.
 Persistent bacterial infections →sinusitis, otitis
and bronchitis.
 Increased susceptibility to opportunistic infections
and recurrent fungal yeast infections.
 Skin and mucous membrane infections.
 Resistant thrush, oral ulcers and conjunctivitis.
 Diarrhoea and malabsorption.

66
Secondary Immunodeficiency
 Drug related
 Disease related
– Cancer
– AIDS
 HIV
 T helper cell as target

67
Acquired Immunodeficiency Syndrome/AIDS
 Caused by Human Immunodeficiency Virus (HIV)
 Human immune system are unable to overcome the
infection.
 The person becomes immunodeficient

68
SIGNS AND SYMPTOMS
 The patient with HIV may present with signs and symptoms
of any of the stages of HIV infection.
 No physical findings are specific to HIV infection
 The physical findings are those of the presenting infection or
illness.
 Manifestations include the following:
 Acute seroconversion manifests as a flulike illness,
consisting of fever, malaise and a generalized rash
 The asymptomatic phase is generally benign
 Generalized lymphadenopathy is common and may be a

69
Oral Manifestation of HIV
 Oral conditions associated with HIV infection are divided into
five major groups:
-Microbiological infections (fungal, bacterial, viral)
-Oral neoplasias
-Neurological conditions
-Lesions of uncertain aetiology
-Oral conditions associated with HIV treatment.
 Other co-infections and conditions associated with HIV
infection, which are significant to dentists are:
-Syphilis

70
Hypersensitivity reactions
 An exaggerated or inappropriate state of normal
immune response with onset of adverse effects
on the body
 The lesions of hypersensitivity are a form of
antigen - antibody reaction.
 Subdivided into four types;
– Type I hypersensitivity
– Type II hypersensitivity
– Type III hypersensitivity
– Type IV hypersensitivity

72
Auto-immune Disease
 The state in which the body’s immune system fails to
distinguish between ‘self’ and ‘non-self’ and reacts by
formation of autoantibodies against own tissue.

73
Etiology
 Genetic factors
 Increased expression of Class II HLA antigens
 Evidence from increased familial incidence
 Infection with microorganisms, particularly viruses (e.g. EBV
infection) and less often bacteria (e.g. streptococci,
Klebsiella) and mycoplasma
 Types of Autoimmunity
 Organ Specific
 Organ non-specific

74
 Systemic lupus erythematosus
 Rheumatoid arthritis
 Scleroderma (Progressive systemic sclerosis)
 Polymyositis-dermatomyositis
 Polyarteritis nodosa (PAN)
 Sjögren’s syndrome
 Reiter’s syndrome
 Wegener’s granulomatosis

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 Sjogren’s syndrome
 Sicca syndrome
 Tried of -
 Keratonjuctivitis sicca
 Xerostomia
 Rheumatoid athritis

76
Conclusion
There is a great deal of synergy between the adaptive immune
system and its innate counterpart and defects in either system
can lead to immunopathological disorders, including
autoimmune diseases, immunodeficiencies and hypersensitivity
reactions. The remainder of this supplement will focus on the
appropriate diagnosis, treatment and management of some of
these more prominent disorders, particularly those associated
with hypersensitivity reactions.

77
References
Ananthanarayan R. Ananthanarayan and Paniker's textbook of
microbiology. Orient Blackswan; 2006.
Baveja CP. Textbook of microbiology. Arya Publications; 2005.
Shafer WG, Hine MK, Levy BM, Rajendran R,
Sivapathasundharam B. A textbook of oral pathology.
Philadelphia: Saunders; 1983 Sep 20.
Sembulingam K, Sembulingam P. Essentials of medical
physiology. JP Medical Ltd; 2012 Sep 30.

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