This document provides an overview of basic immunology. It begins with an introduction by Aditi Singh from the Department of Preventive and Pediatric Dentistry at Seema Dental College & Hospital. The document then covers the following key topics in 3 sentences or less each: nomenclature of immunology, types of immunity, features of immune responses, major immune cells, immunity in the oral cavity, innate and adaptive immunity, properties of adaptive immune responses, active and passive immunity, cells of the immune system, development of B and T lymphocytes, classes of lymphocytes, the CD nomenclature, types of adaptive immunity, phases of adaptive immune responses, naïve, effector and memory lymphocytes, MHC, cytokines, antigens

2. BASIC
IMMUNOLOGY
PRESENTED BY
ADITI SINGH
POST GRADUATE STUDENT
DEPARTMENT OF PREVENTIVE AND
PEDIATRIC DENTISTRY
SEEMA DENTAL COLLEGE & HOSPITAL

3. 
The nomenclature of Immunology

Types of immunity (innate and adaptive; active and
passive; humoral and cell-mediated)

Features of immune responses

The major cells of the immune system

Immunity in the oral cavity

4. Definitions
• Immunity: protection against infections
• Immune system: molecules, cells and tissues that
mediate responses to foreign substances
• Antigens: substances recognized by the cells and
molecules of the immune system and to which the system
responds

5. Innate and adaptive immunity
Innate immunity: always present (ready to attack); many pathogenic
microbes have evolved to resist innate immunity
Adaptive immunity: stimulated by exposure to microbe; more potent

6. Properties of adaptive immune responses
The two features that best distinguish adaptive and
innate immunity are specificity and memory

7. Primary and secondary immune responses illustrate
specificity and memory in adaptive immunity

8. The concept of clonal selection
Lymphocytes with highly specific and diverse antigen receptors develop prior
to exposure to antigens

9. Active and passive immunity
Active immunity: long-lasting protection (memory),
multiple effector mechanisms activated, lag time
Passive immunity: rapid protection, short duration

10. Cells of the immune system
• Lymphocytes
– Mediators of adaptive immune responses; only cells with
specific receptors for antigens
• Antigen-presenting cells (APCs)
– Specialized to capture, concentrate, and display
antigens for recognition by lymphocytes
– Dendritic cells; macrophages, B cells; follicular
dendritic cells
• Effector cells
– Function to eliminate microbes; include lymphocytes,
granulocytes (neutrophils, eosinophils), macrophages

11. Development of B and T lymphocytes
Congenital immunodeficiency diseases are often caused by blocks
at different stages of lymphocyte maturation

12. Classes of lymphocytes

13. The CD Nomenclature
•
Structurally defined leukocyte surface molecule that is
expressed on cells of a particular lineage (“differentiation”)
and recognized by a group (“cluster”) of cell-specific
antibodies is called a member of a cluster of
differentiation (CD)
•
CD molecules (CD antigens, CD markers) are:
•
•
•
Used to classify leukocytes into functionally distinct subpopulations,
e.g. helper T cells are CD4+CD8-, CTLs are CD8+CD4Often involved in leukocyte functions
Antibodies against various CD molecules are used to:
•
•
•
Identify and isolate leukocyte subpopulations
Study functions of leukocytes
Eliminate particular cell populations

14. Types of adaptive immunity
Different types
of immune
responses are
mediated by
different classes
of lymphocytes
and defend
against different
types of microbes

15. Phases of adaptive immune responses
Need for proliferation and differentiation results in delay
(typically 4-7 days) in the adaptive immune response

16. Stages in the life history of lymphocytes
Proliferation: expands number of antigen-specific cells Differentiation:
converts lymphocytes into effective defenders

17. Naïve, effector and memory lymphocytes
• Naïve lymphocytes
– Mature lymphocytes that have not previously
encountered antigen; function -- antigen recognition
– Preferential migration to peripheral lymphoid organs
(lymph nodes), the sites where antigens are
concentrated and immune responses start

18. Naïve, effector and memory lymphocytes
•
Naïve lymphocytes
– Mature lymphocytes that have not previously encountered antigen; function
-- antigen recognition
– Preferential migration to peripheral lymphoid organs (lymph nodes), the
sites where antigens are concentrated and immune responses start
• Effector lymphocytes
– Activated lymphocytes capable of performing the
functions required to eliminate microbes („effector
functions”)
– Effector T lymphocytes: cytokine secretion (helper
cells), killing of infected cells (CTLs)
– B lymphocytes: antibody-secreting plasma cells

19. Naïve, effector and memory lymphocytes
•
•
Naïve lymphocytes
– Mature lymphocytes that have not previously encountered antigen; function
-- antigen recognition
– Preferential migration to peripheral lymphoid organs (lymph nodes), the
sites where antigens are concentrated and immune responses start
Effector lymphocytes
– Activated lymphocytes capable of performing the functions required to
eliminate microbes („effector functions”)
– Effector T lymphocytes: cytokine secretion (helper cells), killing of
infected cells (CTLs)
– B lymphocytes: antibody-secreting cells (e.g. plasma cells)
• Memory lymphocytes
– Long-lived, functionally silent cells; mount rapid
responses to antigen challenge (secondary responses)

20. Naïve, effector and memory lymphocytes
•
•
•
Naïve lymphocytes
– Mature lymphocytes that have not previously encountered antigen; function
-- antigen recognition
– Preferential migration to peripheral lymphoid organs (lymph nodes), the
sites where antigens are concentrated and immune responses start
Effector lymphocytes
– Activated lymphocytes capable of performing the functions required to
eliminate microbes („effector functions”)
– Effector T lymphocytes: cytokine secretion (helper cells), killing of
infected cells (CTLs)
– B lymphocytes: antibody-secreting cells (e.g. plasma cells)
Memory lymphocytes
– Long-lived, functionally silent cells; mount rapid responses to antigen
challenge (secondary responses)

21. MHC

MAJOR HISTOCOMPATIBILITY COMPLEX

The histocompatibility antigens are cell surface antigens that induce an
immune responses.

In human beings, human leukocyte antigens (HLA) (alloantigens), were found
to be the major histocompatibility antigens.

The ability to respond immunologically to an antigen is conditioned by
specific genes called the immune response (Ir) genes.

22. 
HLA molecules:

HLA class I antigens (A, B and C) are found on the surface
of virtually all nucleated cells.

They are the principal antigens involved in graft rejection
and cell mediated cytolysis.

May function as components of hormone receptors.

23. HLA class II antigens

Are more restricted in distribution -- found only on
cells of the immune system-macrophages, dendritic
cells, activated T cells, and particularly on B cells.

HLA class II molecules are primarily responsible for
the graft-versus-host response and the mixed
leucocyte reaction (MLR)

24. HLA class III antigens

They include complement components linked to the formation of
-
C3 convertases.
-
Heat shock proteins and
-
Tumour necrosis factors.

25. 
Many critical interactions among cells of the immune system are
controlled by soluble mediators called cytokines.

Cytokines produced by lymphocytes are known as lymphokines,
whereas those produced by monocytes or macrophages are called
monokines.
Cytokines
-( Interleukins, Interferons, Growth factors)

26. Types:
Interleukin I (Leucocyte Activating Factor):
-IL -I , IL-I
-Stimulation of T Cells
-B cell proliferation, antibody synthesis
-Chemotaxis, Phagocytosis

27. Interleukin – 2 :(T cell growth factor)
-Powerful Mediator of immune response
Interleukin – 3 :(Multi colony stimulating
factor)
-Growth factor for bone marrow stem
cells

28. Interleukin – 4:( B cell growth factor I)
-Growth factor for T cell, mast cells
Interleukin – 5 :(B cell growth factor II)
-Proliferation of activated B cells,
Maturation of Eosinophils

29. Interleukin – 6 :
- Immunoglobulin synthesis
-Stimulatory effects
Colony stimulating factors:
-Stimulates pluripotent stem cells
-Treating haemtopoitic dysfunction
Tumor necrosis factors TNF:
-A serum factor found to induce hemorrhagic
necrosis in tumours
-Cachectin, TNF (activated macrophages)
-TNF (Lymphotoxin)

30. Interferons:IFN
-IFN
(Leucocytes)
-IFN
(Fibroblasts)
-IFN
(T cells)
-Macrophage activation
-Antitumour activity

31. Antigens
Antigen (Ag) – the molecule an antibody (Ab) binds to
•
•
•
•
usually a foreign substance
each antigen has different sites that antibodies can
bind to, so that one antigen can be bound by several
different antibodies
examples in the case of allergy could be pollen, cat
dander, or a chemical in soap
The two attributes of antigenicity are:
(1) Induction of an immune response
(immunogenicity), and
(2) specific reaction with antibodies.

32. 
Complete antigen is able to induce antibody formation and

Haptens are substances which are incapable of inducing

The smallest unit of antigenicity is known as the antigenic
determinant or epitope.
produce a specific and observable reaction with the antibody
so produced.
antibody formation by themselves but can react specifically
with antibodies.
The combining area on the antibody molecule, corresponding to
the epitope, is called the paratope.

33. ANTIBODY

An immunoglobulin that
is capable of combining
with specificity to the
antigen that elicited its
production.
Each is made of two identical heavy and two identical light
amino acid chains, held together by disulfide bonds

34. variable regions of the light chain (grey)
and the heavy chain (yellow) form the
antigen binding site
- light chain constant region is blue while
heavy chain constant region is red. The
two chains are joined by carbohydrate
(purple).

35. How, Why and Where are Antibodies
Produced?

Produced in Vertebrate Cells in response to a
„non-self‟ substance termed an antigen.

The process begins with macrophages roaming in
the bloodstream. Macrophages engulf „non-self‟
molecules and then display portions of the
engulfed molecules on their outer plasma
membranes.

After many recognition steps B-cells are
stimulated to produce specific antibodies.

The antibodies then go off and bind to the
foreign substance thereby marking the
substance for destruction.

36. How an Antibody Works
Antibody binds to
target antigen
Receptor for
constant region of
antibody on NK
cell recognizes a
bound antibody
After binding, the NK
cell is signaled to kill
the target cell
The target cell dies
by apoptosis and/or
membrane damage

37. Primary Response
1.Is slow, sluggish and
short-lived,
2.Long lag phase
SecondaryResponse
1.Is prompt, powerful
and prolonged.
2. Short or Negligible lag
phase
3.Low titre of antibodies 3. Much higher level of
antibodies that lasts
that does not persist
for long periods.
for long.
4. Antibody IgG.
4. Antibody - IgM

38. IMMUNOGLOBULINS

IMMUNOGLOBULIN –‟ PROTEINS OF ANIMAL ORIGIN
ENDOWED WITH KNOWN ANTIBODY ACTIVITY AND FOR
CERTAIN OTHER PROTEINS RELATED TO THEM BY
CHEMICAL STRUCTURE‟ – WHO (1964)

TYPES DEPENDING ON THE PHYSICOCHEMICAL AND
ANTIGENIC DIFFERENCES
-IgG , IgA, IgM , IgD , IgE

39. Stages of development of immunoglobulin

In humans - Peyer's patches develop and lymphoid cells appear in
the spleen and lymph nodes by the 20th week of gestation.

From then on the fetus is able to produce IgM and IgD.

It receives maternal IgG, (but IgA and IgE are not present).

At birth IgM production is enhanced, but IgG level falls steadily, to
reach miminum levels by the 3rd month.

IgG production then picks up and becomes adequate by 2-3 years.

Full immunocompetence is attained only after the first decade of
life.

40. I. IgG
Structure:
Monomer
Percentage
serum antibodies:
80%
Location:
Blood, lymph, intestine
Half-life
in serum: 23 days
Complement
Placental
Known
Fixation: Yes
Transfer: Yes
Functions: Enhances
phagocytosis, neutralizes toxins
and viruses, protects fetus and
newborn.

41. II. IgM
Structure:
Pentamer
Percentage
serum antibodies: 5-
10%
Location:
Blood, lymph, B cell
surface (monomer)
Half-life
in serum: 5 days
Complement
Placental
Known
Fixation: Yes
Transfer: No
Functions: First antibodies
produced during an infection.
Effective against microbes and
agglutinating antigens.

42. III. IgA
Structure:
Dimer
Percentage
serum antibodies: 10-
15%
Location:
Secretions (tears,
saliva, intestine, milk), blood and
lymph.
Half-life
in serum: 6 days
Complement
Placental
Known
Fixation: No
Transfer: No
Functions: Localized
protection of mucosal surfaces.
Provides immunity to infant
digestive tract.

43. IV. IgD
 Structure:
Monomer
 Percentage
serum antibodies: 0.2%
 Location:
B-cell surface, blood, and
 Half-life
in serum: 3 days
lymph
 Complement
 Placental
 Known
Fixation: No
Transfer: No
Functions: In serum function
is unknown. On B cell surface,
initiate immune response.

44. V. IgE
Structure:
Monomer
Percentage
serum antibodies:
0.002%
Location:
Bound to mast cells and
basophils throughout body. Blood.
Half-life
in serum: 2 days
Complement
Placental
Known
Fixation: No
Transfer: No
Functions: Allergicreactions.
Possibly lysis of worms.

45. THE COMPLEMENT SYSTEM

Complement was initially described as a substance in peritoneal fluid and sera
that cooperated with antibodies in the lytic destruction of bacteria
(Bacteriolysis Pfeiffer‟s phenomenon)
NOMENCLATURE

C1q, C1r, C1s, C4, C2, C3, C5, C6, C7, C8, C9.

Enzymatically active form – C1r

Suffix letters a , b etc represents clevage products

Small intial clevage fragment – „a‟ fragment
and the large - „b‟ fragment
eg.C3a, C3b

46. GENERAL FEATURES

Present in all normal mammalian sera

Complement activation by antibody antigen is possible only with
IgM(CH4), IgG1, IgG3(CH2)

Classic activation pathway – cytolytic destruction of membrane
sensitive antigens

Alternate pathway (properdin pathway)

Kinin formation, chemotaxis, opsonisation, anaphylotoxin
formation and immune adherance

47. Functions

Lysis- cells, bacteria, and enveloped viruses.

Opsonization- foreign cells, bacteria, viruses are prepared for
phagocytosis.

Generation of peptide fragments that regulate features of
infammatory and immune responses.

49. Overview of the Immune Response

50. IMMUNOLOGICAL TOLERANCE

Is the condition in which contact with an antigen specifically abolishes the
capacity to mount an immune response against that particular antigen when it is
administered subsequently.

The unresponsiveness of individuals to self antigens was due to the contact of the
immature immunological system with self antigens during embryonic life.

Can occur in adults also.

Tolerance may be
- total or partial.
- short-lived or long-lasting.
The induction, degree and duration of tolerance depend on the species and
immunocompetence of the host, nature and dose of the antigen and the route of
administration.

51. Immunodifficiency Diseases
-
Conditions where the defence mechanisms of the body are impaired, leading
to repeated microbial infections of varying severity and sometimes enhanced
susceptibility to malignancies
Classification :
a.Primary immunodeficiencies:
-Abnormalities in the development of the immune mechanisms
b.Secondary immunodeficiencies:
-Diseases, drugs, Nutritional inadequacies

52. Classification of primary immunodeficiency
syndrome
A.Disorders of specific immunity
I. Humoral immunodeficiencies (B cell defects)
a.X – linked agammaglobulinemia
b.Transient, hypogammaglobulinemia of infancy
c.Common variable immunodeficiency
d. Immunodeficiencies with hyper IgM
e.Selective immunoglobuin deficiency (IgA,
IgM, IgG

53. II.Cellular immuodeficiencies ( T cell defects)
a.Thymic hypoplasia (DiGeorge‟s syndrome
b.Chronic mucocutaneus candidiasis
III.Combined immunodeficiencies(B and T cell defects)
a.Cellular immunodeficiency with abnormal
imunoglobulin synthesis(Nezelof syndrome)
b.Ataxia telengictasia
c.Wiskott aldrich syndrome
d.Immunodeficiency with thymoma
e.Immunodeficiency with short- limbed dwarfism
f.Episodic lymphopenia with lymphocytotoxin

54. B.Disorders of complement
a.Complement component deficiency
b.Complemnt inhibitor defeciencies
C.Disorders of phagocytosis
a.Chronic granulomatos diseases
b.Myloperoxide deficiencies
C.Chediac higashi syndrome
d.Leucocyte G6PD defecie
Secondry immunodeficiencies:
Malnutrition, malignancy, infections, metobolic disorders,
cytotoxic drugs

55. Immunity in the
oral cavity

56. DEVELOPMENT OF ORAL IMMUNE SYSTEMS
DURING INFANCY

During the mid 1960 s Secretory IgA (SlgA) became
recognized as the primary immune mediator of specific host
defenses on mucosal surfaces, specially equipped with four
binding sites and secretory component .

during first years of life the infant‟s oral cavity receives
immune components from several sources :

maternal milk

maternal serum ( igg via placental transfer)

infant saliva

infant serum ( via gcf and teething )

57. INFANT SALIVARY SOURCES :
SALIVARY IgA:

By 4 to 8 weeks of age , saliva from essentially all
immunologically sufficient infants contains detectable
quantities of IgA .

IgA concentration, yields a peak at about 2 to 3 months.
Following this early burst of IgA secretion, salivary IgA
concentrations level off during the middle of the first
year.

Concentrations then gradually increase through early
childhood .Adult levels of salivary IgA are not reached
until at least 5 years of age.

58. 
Secretory IgA has been identified in the meconium
of newborn infants, a substance that is not
considered to be maternally derived.

Low concentrations of IgA (and IgM antibody) to
poliovirus (PV) and E. coli 0 antigens have also been
detected in the saliva of neonates delivered from
normal
mothers
and
from
mothers
with
hypogammaglobulinemia.

These antibodies were synthesized in utero to
placentally transferred maternal IgG antiidiotypic
antibodies to these antigens.

59. SALIVARY IgG

IgG is not considered to be a significant product of adult major
salivary gland tissues.

During fetal life. IgG -producing cells are absent from salivary tissue.
In the neo-natal period, IgG has been found in saliva.Salivary mucosa
is temporarily permeable to the nonspecific passage of
macromolecules from serum.

The presence of serum-derived IgG in saliva at birth could provide
the neonate with passive immunity in the oral cavity because most of
this IgG is maternally derived.

However, this source of protection is transitory because salivary IgG
concentrations and the percentage of infants in whom these
concentrations can be detected rapidly decrease to essentially zero
during the first 2 months of life.

IgG then remains absent from the oral cavity until teeth begin to
erupt.

60. SALIVARY IgD

Salivary IgD is detected in nearly half of the saliva
samples of children up to 1 month of age.

Salivary IgD detected in these young infants may be
locally produced because IgD concentration does not
correlate with other salivary components presumed to
be serum derived (e.g., IgG and albumin).

The initial elevated frequency of infants with salivary
IgD has been reported to fall such that after 5
months of age, IgD could only occasionally be
detected in the saliva of children up to 3 years old.

Source : Parotid gland

61. IgM

Like IgA, IgM does not possess the appropriate Fc
configuration to be transferred to the fetus via the
placenta.so all IgM in neonatal circulation is synthesized
de novo. During the first 1 to 2 months after birth
significant concentrations of IgM are present in the saliva

These immunoglobulins exist in much lower concentrations
than IgA in these pure glandular secretions

Palatine minor salivary glands are relatively enriched in
IgM compared to other major and minor gland salivary
glands


62. THE ORAL CAVITY AS AN
IMMUNOLOGICAL ENTITY
SALIVARY ENVIRONMENT
Components of Innate Immunity

Mucins

Lactoferrin

Salivary peroxidase

Lysozyme

Other Salivary Components-Histidine rich proteins,
Proline rich peptides, Beta-2microglobulins & Fibronectin

63. MUCIN

Mucus secreting cells
located mainly in
submandibular ,sublingual &
minor salivary glands

Lubrication

IgA combines with mucins

Mucin oligosaccharides
mimic tissue receptors
recognized by bacteria
LACTOFERRIN

Serous cells of salivary gland

PMNs also secrete them

High afinity to Fe

Carboxy anion interaction
with bacterial surface

OH- radical generation

64. SALIVARY PEROXIDASES

PAROTID +
SUMBANDIBULAR.,PMNs

H2O2 , Thiocyanate ions

Hypothiocyanate ions
LYSOZYME (muramidase)

Ductal epithelium

N-acetyl muramic acid + Nacetylglucoseamine linkage
of peptidoglycan layer of
bacterial cellwall is cleaved

65. COMPONENTS OF THE ANTIBODY MEDIATED
IMMUNITY
Secretory IgA
-Stable complexes
-Virus Neutralization, Immune exclusion, „Disposal‟ of
bacteria
-Bacterial Enzyme Inhibition
IgM
- „IgM COMPENSATION‟
-Opsonization, Complement mediated Lysis
IgG & IgD
-Occurs in low conc.

66. 
Another function associated with SIgA activity is bacterial enzyme
inhibition.

Salivary IgA antibody has been shown to inhibit the function of a group of
enzymes (glucosyltransferases) from cariogenic mutans streptococci that
synthesize glucans involved in plaque formation.

Inhibition of this process may also change the diffusion characteristics
of plaque, thus allowing bacterial acids to diffuse more readily out of
plaque.

SIgA antibody could interfere with bacterial metabolism by inhibiting
enzymes involved in transport phenomena.

67. GCF ENVIRONMENT

CELLULAR COMPONENTS
 Polymorhonuclear neutrophils
-Realeses Granules containing LYSOSOMAL ENZYMES
 Lymphocytes
-B & T Lymphocytes (1%-2%)
 Monocytes & Macrophages
-Supplement the antibacterial activity of PMN
 Others
-Lipopolysaccharides
-Bacterial proteases
-Prostaglandins
Immunoglobulins:(IgG, IgA, IgM)
Complement:(C3, C4:Additional activated components During disease)

69. COMPLEMENT

In periodontally healthy subjects, C3 and C4 can be detected.

If inflammation occurs, concentrations of GCF C3 and C4
decrease with respect to serum, and activated complement
components such as C3a, C3b, and C5a appear, indicating that
complement activation has occurred in the gingival crevice.

This activation is likely to be in response to the increased
bacterial load associated with the inflammation. Both classic
and alternate complement pathways can be activated.

The biologically active polypeptides released by complement
activation have a variety of antibacterial eftects.

70. PMN‟s

In the GCF environment PMNs defend against
bacterial invasion of the gingival tissue through
phagocytic and bactericidal mechanisms.

The activity of PMNs results in the release of
granules containing lysosomal enzymes that can
disengage bacterial plaque adherent to the tooth.

These enzymes also have the potential to damage
host tissue if present in high enough concentrations.

71. LYMPHOCYTES , MONOCYTES
MACROPHAGES

Both T and B lymphocytes appear in the GCF,
comprising 1 % to 2% of the cells found therein.

Approximately three times as many B cells as T cells
are present in GCF, which is the converse of their
ratio in blood.

Monocytes and macrophages: Approximately 2% to
3% of the remainder of the immune cells in the GCF
are monocytes. These cells may supplement the
antibacterial activity of the PMNs

72. IMMUNOLOGICAL ASPECTS OF DENTAL
CARIES

At least six species of microorganisms constitute this mutans
group. The two most prominent species in humans are S. mutans
(serotypes c, e, and f) and Streptococcus sobrinus (serotypes
d, g, and h).

Most individuals are colonized by mutans streptococci of the c
serotype.

High levels of serum IgG antibody to mutans streptococcal
cells or antigens are associated with low levels of caries in
young adults. Serum antibody from caries-free young adults
inhibits Glucosyltransferases from mutans streptococci to a
greater extent than serum from caries-prone individuals.

73. 


Studies suggested that low numbers of mutans streptococci in
dental plaque are associated with relative elevations in serum
IgG antibody in children approximately 2 to 5 years old.
Serum IgG antibody to mutans streptococcal
antigens is associated with lower caries
experience.
CARIES VACCINE : “Wagner” was the 1st
person to successfully vaccinate rats against
caries. Interestingly S. fecalis was used as
the immunogen

74. SYSTEMIC ACTIVE
IMMUNIZATION

Gregory and Filler observed that ingestion of a
vaccine containing killed Streptococcus mutans
daily for ten consecutive days induced an
increased level of specific secretary IgA
antibodies to Streptococcus mutans cells.

This resulted in reduction in number of viable
Streptococcus mutans organism in dental plaque
and whole saliva

75. SYSTEMIC PASSIVE
IMMUNIZATION

Michalek, et al. used a multivalent vaccine
consisting of whole cell antigen of
Streptococcus mutans (serotype a, b, c, d,
g), to hyperimmunize a group of pregnant
cows.

They observed low plaque scores decreased
number of streptococci in plaque and
decreased caries actually as compared to
the control.

Role of Probiotics
…..

76. HYPERSENSITIVITY

77. CONCLUSION

STUDENT- It is dry .It goes above head .It is difficult to
understand.

RESEARCH SCIENTIST- when I don’t know the cause ,I put
the blame on immunology.

PRACTITIONERS- I use it as a weapon to escape when my
treatment fails.

But actually it is a war between the pathogens and the host
defense system which ends in the “SURVIVAL OF THE
FITTEST” .

78. conclusion

Immune system is a complex functioning system
Acting against various invading pathogens and
preventing the diseases – protective

Helpful in various diagnostic investigations

Acting against the own body tissues – destructive.
IMMUNE SYSTEM , THUS COULD BE A

80. References:

Janis kuby, Immunology, 1st Edition, W.H.Freeman &company, 1992.

Daniel P. Stites, Aba Terr, Tristram G. Parslow Basic and clinical immunology, 8 th
Edition, Prentice-hall international inc,1994.

Ivan Roitt, Jonathan Brostoff, David Male, Immunology, 3rd Edition, Mosby Publication, 1994.

James T Barsel ,Text book of immunology, 5th edition, mosby publication,1998

Jawetz and Melnick, Text book of medical microbiology 3rd edition,elsevier science publishing
company,1999

Gerard.J.Tortora &Grabowski Principles Of Anatomy and physiology,10 thEdition,john Wiley & son’s
inc Publication,2000

Barrot ,Basic immunology and its medical applications ,4 th edition,2000

Harsh Mohan “Essential Pathology for Dental Students 2nd Edition. Jaypee Brothers Medical
Publishers (P) Ltd. New Delhi. 2002.

Ananthanarayan & panissker’s text book of microbiology, 7th edition, orient longman private
limited, 2005.

81. 
Alan Hgowenlock, Varley‟s ,Practical clinical biochemistry,6th edition,2005

Textbook of medical physiology –18th edition by Guyton

Robbins & Cotran pathologic basis of diseases, 7th edition ,Elsevier Publications , 2006.

.Contemporary oral microbiology and immunology.By Slot and Taubmann

Cellular and molecular immunology. Abul K. Abbas, Andrew H. Litchman; 5 th edition

. Immunology : Roitt, Brostoff, Male 6 th edition.

J Virol. 2005 Nov;79(22):14318-29. Human beta-defensins suppress human
immunodeficiency virus infection: potential role in mucosal protection. Sun L et al,

ABIKO .Y et al;Med Electron Microsc. 2003 Dec;36(4):247-52. Defensins in saliva and the
salivary glands.

. E.E. LeClair;Four Reasons to Consider a Novel Class of Innate Immune Molecules in the Oral
Epithelium. ; J Dent Res 82(12):944-950, 2003

. M. Murakami et al.;Cathelicidin Antimicrobial Peptides are Expressed in Salivary Glands and
Saliva. J Dent Res 81(12):845-850, 2002