This document provides an overview of basic immunology. It begins with introductions and definitions of key immunology concepts. It then discusses the history of immunology, types of immunity including innate and acquired immunity. It describes the tissues, cells and basic aspects involved in the immune system such as antigens, antibodies and complement system. It also covers major histocompatibility complex, cytokines and disorders of the immune system. The document is intended as a basic introduction and reference for immunology.

1. BASIC
IMMUNOLOGY
Lecturer: Mr. Osman Hassan Ali

2. • Introduction
• History
• Types of immunity
• Tissues of immunity
• Cells of immunity
• Basic aspects of immunology
• Major histocompatibility complex
• Cytokines
• Disorders of immune system
• Immune responses in periodontal pathogenesis
• Periodontal vaccine
• Host modulation
• Conclusion
• References
Contents

3. INTRODUCTION
 Immunity: resistance to disease, specifically infectious disease.
 Immune system: The collection of cells, tissues, and molecules that
mediate resistance to infections.
 Immune response: the coordinated reaction of these cells and
molecules to infectious microbes.
 Immunology: the study of the immune system, including its
responses to microbial pathogens and damaged tissues and its role in
disease.

4. Traditional concept:
Immunity refers
diseases.
to protection against infectious
Modern concept:
Immunity is a function of which an individual recognizes
and excludes antigenic foreign substances. It is normally
beneficial, but sometimes, it is injurious.

5. •1796 – First demonstration of smallpox vaccination (Edward Jenner)
•1862 – Phagocytosis (Ernst Haeckel)
•1877 – Mast cells (Paul Ehrlich)
•1883 – 1905 – Cellular theory of immunity via phagocytosis by
macrophages and microphages (polymorphonuclear leukocytes) (Elie
Metchnikoff)
•1890 – Demonstration of antibody activity against diphtheria and tetanus
toxins. Beginning of humoral theory of immunity - Emil von Behring
and Kitasato Shibasaburō
•1900 – Antibody formation theory (Paul Ehrlich)
HISTORY

6. • 1965 – Discovery of "immune interferon" (gamma interferon) (E.F.
Wheelock)
• 1971 – Peter Perlmann and Eva Engvall at Stockholm University
invented ELISA
• 1973 – Dendritic Cells first described by Ralph M. Steinman
• 1975 - Discovery of Natural Killer cells (Rolf Kiessling, Eva
Klein, Hans Wigzell)
• 1980-1983 – Discovery and characterization of interleukins (IL-1 IL-
2 ) (Robert Gallo, Kendall A. Smith, Tadatsugu Taniguchi)
• 1985 – Identification of Toll-like receptors (Christiane Nusslein
Volhard)
• 2000 - Characterization of M1 and M2 macrophage subsets
by Charles Mills

7. Importance of the immune system in health
and disease:

8. Types of Immunity
INNATE IMMUNITY:
Non-specific:
• Species
• Racial
• Individual
Specific:
• Species
• Racial
• Individual
ACQUIRED IMMUNITY:
Active
immunity:
• Natural
• Artificial
Passive
immunity:
• Natural
• Artificial

9. • Resistance to infections which, an individual possesses by virtue
of his genetic and constitutional make-up.
• Not affected
immunization.
• Nonspecific -
by prior contact with microorganisms or
when it indicates a degree of resistance to
infections in general.
• Specific - where resistance
concerned.
to a particular pathogen is
Innate or native immunity:

10. • Species immunity:
refers to the total or relative refractoriness, to a pathogen, shown by
all members of a species.
• Racial immunity:
Within a species, different races may show differences in
susceptibility to infections. Such racial differences are known to be
genetic in origin,
• Individual immunity:
The differences in innate immunity exhibited by different individual
in a race.

11. Factors influencing the level of innate immunity:
Innate
Immunity
Age
Hormonal
influence
Nutrition

12. Mechanisms of innate immunity:
 Epithelial surfaces:
 Antibacterial substances in blood and tissues:
• Complement system
• Beta-lysine
• Basic polypeptides- leukins, plakins
• Acidic substances like lactic acid
• Enzymes - lactoperoxidase, lysozymes
• Interferons

13.  Microbial antagonisms:
 Cellular factors:
• Phagocytic cells, discovered by
Metchinikoff Microphages : PMN
Macrophages: Monocytes
• Natural killer cells
• Innate Lymphoid Cells

14.  Inflammation:
 Fever:
A rise of temperature following infection is a natural defense
mechanism.
Accelerates the physiological processes and destroy the infecting
pathogens.
Stimulates the production of interferon. and aids recovery from viral
infections.

15. sudden increase in plasma
 Acute phase proteins:
• Infection or injury leads to a
concentrations of certain proteins.
• These include:
 C reactive protein (CRP),
 Mannose binding protein,
 Alpha-1-acid glycoprotein,
 Serum amyloid P component etc.,
• Activate the alternative pathway of complement.
• Enhance host resistance, prevent tissue injury and promote
repair of inflammatory lesions.

16. Acquired Immunity:
• The resistance that an individual acquires during life is known as
acquired Immunity.
• also known as adaptive immunity as it represents an adaptive
response of the host to a specific pathogen or other antigen.
• Types:

17. Comparison of active and passive immunity:
Activeimmunity: Passive immunity:
Produced actively by host's immune
system.
Received passively. No active host
participation.
Induced by infection or by
immunogens.
Ready made antibody treatment.
Durable effective protection. Transient, less effective.
Immunity effective only after lag Immediate immunity.
period.
Immunological memory present. No memory.
Booster effect on subsequent dose. Subsequent dose less effective.
Negative phase may occur. No negative phase.
Not applicable in the Applicable in immunodeficient.
immunodeficient.

18. Types of acquired immunity:

19. Properties of Acquired Immunity:

20. Phases of adaptive immune response:

21. Tissues of Immune System
• The tissues of the lymphoid organs can be classified into:
1. Central / primary lymphoid organs
2. Peripheral / secondary lymphoid organs
• Central lymphoid organs:
Lymphoepithelial structures in which the precursor lymphocytes
proliferate, develop and acquire immunological capability.
A. Thymus
B. Bone marrow
• Peripheral lymphoid organs:
After acquiring immunocompetence, the lymphocytes migrate
along blood and lymph streams, accumulate in the peripheral
lymphoid organs and following antigenic stimulus, effect the
appropriate immune response.
A. Lymph nodes
B. Spleen
C. Mucosa associated lymphoid tissue (MALT)

22. Thymus:

23. Lymph nodes:
• Encapsulated nodular aggregates of lymphoid tissues.
• Lymph: tissues lymphatic
vessels lymph node blood
circulation.
• APCs :- pick up antigens of microbes from
epithelia and other tissues and transport
these antigens to the lymph nodes.
• On antigenic stimulation: primary
lymphoid follicles germinal centers
• T cell zone: inbetween cortex and medulla
which has t lymphocytes

24. Lymph nodes of head & neck region

25. Spleen:

26. Mucosa associated lymphoid tissue (MALT):

27. Waldeyers ring

28. Cells of Immune System

29. Cell Life span
T cells Weeks to months Memory
cells - years
B cells 5-6 weeks
Macrophages 6-16 days
Monocytes 2-5 days
Neutrophils 2-5 days
Dendritic cells Few months

30. Lymphocytes:
• Circulate through lymphoid organs and nonlymphoid tissues.
• Recognize foreign antigens and initiate adaptive immune
responses.
• O.5 – 1 x 1012 Lymphocytes.
• Arise from stem cells in bone marrow.
• Types:
1. B-lymphocytes:
• B1
• B2
2. T-lymphocytes:
• CD4+ T cells – Helper T cells
• Special subset of CD4+ T cells – Regulatory T
lymphocytes.
• CD8+ T cells – Cytotoxic T
lymphocytes.
3. Null cells/large granular lymphocytes

31. MATURATION OF LYMPHOCYTES

32. CLASSES OF LYMPHOCYTES

33. Stages In The Life History of Lymphocytes

34. Natural killer cells:
 Natural killer (NK) cells recognize infected and stressed cells and
respond by killing these cells by secreting the macrophage-activating
cytokine IFN-γ

35. Dendritic cells:
• Leucocytes with cytoplasmic processes.
• Dermal dendrocytes are also known as histiocytes.
• Langerhans cells peripheral dendritic cells
• Possess receptors for C3a
• Express MHC class II, ICAM Molecules.
• Bridge between innate and adaptive immune response.
• Can express MMP in response to bacterial challenge and can
contribute to periodontal destruction.

36. Mast cells:
• Important in immediate inflammation
• Has receptors for complement components (C3a, C5a) and Fc portion of
IgE and IgG (Fcxr and Fcyr).
• Express Toll like receptors
• Stimulation of receptors causes activation of vasoactive substances
leading to inflammatory process.
• Contain lysozymes, histamine, neutrophil chemotactic factor, heparin.
• They can synthesize slow reactive substances like SRS-A, TNFa and
IL6.

38. Neutrophils:
• First cells to arrive at the site of
inflammation
• Possess receptors for c1,c3,c4 & c5
• Primary granules: Beta
glucoronidases, betagalactosidase,
Elastase, Myeloperoxidase,
Lysozyme
• Secondary granules: Lactoferrin,
Lysozyme,
Antimicrobial peptides Beta
defensins Cathelicidins

39. Macrophages:
• Monocytes enter tissue and differentiate into macrophages
• Antigen presenting cells
• Ingest antigens and coat with MHC molecules and present to T cell
receptor
• Secrete variety of cytokines like IL1, IL6, TNFA, IFN,
Complements and growth factors and can phagocytose antigens.

40. Phagocytosis:

41. Transendothelial migration

42. Basic Aspects of Immunology
 Antigens
 Antibodies
 Antigen-antibody reactions
 Complement system

43. Antigens
• Antigen has been defined as any substance which
when introduced parenterally into the body, stimulates the
production of an antibody with which it reacts specifically
and in an observable manner.
• Attributes of antigenicity:
1. Immunogenicity – induction of an immune response
2. Immunological reactivity – specific reaction with
antibodies

44. • Based on the ability of antigens to carry out these two functions,
they are classified as :
1. Complete antigen – able to induce antibody formation and produce a specific
and observable reaction with the produced antibody.
2. Haptens: substances incapable of inducing antibody formation on their own.
• Complex haptens – can precipitate with specific antibodies
• Simple haptens - nonprecipitating.
• Biological classes of antigens:
• T cell dependent antigens (TD) Antigens that require the help of T cells
for B cell activation are thymus-dependent (T-dependent) antigens.
• T cell independent antigens (TI) is an immunogen that can stimulate B
cells to synthesize antibodies without participation by T cells.

45. Epitope
Antigen
Paratope
The combinig area on the antibody molecule, corresponding to
the epitope

46. Determinants
of
antigenicity:
Size
Chemical
nature
Susceptibilit
y to tissue
enzymes
Foreignness
Antigen
specificity
Species
specificity
Isospecificity
Autospecifici
ty
Organ
specificity
Heterogenic
specificity

47. Synthesized by plasma cells & to some extent by lymphocytes.
Immunoglobulins are glycoproteins, each molecule consisting of
two pairs of polypeptide chains, the light (L) & heavy (H) chains.
ANTIBODIES

49. Abnormal Immunoglobulins:
• Bence jones proteins in multiple myeloma.
• IgM in waldenstrom’s macroglobulinemia.
• Cryoglobulinemia
•A different disorder is found in ‘ heavy chain disease’, a
lymphoid neoplasia characterized by over production of Fc parts of
heavy chains.

50. Antigen – Antibody Reactions
They serve several functions. In the body, they form the basis
of humoral immunity.
In the laboratory, they help in the diagnosis of infections, in
epidemiological surveys, in the identification of infectious
agents.
The reaction occur in 3 stages
1.Primary reactions
2.Secondary reactions
3.Tertiary reactions

51. When an antigen is bound by an antibody, any of four
actions may occur:
• Antigen may no longer function properly (inactivation by
antibody)
• Complement may be activated
• antigen and/or attached microorganism may clump
(agglutination) or even precipitate out of solution
• Antibody-dependent cell-mediated cytotoxicity may
occur.

52. General Features:
• Reaction is specific.
• Entire molecule react & not fragments.
• No denaturation during the reaction.
• Combination occurs at the surface
• Combination is firm but reversible. AFFINITY–
intensity of attraction AVIDITY– strength of the bond

53. Serological Reactions:
Precipitation Reaction
Agglutination Reaction

55. Radio Immunoassay (RIA)
Enzyme Immunoassay
A technique for determining antibody levels by introducing an antigen
labelled with a radioisotope and measuring the subsequent
radioactivity of the antibody component.

56. IMMUNOCHROMATOGRAPHIC TESTS

57. The Complement System
Coined by Ehrlich.
Refers to a system of factors which occur in normal serum & are activated
by Ag- Ab reaction & subsequently mediate a number of biologically
significant consequences.
 Acts as mediator & amplifier of many immune responses & inflammation.
The complement system belong to a group of biologic effector mechanisms
called Triggered enzyme mechanisms.
 Only IgM & IgG1,2,3 fixes the complement.
Complement as a whole is heat labile.

58. Components:
A complex 9 different fractions called C1- C9.
C1 is present in serum as a calcium dependant ion which chelates
with EDTA.
Complement Activation:
C cascade is a series of reactions in which the preceding
components act as enzymes on the succeeding components, cleaving
them into dissimilar components.
Larger fragment join the cascade, smaller fragments often possess
the biologic effects which contribute to defense mechanisms by
various mechanisms.

59. C cascade can be activated by
1.Classical pathway
2.Alternative pathway
3.lectin pathway

60. Ag-ab,DNA,trypsin like
enzymes,retro viruses
Properidin, factor D, Zymogen,
bacterial endotoxins & IgA
MBL binds
to mannose

62. REGULATION OF C- ACTIVATION:
Unchecked C-activity can cause not only exhaustion of the C- system
but also serious damage to tissues.
 Two different type of regulators are
A)Inhibitors
B)Inactivators
Various inhibitors include inhibitor of C1a esterase. This does not
prevent normal C-cascade but checks it’s autocatalytic prolongation.
The S protein binds to C567a & modulates the cytolytic action of
the MAC.

63. Various inactivators are
1. Factor I
2. Factor H
3. Anaphylatoxin inactivator
4. C4 binding protein

64. Major Histocompatibility Complex (MHC)
• MHC is a locus in the short arm of Chromosome 6 that encodes for
MHC classI, II & III molecules which are involved with antigen uptake
and presentation.
• Class I – present in all cells in association with self derived
antigens (intracellular) presented to CD8 & NK cells
• Class II – Antigens from Extracellular sources are presented by APCS
(peripheral DCs, monocyte derivitives & B cells) in association with
Class II molecules – HLA- DR, DP, DQ
• Class III – complement factors B, C2and C4

66. Genes of MHC Organized In 3 Classes
⚫ Class I MHC genes
⚫ Glycoproteins expressed on all nucleated cells
⚫ Major function to present processed Ags to TC
⚫ Class II MHC genes
⚫ Glycoproteins expressed on B-cells, dendritic cells.
⚫ Major function to present processed Ags to TH
⚫ Class III MHC genes
⚫ Products that include secreted proteins that have immune
functions.
Ex. Complement system, inflammatory molecules.

67. Defensins
• Endogenous, small, cysteine-rich antimicrobial peptides that are
produced by leukocytes and epithelial cells.
• Multifunctional and, by interacting with host cell receptor(s),
participate in both immune responses.
• Contain cysteine residues that form characteristic disulfide
bridges.
• Human defensins are classified into two subgroups:
• Six alpha-defensins (hND-1 to hND-6) PMNs
• Four beta-defensins (hBD-1 to hBD-4) Mucosal epitheial cells

68. Cytokines
•Low molecular wt. proteins secreted by many cells (previously
known as Lymphokines)
•Assist in the regulation and development of Immune effector cells
•Cell to Cell communication
•Direct effector function
•Autocrine, Paracrine or endocrine
•Pleiotrophic

71. Cellular Receptors For Microbes and Damaged Cells
Receptors used to detect microbes and damaged cells are expressed on
phagocytes, dendritic cells and many other cell types.
Based on their location, they are of 3 types:

72. These receptors for PAMP and DAMP belong to several
protein families.
1. Toll-like receptors
2. NOD-like receptors and the inflammasome
3. Others: the RIG-like
receptor Cytosloic
DNA sensors lectin
receptors

74. Signaling functions of TLRs

75. The Inflammasome

76. Immunodeficiency Diseases
• Conditions where the defense mechanisms, of the body are impaired,
leading to repeated microbial infections of varying severity and
sometimes enhanced susceptibility to malignancies.
• Deficiencies of defence mechanisms may involve:
• Specific immune functions - humoral immunity, cell mediated
immunity or both
• Nonspecific mechanisms - such as phagocytosis and complement.
• Immunodeficiencies may be classified as:
• Primary or Secondary.

77. Conti…..
• Primary immunodeficiencies: from abnormalities in the
development of the immune mechanisms.
• Secondary immunodeficiencies: are consequences of
disease, drugs, nutritional inadequacies and other processes
that interfere with the proper functioning of the mature
Immune system.

78. Classification of primary Immunodeficiency
syndromes:
iniI. Humoral immunodeficiencies {B cell defects):
•a. X-linked agammaglobulinemia
•b. Transient hypogammaglobulinemia of infancy
•c. Common variable immunodeficiency (late onset
hypogammaglobuilnemia)
•d. Selective immunoglobulin deficiencies (IgA, IgM or IgC subclasses)
•e. Immunodeficiencies with hyper-IgM
•f. Transcobalamin II deficiency
•II. Cellular immunodeficiencies. (T cell defects):
•a. Thymic hypoplasia (Digeorge's syndrome)
•b. Chronic mucocutaneous candidiasis
•c. Purine nucleoside phosphorylase (PNP) deficiency.

79. Conti……..
•III. Combined immunodeficiencies (B and T cell defects):
•a. Cellular immunodeficiency with abnormal immunoglobulin -synthesis
•b. Ataxia telangiectasia
•c. Wiskott-Aldrich syndrome
•d. Immunodeficiency with thymoma
•e. Immunodeficiency with short-limbed dwarfism
•f. Episodic lymphopenia with lymphocytotoxin.
•g. Severe combined immunodeficiencies
•'Swiss type’ agammaglobulinemia
•Reticular dysgenesis of de Vaal
•Adenosine deaminase (ADA) deficiency

80. B. Disorders of
complement:
• a. Complement component deficiencies
• b. Complement inhibitor deficiencies
• Chronic granulomatous disease
• Myeloperoxidase deficiency
• Chediak-Higashi syndrome
• Leucocyte G6PD deficiency
• Jobs’s syndrome
• Tuftsin deficiency
• Lazy Leucocyte syndrome
• Hyper-IgE syndrome
• Actin-bindlng protein deficiency
• Shwachman's disease

81. Autoimmunity
• Condition in which structural or functional damage is produced by the
action of immunologically competent cells or antibodies against the
normal components of the body.
• Pathogenesis :
 Autoantibody formation may be a result of tissue injury
 They may cause damage by the cytotoxic (type II) or by toxic
complex (type III) reactions
 Sensitized T-lymphocytes may also result in autoimmune
diseases through type IV reactions.
Humoral and cellular responses may act synergistically in the
production of some autoimmune diseases.

82. Hemolytic autoimmune diseases:
• Autoimmune hemolytic anemias
• Autoimmune thrombocytopenia
• Autoimmune leucopenia
Localized autoimmune diseases:
• Autoimmune diseases of thyroid gland
• Addisons disease
• Pernicious anemia
• Myasthenia gravis
• Autoimmune orchitis
• Autoimmune diseases of the eye
• Autoimmune diseases of the nervous system
• Autoimmune diseases of the skin.
Systemic autoimmune diseases:
• Sjogrens syndrome
• Systemic lupus erythematosus
• Rheumatoid arthritis
• Polyarteritis nodosa
Classification of autoimmune diseases:

83. Hypersensitivity
• The term hypersensitivity refers to the injurious consequences in
the sensitized host, following contact with specific antigens.
• Traditionally they are classified into:
1. Immediate hypersensitivity:
• Anaphylaxis
• Atopy
• Antibody mediated cell damage
• Serum sickness
2. Delayed hypersensitivity:
• Infection (tuberculin) type
• Contact dermatitis

84. Coombs and Gell (1963) classification:
1. Type I reactions (IgE dependent):
cytotropic IgE antibodies fixed on the surface of tissue cells (mast and
basophils) in sensitized individuals binds to Ag.
Occurs in two forms:
a. Anaphylaxis – acute, fatal and systemic
b. Atopy – chronic, recurrent, nonfatal, localized form Tissues
involved - target tissues or shock organs.

85. Primary
mediators
:
Histamine
Serotonin
Heparin
Chemotactic
factors
Enzymes like
proteases and
hydrolases
Secondary
mediators:
Prostaglandins
Leukotrienes
Platelet
activatingfactor
Other
mediators:
Anaphylotoxins
Bradykinin

86. Type II reaction: cytolytic and cytotoxic:
Antibodies bind with the antigenic determinants on the surface
of cells leading to cytotoxic or lytic effects Ex:
• Autoimmune anemias and hemolytic disease of new born
• Long acting throid stimulators (LATS) in graves disease.
• Myasthenia gravis

87. Type III reactions: Immune complex diseases:
1. Arthus reaction:
• Local manifestation of generalized hypersensitivity.
• Seen as an intense local reaction with edema,induration and
hemmorhagic necrosis.
2. Serum sickness:
• Systemic form of type III hypersensitivity.
• The clinical syndrome consists of fever, lymphadenopathy,
splenomegaly, arthritis, glomerulonephritis, endocarditis,
vasculitis,urticarial rashes, abdominal pain, nausea and vomiting.

88. Type IV reactions: Delayed hypersensitivity:
Induced by sensitized t cells (Tdth, Th1,Th2,Tc), which on contact with
specific antigens causes biological effects on leucocytes, macrophages and
tissue cells
1. Tuberculin type (infection):
Small dose of tuberculin when injected intradermally in an sensitized
at the site
individual, an indurated inflammatory reaction develops
within 48-72 hours.
2. Contact dermatitis type:
DH develops from skin (esp. inflamed area)contact with chemicals.
Contact with the allergen in sensitized individuals.
Varies from macules, papules to vesicles.

89. DRUG ALLERGY TESTS

90. PERIODONTAL DISEASE IMMUNOLOGY
Initiated by small subset of
endogenous gram-negative
periodontal bacteria.
Trigger innate, inflammatory, and
adaptive immune responses.
Destruction of the
PERIODONTIUM

91. • First line of defense.
• Includes:
 Saliva
 GCF
 Epithelial barrier
 Commensals
• Orchestrated by a broad
range of cytokines,
chemokines, cell surface
receptors.
Innate immunity in periodontal diseases:

92. The PRR’s
• The primary response to pathogens in the innate immune system is
triggered by Pattern Recognition Receptors (PRRs) that bind
Pathogen-Associated Molecular Patterns (PAMPs), found in a
broad type of organisms.
• These receptor types include:
 toll-like receptors (TLR),
 nucleotide-binding oligomerization domain (NOD)
proteins,
 cluster of differentiation 14 (CD14),
 complement receptor-3,
 lectins and scavenger receptors.

93. Toll Like Receptors
• 10 TLRs are identified so far.
• Among them TLR-2 and TLR-4 are most defined members.
• TLR 2 responds to lipoteichoic acid and microbial lipoproteins
• TLR 4 responds to LPS
• TLR 5 responds to Flagellin
• TLR 9 responds to bacterial DNA
• Porphyromonas gingivalis LPS stimulates TLR-2, and not TLR-4
• Only Aggregatibacter actinomycetemcomitans and Veillonella
parvula were capable of stimulating both TLR-2 and TLR-4.
• Chronic stimulation of TLRs results in over-production of pro-
inflammatory cytokines and may lead to tissue destruction.

94. Adaptive immunity in periodontal disease:
• The importance of adaptive immunity in periodontal diseases is
endorsed by the histologic studies of established lesions, which
revealed:
 B cells and plasma cells in progressive lesions.
 T cells especially T-helper subset (CD4) in stable lesions.
• Antigen presenting cells – Generate Ag specific response
• T cells – alterations in th1 and th2 balance leads to tissue destruction
• B cells – control extracellular antigens.
• Antibodies – mainly IgG, but also IgM and A.
• Complement system - Provide barrier against spread of bacterial
infections.

95. Cytokines & Periodontal Disease

96. The MMPs
• Family of proteolytic enzymes that degrade extracellular matrix molecules.
• Produced by variety of cells like PMN, macrophages, fibroblast, epithelial cells.,
Key inhibitors of mmps: glycoprotein, antitrypsin, macroglobulin.

97. Periodontal Disease Osteoimmunology
tnfa, il1a, 1b, 6, 11,15, 17 stimulate bone resorption
Il 4,5,10,13,18,tgfb inhibit bone resorption.
Th2 cells: inhibit ocl by il 4,10
Th17 cells: promote ocl by il 23,17 and RANKL.

98. Immunologic Considerations Of:
1. Gingivitis:
• Initial lesion - PMNs
• Early lesion – T Lymphocyte
• Established lesion - Plasma cells & B lymphocytes
• Advanced lesion - Plasma cells
2. Chronic periodontitis:
• Involves mainly alternative pathway of complement
• P gingivalis produces an enzyme that can cleave C5
• MMP-8 is elevated & TIMP-1 are not
• Chymotrypsin released by T denticola activates MMPs
• Most of the collagenase activity of C.P is due to the MMP-8 released
by PMNs.
3. Aggressive periodontitis:
• 75% of LAP patients have dysfunctional neutrophils.
• Elevated levels of MMP-1 & TIMP-1 are present.
• Demonstrate elevated IgG2 antibodies against Aa.
• GAP is often characterized by defects in either PMNs/monocytes.

99. Immunological differences between chronic and
aggressive periodontitis
• Clinically the gingival lesion is often absent in aggressive
periodontitis suggesting that it may not follow the same sequence of
initiation and progression as chronic periodontitis (from gingival T-
cell lesion to progressive B-cell lesion).
• Ford et al. Examined the possibility of subtle immunological
differences.
• There are differences between these two forms of periodontitis with
• respect to the synthesis of b-defensins by host cells.
• In components of the adaptive immune system

100. • Differences in neutrophil function:
• Patients with localized aggressive periodontitis had an inherited
trait characterized, by lower than normal chemotaxis
phagocytosis and intracellular microbial killing responses.
• Ryder believed that some of the differential functions of
neutrophils in aggressive forms of periodontitis may be due to a
combination of inherited and acquired characteristics.
• At present it is not possible to identify real differences in the
immunopathology of the two diseases.
• This may be because there are no differences, or because the
differences only reflect variations in the degree of severity or
susceptibility rather than actual different immunopathologies.

101. Periodontal vaccine
• The complexity of periodontopathic bacteria might be a problem in
developing a periodontal vaccine.
• The vaccine development program involves identifying the bacterial
peptides and proteins that trigger the immune response, and using
these as the basis of vaccines.
• The vaccines are being trialed in mouse models of periodontal
disease and following a positive response, a vaccine will progress
to clinical trials.
• Administering the vaccine, in early adolescent age before there is
any sign of periodontitis, helps in prolonging the healthy life of the
periodontium and risk of any inflammation is reduced.

103. Host Modulation
• Modulation of ArachidonicAcid metabolites (NSAIDS)
• Modulation of MMPs – SDD (Doxycline - 20 mg twice daily)
• Modulation of bone remodeling (Bisphosphanates)
• Inhibit Inflammatory cytokines (IL1 & TNFα) through
recombinant human IL11 (rhIL-11)
• Inhibition of Nitric Oxides by MEG (Mercaptoalkylguanidines)

104. CONCLUSION
• Immunity is a war between pathogens and host defense system
which ends in the “SURVIVAL OF FITTEST”.
• The immune responses team in unique ways, depending upon
host, microbial and environmental controls, to maintain or re-
establish homeostasis.
• However, these inherent good guys if went rogue would result
in collateral damage of the periodontium.
• Immune system, thus could be a

105. REFERENCES
• Text book of microbiology-R .AnanthanarayAan, 6th edition.
• Carranza’s Clinical periodontology-11th edition.
• Clinical periodontology and implant dentistry-Jan Lindhe.
• Mim’s medical microbiology-4th edition.
• Basic Immunology - Functions and disorders of the immune
system 5e - Abbas (2016)
• Textbook of periodontics – jaiganesh r, 1st edition.