This is not a substitute for textbook learning. Adequate References have been added.

1. HOST DEFENSE
Dr. Aneetinder Kaur
PG 1st year
Department of Conservative
Dentistry & Endodontics

2. Defense Lines
01
Inflammation
02
Immunity
03
Structure and
Functions of Immunity
05
Immune Response
06
Hypersensitivity
07
CONTENTS
Components of Immunity
04
08
References

3. Defense Lines

4. FIRST LINE (PHYSICAL ) BARRIERS
Body Systems &
Factors Involved
Active Components
Skin Squamous Cells, Sweat & Sebaceous Glands
Mouth Saliva
GIT Wall, Gastric Secretions
Respiratory Tract Tracheal Cilia, Coughing Reflex
Nasopharynx Nasal Hair & Mucus
Eye Tears
CVS Phagocytic Cells, NK Cells
Serum Lactoferrin, Transferrin, Interferons, TNF α,
Lysozyme, Fibronectin, Complement Proteins
Acute Phase Proteins Alpha 1 Acid Glycoprotein
Urinary System Acidic pH & Flow
Breast Milk Antibodies, Lactoferrin, Transferrin,
Interferons, Mucin, Lysozyme, Fibronectin
Fever High Temperature
Paniker’s 9th Edition

5. SECOND LINE (DEFENSIVE
MECHANISM) BARRIERS
◦ Inflammation
◦ Defensive cells
◦ Complement System
THIRD LINE BARRIER
◦ Immune system
Paniker’s 9th Edition

6. Inflammation

7. INFLAMMATION
◦ Inflammation is a protective
response involving host cells, blood
vessels, and proteins and other
mediators that is intended to
eliminate the initial cause of cell
injury, as well as the necrotic cells
and tissues resulting from the
original insult, and to initiate the
process of repair.
Pathologic Basis of Disease – Robbins & Cotran

8. Pathologic Basis of Disease – Robbins & Cotran

9. SEQUENCE OF
EVENTS IN
INFLAMMATION
RECOGNISE
RECRUIT
ACTIVATE
CONTROL AND
TERMINATE
DAMAGE
REPAIR
Pathologic Basis of Disease – Robbins & Cotran

10. ACUTE INFLAMMATION
Pathologic Basis of Disease – Robbins & Cotran

11. Pathologic Basis of Disease – Robbins & Cotran

12. Pathologic Basis of Disease – Robbins & Cotran

13. Pathologic Basis of Disease – Robbins & Cotran

14. Pathologic Basis of Disease – Robbins & Cotran

15. CHRONIC INFLAMMATION
INFILTRATION
TISSUE
DESTRUCTION
ATTEMPTS AT
HEALING
CELLS AND MEDIATORS
➢Macrophages
➢Lymphocytes
➢Eosinophils
➢Mast Cells
➢Neutrophils
Pathologic Basis of Disease – Robbins & Cotran

16. TISSUE REPAIR
Pathologic Basis of Disease – Robbins & Cotran

17. Immunity

18. TYPES OF IMMUNITY
IMMUNITY
INNATE/
NATIVE
NON-
SPECIFIC
SPECIFIC
ACQUIRED/
ADAPTIVE
ACTIVE PASSIVE
Paniker’s 9th Edition

19. MECHANISMOFINNATE
IMMUNITY
EPITHELIAL SURFACES
ANTIBACTERIAL SUBSTANCES IN
BLOOD AND TISSUES
MICROBIAL ANTAGONISMS
CELLULAR FACTORS
INFLAMMATION
ACUTE PHASE PROTIENS
TOLL-LIKE RECEPTORS
INNATE IMMUNITY
FACTORSAFFECTING
INNATEIMMUNITY
AGE
HORMONES
NUTRITION
Paniker’s 9th Edition

20. TYPES OF ACQUIRED
IMMUNITY
• NATURAL ACTIVE
• ARTIFICIAL ACTIVE (Vaccines)
ACTIVE
• NATURAL PASSIVE
• ARTIFICIAL PASSIVE
(Sera of animal / human origin , Gamma Globulin , Convalescent
sera)
PASSIVE
COMBINED IMMUNISATION
Paniker’s 9th Edition

21. ACTIVE IMMUNITY PASSIVE IMMUNITY
Produced Actively by Hosts Immune
System
Received Passively No Active Host
Participation
Induced by Infection or Immunogens Readymade Antibody Transfer
Durable Effective Protection Transient, Less Effective
Effective only after Lag Period Immediate Immunity
Booster Effect on Subsequent Dose Less Effective Subsequent Dose
Negative Phase May Occur No Negative Phase
Not Applicable in Immunodeficient Applicable in Immunodeficient
Paniker’s 9th Edition

22. Components of
Immunity

23. ANTIGENS
◦ An antigen is a substance which
when introduced into a body
evokes immune response to
produce a specific antibody with
which it reacts in an observable
manner.
◦ Attributes:
◦ Immunogenicity
◦ Immunological Reactivity
Types
Complete Antigen
Haptens
(Simple/Complex)
Epitope
Paniker’s 9th Edition

24. Size
Chemical
Nature
Susceptibility to
Tissue Enzymes
Foreigness
Antigenic
Specificity
Heterogenic
Specificity
Determinants of Antigenicity
Biological
Classification of
Antigens
T Cell Dependent T Cell Independent Super Antigens
Paniker’s 9th Edition

25. ANTIBODIES -
IMMUNOGLOBULINS
Immunoglobulin – Proteins of
animal origin endowed with
known antibody activity and /for
certain other protein related to
them by chemical structure.
◦ Antibodies have unique structural
features and motifs and bind to
antigens to destroy them
effectively.
◦ Synthesised by endoplasmic
reticulum of plasma cells and to some
extent by lymphocytes.
◦ Constitute 20~25% of total serum
proteins.
WHO (1964)
Paniker’s 9th Edition

26. Textbook of Microbiology – CP Baveja 4th Edition

27. Criteria IgG IgM IgA IgD IgE
Half Life
(Days)
23 5 6-8 3 2
Percentage
in Serum (%)
80 5-8 10-13 1 1
H chain gamma alpha mu delta epsilon
Serum
Concenratio
n (mg/ml)
8-16 0.5-2 0.6-4.2 0.03 In nano grams
Molecular
Weight
150000(7S)
900000-
1000000(19S)
160000(7S)
400000
180000(7S) 190000(8S)
Protective
function
mainly
Body Fluids
(GCF)
Blood Stream
Body Surfaces
(Colostrum
Saliva Tears)
Recognition
Molecule
Reagenic
Hypersenstivit
y
Main Serum Ig,
only maternal
Ig (across
placenta), Late
antibody
Millionaires
Molecule ,
oldest Ig class,
synthesised by
fetus (20 wks)
2ndmost
abundant
Resembles IgG
Heat Labile
(56Deg.C),
Anaphylactic Ig
Paniker’s 9th Edition

28. COMPLEMENT SYSTEM
◦ Refers to a system of factors that occurs in
the normal serum and is activated
characteristically by antigen – antibody
interaction which subsequently mediates a
number of biologically significantly
consequences.
• Classical Complement pathway
• Alternative Complement
pathway
• Lectin Complement pathway
TYPES
Phagocytosis
Inflammatory Response
Hypersenstivity Rxns
Autoimmune Disease
Endotoxic Shock
Immune Adherence
Conglutination
BIOLOGICALEFFECTS
Paniker’s 9th Edition

29. Pathologic Basis of Disease – Robbins & Cotran

30. Paniker’s 9th Edition

31. Paniker’s 9th Edition

32. Structure and
Function
Of Immunity

33. LYMPHORETICULAR SYSTEM
Is a complex organisation of cells of
diverse morphology distributed widely in
different organs and tissues of body
responsible for immunity
TYPES
◦ Humoral immunity (antibody mediated )
◦ Cellular immunity
Paniker’s 9th Edition

34. Paniker’s 9th Edition

36. CELLS of IMMUNE SYSTEM
◦ Granulocytes
◦ (polymorphonuclear leukocytes,
PMNs) neutrophils, eosinophils,
and basophils; lymphocytes.
◦ Monocytes.
◦ Tissue macrophages
◦ Mast cells .
◦ LYMPHOCYTES –
◦ B Cells
◦ Plasma B-Cells
◦ Memory B-Cells:
◦ Types of T Cells
◦ Regulatory or Effector Cells
◦ CD4 + or CD8+
◦ Helper/Inducer (TH Cells)
◦ TReg Cells
◦ Cytotoxic/Cytolytic (TC )
◦ Memory cells (TM )
◦ Antigen-presentingcells
◦ Dendriticcell
◦ Natural Killer Cells
Paniker’s 9th Edition

37. Paniker’s 9th Edition

39. Immune
Response

40. TYPES OF IMMUNE RESPONSES
Humoral/Antibody mediated
Immunity
Cell mediated Immunity
Paniker’s 9th Edition

41. Humoral/Antibody mediated Immunity
ANTIBODY RESPONSES
◦ Primary response
◦ Secondary response
ANTIBODY PRODUCTION
Paniker’s 9th Edition
• Genetic Factors
• Age
• Nutritional Status
• Route of Administration
• Size and No. of Doses
• Multiple Antigens
• Adjuvants
Factors Affecting
Antibody Production
(AMI)

42. Cell mediated Immunity
Antigen Presentation
by APC to T
Lymphocytes
Sensitised T
Lymphocytes change
into Memory and
Effector Cells
Activated
Lymphocytes release
Lymphokines
T Cell recognises
Antigens when
presented with MHC
Molecules
CD4+ Cells recognise
MHC2 and Antigen,
change into Th and Td
cells
Tc attach to target
cells and release
cytolysins
Paniker’s 9th Edition

43. Pathologic Basis of Disease – Robbins & Cotran

44. Hypersensitivity

45. HYPERSENSITIVITY
◦ Immune responses that normally are protective are also
capable of causing tissue injury. Injurious immune reactions
are grouped under hypersensitivity, and the resulting diseases
are called hypersensitivity diseases.
Paniker’s 9th Edition

46. Pathologic Basis of Disease – Robbins & Cotran

47. Pathologic Basis of Disease – Robbins & Cotran

48. Pathologic Basis of Disease – Robbins & Cotran

49. Pathologic Basis of Disease – Robbins & Cotran

50. Pathologic Basis of Disease – Robbins & Cotran

51. Pathologic Basis of Disease – Robbins & Cotran
Systemic Inflammation as a Consequence of
Local Infection

52. References
• Pathologic Basis of Disease – Robbins & Cotran (SAE)
• Essential Pathology for Dental Students –
Harshmohan, 4th Edition
• Textbook of Microbiology – Ananthanarayan &
Paniker’s, 9th Edition
• Textbook of Microbiology – CP Baveja 4th Edition
• Abbas & Lichman, Cellular & Molecular Immunology,
5th Edition

54. Doubt Session

55. 1 . Type of T cells that predominate
Pulpal tissue .

56. 2. Hypersensitivity v/s
Hypereactivity

58. 3. Acquired Immunologic Tolerance
◦ Immunological tolerance is defined
as a state 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 immune reactivity
to other antigens being unaffected.

62. ◦ Management hinges on confirming the diagnosis. All individuals with confirmed asthma should
receive self-management education, including a written action plan. Very mild intermittent asthma
may be treated with a short-acting beta2-agonist (SABA) taken as needed. SABAs are
recommended for relief of symptoms; individuals 12 years of age and over with moderate to
severe asthma (particularly those who are exacerbation prone and have poor control) who are
taking an ICS/LABA formulation approved also for use as a reliever may do so. Inhaled
corticosteroids (ICS) should be introduced early as the initial maintenance treatment for asthma
even in individuals who report asthma symptoms less than three times a week. LTRA are second-
line monotherapy for mild asthma. If asthma is not adequately controlled by low doses of inhaled
corticosteroids, additional therapy should be considered. In children 6 years of age and over, the
ICS should be increased to a medium dose before adding an adjunct agent such as a long-acting
beta2-agonist (LABA) or LTRA. In children 12 years of age and over and adults, a LABA should
be considered first as adjunct therapy. A LABA should only be used in combination with an ICS.
Increasing to a medium dose of ICS or the addition of an LTRA are third-line therapeutic options.
Theophylline may be considered as a fourth-line agent in adults. Severely uncontrolled asthma may
require additional treatment with prednisone. Omalizumab may be considered in individuals 12
years of age and over with atopic asthma poorly controlled despite high doses of ICS and
appropriate add-on therapy, with or without prednisone. Asthma symptom control and lung
function tests, inhaler technique, adherence to asthma treatment, exposure to asthma triggers in the
environment, and the presence of co-morbidities should be reassessed at each visit and before
altering the maintenance therapy. Consider also assessment of sputum eosinophils in adults with
uncontrolled moderate to severe asthma managed in specialized centres. After achieving acceptable
asthma control for at least a few weeks to months, the medication should be reduced to the
minimum necessary dose to achieve adequate asthma control and prevent future risk of
exacerbations. HFA: Hydrofluoroalkane; IgE: Immunoglobulin E; mcg: Micrograms; PEF: Peak
expiratory flow; yrs: Years

63. 4. Role of DPSCs in Inflammation

64. 5. Endogenous and Exogenous Antigen
◦ Endogenous antigens are proteins
found within the cytosol of human
cells. Examples of endogenous
antigens include:
◦ Viral proteins produced during viral
replication;
◦ Proteins produced by intracellular
bacteria
◦ Proteins that have escaped into the
cytosol from the phagosome of
phagocytes such as antigen-
presenting cells;
◦ Tumor antigens produced by cancer
cells; and
◦ Exogenous antigens are antigens
that enter from outside the body,
such as bacteria, fungi, protozoa,
and free viruses. These exogenous
antigens enter macrophages,
dendritic cells, and B-lymphocytes
through phagocytosis or
pinocytosis.

65. 6. Epitope, Idiotope, Paratope
◦ The actual portions or fragments of
an antigen that react with
receptors on B-lymphocytes and
T-lymphocytes, as well as with free
antibody molecules, are called
epitopes or antigenic determinants.
The size of an epitope is generally
thought to be equivalent to 5-15
amino acids or 3-4 sugar residues.
◦ An idiotope is the unique set of
antigenic determinants (epitopes) of
the variable portion of an antibody.
In some cases it can be the actual
antigen-binding site, and in some
cases it may comprise variable
region sequences outside of the
antigen-binding site on the antibody
itself
◦ A paratope, also called an antigen-
binding site, is a part of an antibody
which recognizes and binds to an
antigen. It is a small region (of 5 to
10 amino acids) of the antibody

66. 7. Complementarity-Determining Regions
◦ The variable domain is also referred
to as the FV region and is the most
important region for binding to
antigens. To be specific, variable
loops of β-strands, three each on
the light (VL) and heavy (VH) chains
are responsible for binding to the
antigen. These loops are referred to
as the complementarity-determining
regions (CDRs). In the framework
of the immune network theory,
CDRs are also called idiotypes.