The document discusses the immune system, detailing its components, mechanisms, and classifications, including innate and adaptive immunity. It outlines the roles of various cells and proteins involved in immune responses, as well as factors affecting immunity and types of immunodeficiencies and autoimmune diseases. Additionally, it emphasizes the importance of maintaining a healthy lifestyle to support immune function and addresses clinical implications of immune system disorders.

1. IMMUNITY
Presented by :- Dr. Rohan Shrivastava
MDS – JR1

2. CONTENTS
Immunity
• Introduction
• Components of immune system
• Classification
• Innate immunity & mechanism
• Adaptive immunity & mechanism
Antigen
• Antigen
• Classification
Antibody Immunoglobulin
• Structure
• Classification
• Functions of each antibody
Auto-Immune diseases
Conclusion
References

3.  Introduction –
Our environment contains infectious microbes-
viruses, fungi , protozoa, multicellular parasites-
can cause diseases in host.
Body is protected against invading
microorganisms by physical barriers- skin, bile,
mucus, epithelial linings- first line of defence.
If these fail- second line of defence – immune
system is activated.

4.  Immunity
• Resistance exhibited by the host against injury caused by
microorganisms and their products.
• This resistance plays a major role in prevention of infectious diseases
• Immune system- Biological structures & processes within an organism
that protect against diseases by identifying & killing pathogens &
tumour cells.

5.  Classification

6.  Line of Defense

7. Innate Immunity
• Also known as NATIVE IMMUNITY.
• Resistance possessed by birth.
• By virtue of his genetic and constitutional make-up.
• Does not depend on prior contact with foreign antigen.
 SPECIFIC – Resistance to a particular pathogen is concerned.
 NON SPECIFIC- Indicate a degree of resistance to infections in general.

8. • Again classified as
• SPECIES IMMUNITY - Entire human species is resistant to plant
pathogen.
• RACIAL IMMUNITY- Particular races of that species are resistant.
E.g.- American negroes are more susceptible to TB than the white race.
• INDIVIDUAL IMMUNITY- Resistance to infection varies with different
individuals of same race and species.
E.g- Homozygous twins show similar resistance/ susceptibility to Leprosy/
TB , not seen in heterozygous twins.

9. FACTORS INFLUENCING INNATE IMMUNITY
1. AGE-
Two extremes of life- fetus and old persons – higher susceptibility to various
infections.
Foetus- immature immune system , Old age- gradual waning of immune
response.
2. HORMONES-
Hormonal disorders – Diabetes mellitus , Hypothyroidism enhance
susceptibility to infections.
3. NUTRITION-
Immune response is reduced in malnutrition patients.

10.  Mechanism of Innate Immunity
1. EPITHELIAL SURFACES – First line of defence (Mechanical barrier)
• Skin – Bactericidal property.
High concentration of salts in drying sweat .
Sebaceous secretions
• Respiratory tract- Inhaled particles arrested in nasal passages.
Mucous secretion act as trapping mechanisms .
Cough reflex- important defence mechanism.

11. • Intestinal Tract- Saliva – inhibitory effect on micro-organisms.
Digestive juices.
• Conjunctiva-
Lysozymes present in tears- bactericidal action.
• Genitourinary tract- Urine’s flushing action eliminate bacteria from urethra.
Semen- contains some antibacterial substances.
Acidity of adult vagina- inhospitable to many pathogens.

12. 2. ANTIBACTERIAL SUBSTANCE-
• Present naturally in blood and tissues.
• Beta lysin- thermostable substance active against anthrax and related bacilli.
• Lactic acid- muscle tissues and inflammatory zones.
• Lysozymes- present in tears
• Interferons- activated against viral infection.
• Complement system- destruction of pathogenic micro-organisms invading
blood and tissues.

13. 3. CELLULAR FACTORS
• Phagocytic cells are –
Microphages- Polymorphonuclear leucocytes( neutrophills)
Macrophages- Mononuclear phagocytic cells
• Natural killer cells (NK)- A class of lymphocytes- non specific defence
against viral infection and tumours.

14. 4. INFLAMMATION
• Occurs as a result of tissue injury/ irritation.
• Important nonspecific defence mechanism.
• Inflammation Vasodilation Inc. vascular permeability &
cellular infiltration
Microorganisms phagocytosed & destroyed, fibrin barrier laid at infection site.

15. 5. FEVER
• Rise in body’s temperature - natural defence
mechanism.
• Accelerates physiological process.
• Destroys infecting pathogens.
• Stimulates production of interferons.

16. 6. ACUTE PHASE PROTEINS
• Sudden increase in plasma concentration of certain proteins following injury/
infection- acute phase proteins.
• This include-
- C reactive proteins
- Mannose binding proteins
- Alpha- 1 - acid glycoprotein
• Enhance host resistance, prevent tissue injury, repair of inflammatory lesions.

17.  Acquired Immunity
• Resistance acquired by individual during his life .
• Adaptive immunity .

18.  ACTIVE IMMUNITY
• Resistance developed by individual – antigenic stimulus .
• Involves active functioning of host’s immune apparatus to produce
antibodies & immunologically active cells.
• Once developed , it is long lasting.
• When actively immunised individual encounters subsequent attack of same
antigen , immune response occurs more quickly.

19.  A. Natural active immunity
• Results from clinical / inapparent
infection by microbe .
• E.g- Person recovered from attack of
measles develop natural active
immunity.
• Life long immunity following many
viral diseases
• Immunity following bacterial infection
is generally less permanent.

20.  B. Artificial active immunity
• Resistance induced by vaccine
• Examples of vaccines-
• Bacterial vaccine –
- Live (BCG for tuberculosis )
- Killed (Cholera vaccine)
- Killed whooping cough (pertussis) vaccine
- Bacterial products(Tetanus toxoid)
- Viral vaccines-
- Live (Oral polio vaccine- Sabin)
- Killed Covid19 vaccine

21.  Mechanism of Active Immunity – Stimulates both humoral
immune response & cell mediated immune response
Humoral/ antibody mediated immunity (HMI/AMI)
• Primary defence against viruses that infect respiratory / intestinal tract.
• pathogenesis of hypersensitivity (Type I, II,III) & autoimmune diseases.
• Synthesis of antibodies by plasma cells.

22.  Cell- mediated immunity (CMI)
• mediated by T lymphocyte cells.
• Protects against fungi, viruses, intracellular bacteria
• allograft rejection , graft vs host reactions
• mediates pathogenesis of delayed hypersensitivity(type IV)
• immunity against cancer

23.  PASSIVE IMMUNITY
• Resistance transmitted passively to recipient in a readymade form
• Recipient immune system plays no active role
• No antigenic stimulus, preformed antibodies administered
• Immunity lasts for days to weeks
• Less effective , employed when instant immunity is desired.

24.  A. Natural passive immunity
• Resistance passively transferred from
mother to baby.
• Human infants- maternal antibodies
transmitted through placenta.
• Human foetus acquires ability to produce
antibodies – 20th week of life.
• Till then, maternal antibodies give passive
protection against diseases.

25.  B. Artificial passive immunity
• Resistance passively transferred to
recipient by administration of antibodies.
• Agents used-
• HYPERIMMUNE SERA OF
ANIMAL/HUMAN ORIGIN
- Antitetanus serum prepared from
hyperimmune horses.
- Temporary protection
- Disadvantage- hypersensitivity & immune
elimination

26.  DIFFERENCE-

27.  IMMUNE SYSTEM
• LYMPHOID ORGANS
A. Central lymphoid organs –
- Thymus
- Bursa of Fabricius in birds.
- Bone marrow in mammals
B. Peripheral lymphoid organs-
- Spleen
- Lymph nodes
- Mucosa associated lymphoid
tissues(MALT)
- Lymphoid tissues in gut, lungs,
liver, bone marrow.

28. • CELLS-
1. Lymphocytes In
circulating blood-
70% are T Lymphocytes
{T for thymus dependent} ,
20% B Lymphocytes
{B for Bursa/ Bone marrow
10% Null cells}
2. Plasma cells

29.  Difference between B cells & T cells

30.  ANTIGEN
• Antigen is a molecule which introduced into a body evokes immune
response.

31.  CLASSIFICATION OF ANTIGEN

32.  They may also be classified as-
1. Complete antigen- Substances which induce antibody formation by
themselves & react specifically with these antibodies.
2. Haptens- Substances incapable of inducing antibody formation by
themselves but can react specifically with antibodies.
• Haptens are of 2 types- COMPLEX HAPTENS
SIMPLE HAPTENS

33.  ANTIBODIES- IMMUNOGLOBULINS
• Substances which are formed in serum & tissue fluids in response to
antigen and react with that antigen specifically and in some observable
manner.
• CHEMICAL NATURE- GLOBULIN – named as
IMMUNOGLOBULIN.
• Immunoglobulin 20 -25% total serum protein.
• Synthesised by plasma cells.
• NOTE: All antibodies are immunoglobulins , but all
immunoglobulins may not be antibodies.

34.  STRUCTURE OF IMMUNOGLOBULINS

35.  CLASSES OF IMMUNOGLOBULIN

36.  FUNCTIONS OF IMMUNOGLOBULINS

38.  ROLE OF ANTIBODIES IN IMMUNITY
• NEUTRALIZATION- Pathogen can no longer infect host because it is
bound to an Ab
• OPSONIZATION- Ab bound to Ag increases phagocytosis
• Antibodies together with proteins of complement system- cell lysis

39.  ANTIGEN- ANTIBODY REACTION
• Morphologically,
 PRECIPITATION REACTION
 AGGLUTINATION REACTION
• Functionally,
 NEUTRALIZATION
 COMPLEMENT FIXATION
 RADIOIMMUNOASSAY
 IMMUNOFLUORESENCE
 ENZYME LINKED IMMUNOSORBENT
ASSAY(ELISA)

40. USES
• IN VIVO- Basis of immunity against infectious diseases.
Lead to tissue injury in some hypersensitivity reaction/
autoimmune diseases.
• IN VITRO- Diagnosis of infections.
Detection of antigen/ antibody.

41. IMMUNITY BOOSTER
• Healthywaysto strengthenour immune system
• Diet rich in fruits & vegetables
• Regular exercise
• Maintain a healthy weight
• Adequate sleep
• Avoid smoking & drinking
• Measures to avoid infection- washing our hands
frequently
• Minimizing stress

42.  FOOD THAT ENHANCE IMMUNITY
• CITRUS FRUITS
• RED BELL PEPPER
• BROCCOLI
• SPINACH
• GINGER
• YOGURT
• TURMERIC

43. • ALMONDS
• SUNFLOWER SEEDS
• GREEN TEA
• PAPAYA
• HONEY

44.  PROBIOTICS
• Include Good Bacteria
• Live micro organisms that can be consumed
through fermented foods & supplements.
• Helps to boost our immunity
• Inhibit growth of harmful gut bacteria
• Promote production of natural antibodies
• Boost immune cells – T lymphocytes, IgA
producing cells, NK cells
• Lactobacillus acidophillus- common
probiotic strain – boost immunity

45. CLINICAL CONSIDERATIONS

46.  IMMUNODEFICIENCY SYNDROMES
• A state in which immune system ability to fight infectious disease is
compromised / entirely absent.
• 2 Types
• Primary- Congenital- resulting from genetic defects in some components
of immune system.
• Secondary- Acquired- As a result of other disease / condition – HIV
infection, malnutrition, immunosuppression.

47. Primary Immunodeficiency syndromes & classification
A) HUMORAL IMMUNODEFICIENCIES (B Cell defect)
X linked agammaglobulinemia
Transient Hypogammaglobulinemia
of infancy
• Failure of pre - B cells to
differentiate into mature B cells.
• Pt suffers from recurrent
infections.
• Abnormal delay in initiation of
IgG synthesis in some infants.
• Ig concentration in majority
patients normalise by 2-4 yrs of
age.

48. Selective Immunoglobulin
deficiencies
Selective IgA deficiency
• selective deficiency of one / more
immunoglobulin classes
• other immunoglobulin classes
remain normal / elevated.
• Absence/ near absence of
serum & secretory IgA.
• Increased susceptibility to
respiratory & GIT infections.

49. B) CELLULAR IMMUNODEFICIENCIES (T CELL DEFECT)
• Thymic Hypoplasia
(DiGeorge’s Syndrome)
• Development defect –
affects 3rd & 4th pharyngeal
pouches
• aplasia / hyperplasia of
thymus & parathyroid
glands.
• T cells absent/ deficient.

50. C) COMBINED IMMUNODEFICIENCIES (BOTH T & B CELL
DEFECTS)
Ataxia Telangiectasia
• Majority pt lack IgA & IgE, some
posses antibody to IgA
• . Cell mediated immunity also
defective
• results in delayed hypersensitivity
& graft rejection.

51. • Wiskott- Aldrich syndrome
• X linked recessive disease
• Thrombocytopenia
• eczema, bleeding
• recurrent infections
• Cellular immunodeficiency with
abnormal Ig synthesis
• Depressed cell mediated
immunity
• . Pt susceptible to recurrent
diseases.
• Haemolytic anaemia common.

52. Secondary Immunodeficiency
• Depression of Humoral
Immune responses
• Depression of Cell- Mediated
Immunity
• Results when B cells are depleted
– Lymphoid malignancy –
Chronic lymphatic leukaemia
• Excessive loss of serum proteins –
Exfoliative skin diseases
• Multiple myeloma – Excessive
production of abnormal Ig.
• Occurs in AIDS , Hodgkin’s
lymphoma , Lepromatous leprosy

53.  AUTOIMMUNE DISEASE
Autoimmune disorders
affecting orofacial region
predominantly-
Systemic Autoimmune
diseases with oral
manifestations
• Sjogrens syndrome
• Benign lymphoepithelial
lesion(mikulicz’s disease)
• Aphthous stomatitis
• Periodontal disease
• Pemphigus
• Bullous pemphigoid
• Epidermolysis bullosa
• SLE
• Myasthenia gravis

54.  SJOGRENS SYNDROME
• Autoimmune disorder
• Diminished lacrimal & salivary gland
secretion (sicca complex)
• Results in Keratoconjuctivitis sicca &
Xerostomia
• Primary- Xerostomia & Xerophthalmia
• Secondary- Triad – Xerophthalmia,
Xerostomia & Connective tissue
disorders(Rheumatoid arthritis, SLE)

55.  BENIGN LYMPHOEPITHELIAL LESION
(Mikulicz’s Disease)
• Systemic/bilateral chronic,
enlargement of lacrimal, parotid,
submandibular salivary gland ,
attributed to chronic infection
• Related to Sjogrens syndrome
• Mild pain, local discomfort &
xerostomia.
• Associated with fever, respiratory
disorders, oral infections

56.  APHTHOUS STOMATITIS(Aphthous ulcers,
canker sores, recurrent aphthous stomatitis)
• oral ulceration
• Hereditary, trauma, dietary deficiency,
psychological , allergic, infections, drugs,
Immunological
• Elevated levels- IgA & IgG in patient sera
• Females(10-30 yrs)
• Burning sensation
• Initially localised area – erythema, small white
papule forms, Ulcerates & enlarges.
• Yellowish grey Pseudo membrane

57.  PERIODONTITIS
• Inflammatory disease –
destruction of both soft & hard
tissues in periodontal region .
• Over activation of host
immune response activates
osteoclastic activity & alveolar
bone loss.

58.  PEMPHIGUS VULGARIS
• Rapid appearance of
vesicles/ bullae
• NIKOLSKY
SIGN- loss of
epithelium by
rubbing apparently
unaffected skin.
• ASBOE HANSEN
SIGN- bulla spread
phenomenon

59.  BULLOUS PEMPHIGOID
• Rashes – remains for several week-
vesicles & bullae
• Rarely painful
• Buccal mucosa, gingiva commonly
involved
• Edema & gingival inflammation

60.  SYSTEMIC LUPUS ERYTHEMATOSIS
• Autoantibodies , immune complex
formation & immune dysregulation
• Damage to kidney, skin, blood cells & CNS
• Oral lesions- Multiple white plaques with
dark reddish purple margins
• Hyperaemia & oedema
• Bleeding & superficial ulceration
• Xerostomia, Glossitis, dental caries,
periodontitis

61.  MYASTHENIA GRAVIS
• Life threatening condition
• Drooping of one/more eyelids
• Double vision
• Difficulty in speech/ swallowing
• Limited facial expression
• Weakness in muscles

62.  CONCLUSION
• The immune system is like an army- With the task of protecting the host
against infection by potential pathogens
• There is always a synergy between adaptive immune system & its innate
counterpart
• Defects in either system can lead to autoimmune diseases,
immunodeficiencies & hypersensitivity reactions.
• Thus a thorough knowledge of immune reactions is of prime concern in our
day to day clinical treatment procedures.

63.  REFERENCES
• Textbook of microbiology for dental students – C P Baveja
• Essential Pathology for Dental students- Harsh mohan
• Oral health & disease- Nisengard & Newman
• Shafer’s Textbook of oral pathology
• General medicine for dental students- Harmanjit singh hira