This document discusses innate and acquired immunity. Innate immunity is inborn and provides non-specific resistance to pathogens. It includes barriers like skin and mucous membranes, antimicrobial substances, and phagocytic cells. Acquired immunity develops from exposure to pathogens and results in long-lasting, pathogen-specific protection. It can be active, arising from natural infection or artificial vaccination, or passive, through transfer of antibodies from mother to fetus or through administration of antisera.

1. - Department Of Conservative Dentistry And Endodontics
Second Year
Shubham Parmar
IMMUNITY

2. DEFINITION
Resistance exhibited by the host towards injury
caused by microorganism & their products
Immunity is concerned with reaction of body
against any foreign antigen

3. ACQUIRED (ADAPTIVE)
IMMUNITY
Active
Natural
Artificial
Passive
Natural
Artificial

4. INNATE IMMUNITY
Resistance to infections that an individual
possesses by virtue of his genetic constitutional
make-up
Immunity present since birth (inborn)
It is not affected by prior contact with
microorganisms or immunisation
Non-specific: degree of resistance to infections in
general
Specific: resistance to particular pathogen

5. 3 levels of innate immunity: species, racial, individual
Species immunity:
Total or relative resistance to pathogen, shown by all
members of species
Eg: All human beings are resistant to plant pathogens
& many animal pathogens
Mechanism is not clearly understood but may be due
to physiological & bichemical differences between
tissues of different species

6. Racial immunity:
Different races within same species may show
differences in susceptibility to infection
Eg: high resistance of Algerian sheep to anthrax
Another example: genetic resistance to Plasmodium
falciparum in some parts of Africa
Racial differences are genetic in origin, by selection
& inbreeding

7. Individual immunity:
Difference in immunity exhibited by different
individuals in race
It is well documented that homozygous twins show
similar degrees of susceptibility to leprosy & TB
This immunity is due to genetic constitution of
individual

8. 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

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

10. 3. Nutrition:
Malnutrition: reduced cell mediated & humoral
immunity
Cell mediated immune responses decrease in severe
protein deficiency

11. MECHANISMS OF INNATE
IMMUNITY
1. Epithelial surface:
Skin & mucus membrane covering body protect it
against invasion by microorganisms
Skin:
Mechanical barrier
Possesses bactericidal activity due to high salt
concentration in drying sweat, sebaceous secretions &
long chain fatty acids
Normal flora on skin: prevents colonisation by
pathogens

12. Respiratory tract:
Inhaled particles are arrested in nasal passages on
moist mucus membrane surface
Pathogens are trapped by mucus lining epithelium &
given to pharynx where they are swallowed or
coughed out
Cough reflex: important defense mechanism
Nasal & respiratory secretions contain
mucopolysaccharides that combine with influenza &
other viruses
Particles that reach alveoli are ingested by phagocytic
cells

13. Digestive tract:
Mouth saliva: inhibitory effect on many microbes
Swallowed pathogens: destroyed by acidic pH of
gastric juice
Normal flora of ileum inhibits growth of pathogens
Conjunctiva:
Tear secretion flush away bacteria & other foreign
particles
Tear contains antibacterial lysozyme: break down
polysaccharide of bacterial cells

14. Genitourinary tract:
Flushing action of urine: eliminates bacteria from
urethra
Spermine & zinc in semen: antibacterial activity
Acidic pH of vaginal secretions in females, due to
fermentation of glycogen by lactobacilli, inhibit
pathogens

15. 2. Antibacterial substances in blood & tissues:
Complement system: bactericidal activity & result in
destruction of pathogenic bacteria
Antibacterial substances:
beta lysin, leukins, plakins, lactic acid,
lactoperoxidase, lysozyme
Interferons produced by cells: antiviral activity

16. 3. Cellular factors:
Pathogens invading blood & tissue: destroyed by
phagocytic cells
Phagocytes: microphages & macrophages
Microphages are polymorphonuclear leucocytes
Macrophages are wandering amoeboid cells in
tissues, reticuloendothelial cells & monocytes in
blood

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

18. 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

20. 4. Inflammation:
Entry of pathogens → tissue injury & irritation →
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

21. INFLAMMATION IS CHARACTERISED BY: PAIN
(DOLOR), REDNESS (RUBOR), HEAT (CALOR),
SWELLING (TUMOR)
Plasma helps in diluting toxic products
Fibrin barrier forms wall around site of infection

22. 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

23. ACQUIRED IMMUNITY
Resistance that an individual acquires during life
Two types:
o Active immunity
o Passive immunity
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

24. 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 Ag combines with pre-existing Ab
in circulation
Once developed, it is long-lasting
When actively immunised individual encounters
subsequent attack of same Ag, immune response
occurs more quickly (called as secondary response)
Besides cell mediated & humoral immune response, it
is also associated with immunological memory
Active immunisation is more effective & confers
better protection than passive immunisation

25. 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 Ab
are administered
No latent period
No negative phase
Immunity is transient lasting for days or weeks

27. Both Active & Passive immunities are further
classified as Natural & artificial
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

28. Artificial active immunity:
Resistance induced by vaccine
Examples of vaccines:
Bacterial vaccines:
o Live (BCG for tuberculosis)
o Killed (Cholera vaccine)
o Subunit (Typhoid Vi antigen)
o Bacterial products (Tetanus toxoid)
Viral vaccines:
o Live (Oral polio vaccine- Sabin)
o Killed (Injectable polio vaccine- Salk)
o Subunit (Hepatitis B vaccine)

29. 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

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

31. Artificial passive immunity:
Resistance passively transferred to recipient by
administration of Ab
Agents used for this purpose:
- Hyperimmune sera of animal or human origin
- Convalescent sera
- Pooled human gammaglobulin
These are used for prophylaxis & therapy

32. 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 Ab

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

34. Active immunity Passive immunity
Produced actively by host’s immune
system
Received passively. No active host
participation
Induced by infection or by
immunogens
Readymade Antibody transferred
Durable effective protection Transient, less effective
Immunity effective only after lag
period
Immediate immunity
Immunological memory present No memory
Booster effect on subsequent dose Subsequent dose less effective
Negative phase may occur No negative phase
Not applicable in immunodeficient Applicable in immunodeficient

35. THANK YOU