IMMUNITY

Definition:
State or quality of being resistant either by
virtue of an inherent trait or as previous
exposure to an infectious agents

The immune system produces antibodies or

cells that can deactivate pathogens
Types of immunity:
Innate Immunity:
any inborn resistance that is already present.

does not require prior exposure.

Types:
Racial
Individual
Species
 Component of Innate Immunity

First line Second line

1) Mechanical barriers A- Cells
2) Chemical & biochemical inhibitors 1- Natural killer
3) Normal flora 2- Phagocytes, etc.
B- Chemical factors
C- Inflammatory barriers
 First line
Mechanical barriers

 Intact skin

 Mucous coat

 Mucous secretion

 The hair at the nares

 Coughing and sneezing reflex

 First line
Chemical & biochemical inhibitors

 Sebaceous secretion

 Hydrolytic enzymes in saliva

 HCl of the stomach

 Proteolytic enzyme in small intestine

 Lysozyme in tears
 First line
Normal bacterial flora

 Competition for essential nutrients

 Production of inhibitory substances

If a pathogen is able to get past the

body's first line of defense,

 the body can rely on

it's second line of defense

 Second line
Cellular Factors:

 Mast Cells

 Natural Killer Cells

 Eosinophils

 Basophils

 Phagocytes (Macrophage, Neutrophils, and

Dentritic cells)
Phagocytosis:
 Second line
Chemical Factors :

Pepsin – hydrolyzes proteins

Lysozyme – cleaves peptidoglycan of bacterial cell wall
Antimicrobial substances :
◦ Cryptidins & α-defensins: in the crypts of small
intestine damage bacterial cell membranes
◦ Surfactant proteins A & D: in lungs function as
opsonins.
Chemical Factors : Interferons
IFN α&β
◦ Source:
 Macrophages, neutrophils, somatic cells
◦ Effects:
 Antiviral
 Induction of MHC-I on cells
 Activation of macrophages & NK cells

IFN γ
◦ Source:
 Activated TH1 & NK cells
◦ Effects:
 Induction of MHC-I on cells
 Induction of MHC-II on APCs
 Activation of macrophages, neutrophils & NK cells
 Promotion of CMI (inhibits TH 2 cells)
 Antiviral
 Second line
Chemical Factors :
Inflammatory Barriers:

Tissue damage by a wound or by invasion by a

pathogen induces a complex sequence of

events collectively known as the

inflammatory response
CARDINAL SIGNS

Heat Redness Swelling Pain Loss of function

Celsius (30 BC) Virchow (1902)

Inflammation Components

Physiological Symptoms
Responses
Release of soluble mediators
Heat (calor)
Vasodilation

Increased blood flow Redness (rubor)

Extravasation of fluid (permeability) Swelling (tumor)

Cellular influx (chemotaxis)
Pain (dolor)
Elevated cellular metabolism
Inflammation Components

Physiological Symptoms
Responses
Release of soluble mediators
Heat (calor)
(calor
Vasodilation
Redness (rubor)
Increased blood flow
Swelling (tumor)
Extravasation of fluid (permeability)
Pain (dolor)
Cellular influx (chemotaxis)

Elevated cellular metabolism

Inflammation Components

Physiological Symptoms
Responses
Release of soluble mediators
Heat (calor)
Vasodilation
Redness (rubor)
Increased blood flow
Swelling (tumor)
Extravasation of fluid (permeability)
Pain (dolor)
Cellular influx (chemotaxis)

Elevated cellular metabolism

Inflammation Components

Physiological Symptoms
Responses

Release of soluble mediators Heat (calor)

Vasodilation Redness (tubor)

Increased blood flow Swelling (tumor)

Extravasation of fluid (permeability) Pain (dolor)

Cellular influx (chemotaxis)

Elevated cellular metabolism

Inflammation Components

Physiological Symptoms
Responses
Release of soluble mediators
Heat (calore)
Vasodilation
Redness (tubor)
Increased blood flow
Swelling (tumor)
Extravasation of fluid (permeability)
Pain (dolor)
Cellular influx (chemotaxis)

Elevated cellular metabolism

 Events during an inflammatory response:  
 Vasoconstriction 

 Vasodilation: Increased volume of blood flow.

 Decreased velocity of blood flow: leucocytes slow down and

adhere to vascular endothelium

 Increased expression of vascular endothelial adhesion

molecules: leucocytes attach to vascular endothelium

 Increased vascular permeability: fluid enters tissues 

 Influx of phagocytes into tissues: migration and

extravasation
Third-Line Defenses- body's last line of defense

recognizes, attacks, destroys, remembers by

making specialized cells and antibodies that
render the pathogens harmless.
 
Unlike the first line and second line defense the
immune system differentiates among pathogens.

For each type of pathogen, the immune system

produces cells or Ab. that are specific for that
particular pathogen
Innate To Acquired
Adaptive/Acquired Immunity:
Acquiredby an individual during life
Types: Active and Passive

Active:
 Involves active functioning of immune apparatus

 Long lasting
Active Immunity:
 Types:
 Natural (getting infection)

 Artificial (vaccines)
Passive:
 Resistance transmitted to a recipient in a ready
made form

 Recipient’s immune system play no roles

Passive:
 Types:
 Natural (mother to child)

 Artificial (immune sera)

Thank you