The study in immunology provides the fundamental understanding of how the human body defend itself against foreign organisms, materials or particles that have the ability to cause harm to host tissues.

1. Presented by:
Mr. Abraham G. Dayklee
Lecturer
Mother Patern College of Health Sciences

2. Chapter One(1)
An Overview of the Immune System
Chapter Outline:
1.1. Overview of the Immune System
1.2 Terminologies in Immunology
1.3 History of Immunology
1.4 The Immune System
1.5 Natural Immune system
1.6 Adaptive Immune System

3. Learning Objectives:
Upon completion of this lecture the student will be able to:
 Define the terms immunology, immunity
 Describe major historical events in the development of
immunology
 Differentiate innate and adaptive immunity in terms of
components and type of immune response.
 Explain the major defenses of innate immunity
 Describe the mechanisms used by the body to defend
itself in an innate /adaptive responses.

4. He that Thinks Logically is WISE….
WHAT IS IMMUNOLOGY ????
How does it differs from IMMUNITY?

5. 1.1 Overview of Immunology
The Science of Immunology is primarily directed towards
understanding the Immune system- how it develops, functions
and sometimes malfunctions, thereby causing Disease(s)
The word immunology owes its origin to the Latin words
Immunitas and Immunes. Initially, in Rome, these words
implied ‘’ Exemption of an Individual from Service or Duty’’.

6.  Later in the Middle age it came to mean ‘Exemption of the
Church and its properties and personnel from Civil control’’
 The Roman poet Marcus Annaeus Lacanus (AD 39-65) first
applied the word immunes in the present –day biological context
in his book The History of Immunology stated A.M. Silverstein
 The WORD IMMUNOLOGY attained currency only in the 19th
century, following the rapid spread of Edward Jenner’s historic
technique for small pox Vaccination
1.1 Overview of Immunology

7.  Since then, Immunity came to be known as ‘ The Ability of an
Individual to Resist Diseases’. The study of immune reaction
was initially referred to as Immunochemistry, coined by Marcus
Annaeus Lucanus.
 Gradually, the meaning of the word immunology evolved to mean
an ‘EXPERIMENTAL DISCIPLINE THAT MANIPULATES THE
FUNCTION OF THE IMMUNE SYSTEM’.
1.1 Overview of Immunology

8. 1.2. Definition of Terminologies
 IMMUNOLOGY:
 The study of Immune System Or Immunity:
 Looking at the molecules, cells, organs, and systems
responsible for the recognition and disposal of foreign
material.
• The study of all aspects of Host Defense against Infection and
of adverse consequences of immune responses.

9.  IMMUNOLOGY is also the study of the physiological
mechanisms which enable the body to recognize materials
as foreign agents and to neutralize, metabolize or
eliminate them without injury to the host tissue.
1.2. Definition of Terminologies

10.  Immunity:
 State of Protection from Infectious Diseases
 Immune System:
 A remarkably versatile DEFENSE SYSTEM that has
evolved to PROTECT animals from Invading
Pathogenic Microorganisms and Cancer.
 It is able to generate an enormous variety of cells and
molecules capable of specifically recognizing and
eliminating an apparently limitless variety of foreign
invaders.

11.  Antigens are molecules capable of stimulating
an immune response. Each antigen has distinct
surface features, or epitopes, resulting in
specific responses.
 Antibodies (immunoglobins) are Y-shaped
proteins produced by B cells of the immune
system in response to exposure to antigens. It
contains paratope
Definition of Terminologies

12.  Each antibody contains a paratope which
recognizes a specific epitope on an antigen,
acting like a lock and key binding mechanism.
 A paratope, also called an antigen-binding site,
is a part of an antibody which recognizes and
binds to an antigen.
• This binding helps to eliminate antigens from
the body, either by direct neutralization or by
‘tagging’ for other arms of the immune system.

13.  Antigen:
• A 'hook' in the cell's surface,
partially responsible for what
goes in and out of the body.
• Exists in almost every cell in the
entire world.
• Exists due to random mutations
in the cell's gene.
• Antigens are locks or security
gates in a cell.
 Antibody:
• A chemical that attaches to the
antigen in order to sterilize or kill
the cell.
• Needed for the destruction of
pathogens in the body.
• Complex chemical that bonds to
a very specific Antigen
• Antibodies are weapons or keys
to attack and destroy a cell.
Antibodies cling onto antigens to either sterilize or kill the target cell

14. Overview Substance that can induce
an immune response
Proteins that recognize and
bind to antigens
Molecule type
Usually proteins, may also
be polysaccharides, lipids
or nucleic acids
Proteins
Origin Within the body or
externally Within the body
Specific binding site Epitope Paratope
Antigen Antibody

15.  It was Edward Jenner who first studied the
response of the body to foreign substances.
 He observed that dairy maids who had naturally
contracted a mild infection called cowpox
seemed to be protected against smallpox
 n 1796, Jenner inoculated an eight year-old
boy with fluid from cowpox blisters on the hand
of a dairymaid. The boy contracted cowpox.
1.3. History of Immunology

16.  Then two month later Jenner inoculated him with fluid
from a small pox blister, the boy only developed a
small sore at the site of inoculation.
 His exposure to the mild disease cowpox had made
him IMMUNE to the Small Pox Infection.
1.3. History of Immunology

17.  Individuals recovering from certain disease rarely contracted
that same disease again.
 Observation promoted deliberate attempts to induce immunity
 Athens plague as of Thucydides in 430BC (Recovered People
Only Nurse Sick One)
1.3. History of Immunology
 ITS PRINCIPLES AMONG THE EARLIEST WRITTEN
OBSERVATIONS:

18.  Chinese(1500A.D) custom of inhaling crusts from smallpox
lesions to prevent development of small pox in later life.
 Injecting materials from crusts or fluid from smallpox blisters
(“variolation”), used through out the eastern world, in 1718 was
introduced into western medicine by British ambassador’s wife, to
Turkey, had her children so treated.
 Note- The virus used could be transmitted => protection by
variolation was hazardous to the community at large!!
1.3. History of Immunology

19.  In 1798, Jenner’s work on vaccination, describing
a related, yet safe procedure.
 Noted people, who had cow pox, were spared
in small pox epidemics
 Inoculated boy with pus from milk maid with
cow pox, and
 Re-inoculated same boy with infectious pus
from a patient in the active small pox.
 No disease state followed these inoculations,
and experiment was repeated several times
with great success!

20. Wood engraving of Louis Pasteur watching Joseph Meister receive the rabies vaccine. [From Harper’s
Weekly 29:836; courtesy of the National Library of Medicine.]
Louis Pasteur - demonstrating that it was
possible to attenuate, or weaken, a
pathogen and administer the attenuated
strain as a vaccine.
In 1885, Pasteur administered his first
vaccine to a human, a young boy who had
been bitten repeatedly by a rabid dog
1.3. History of Immunology

21.  Jenner`s provided first clear evidence that
active immunization could be used safely to
prevent an infectious disease.
 Almost 70 Years later, Pasteur - introduced
Pasteurization also
Recognized and exploited the general
principle underlying vaccination
 At about 1900,
 Role of phagocytes and cellular immunity
were elucidated
1.3. History of Immunology

22.  In 20th
century,
 Acquired immunity resulted from both cellular and humoral elements
were demonstrated.
 Opsonization was described: The process by which the pathogen is
marked for ingestion and eliminated by the phagocytes.
 Opsonin (from the Greek OPSŌNEÎN, to prepare for eating) is any molecule that
enhances phagocytosis by marking an antigen for an immune response or marking
dead cells for recycling (i.e., causes the phagocyte to "relish" the marked cell)

23.  Opsonin (make a foreign cell) more susceptible to
phagocytosis. After opsonin ( an antibody) binds to the
membrane of a pathogen, phagocytes are attracted to
the pathogen for elimination or ingestion.
 The term Antigen came in to regular use

24.  1901 Emil von Behring, Serum antitoxins
 1905 Robert Koch, Cellular immunity to tuberculosis
 1908 Elie Metchnikoff, Role of phagocytosis
 1908 Paul Ehrlich, antitoxins in immunity
 1913 Charles Richet, Anaphylaxis
 1919 Jules Border, Complement-mediated bacteriolysis
 1930 Karl Landsteiner, Discovery of human blood groups
 Noble Prize Winners for Immunologic Research
1.3. Historical Events of Immunology

25.  1951 Max Theiler, Development of yellow fever vaccine
 1957 Daniel Bovet ,Antihistamines
 1960 F. Macfarlane Burnet and Peter Medawar, Discovery of acquired
immunological tolerance
 1972 Rodney R. Porter and Gerald M. Edelman, Chemical structure of
antibodies
 1977 Rosalyn R. Yalow, Development of radioimmunoassay
 1980 George Snell, Jean Daussct and Baruj Benacerraf
Major histocompatibility complex
 Noble Prize winners for Immunologic Research

26.  1984 Cesar Milstein and Georges E. Köhler, Monoclonal
antibody
 1984 Niels K. Jerne, Immune regulatory theories
 1987 Susumu Tonegawa, Gene rearrangement in
antibody production
 1991 E. Donnall Thomas and Joseph Murray
Transplantation immunology
 1996 Peter C. Doherty, Role of major histocompatibility
complex
 1996 Rolf M. Zinkernagel, in antigen recognition by by T
cells
 Noble Prize winners for Immunologic Research

27. THE COMPONENTS OF THE IMMUNITY
1. The Non- Specific
Resistance or Innate Immunity
From the ‘Innasci’ meaning ‘to
be born in’ i.e., it is active right
from the time the child is born,
hence innate.
It provides the Early Lines of
defence against microbes
First line of defence
2. The Specific Resistance or
Adaptive Immunity
It is Acquired, active five to six
days of antigen exposure.
Antigenic specificity , has the
ability to ‘ remember’ different
types of antigens
Self from Non-Self
The Human Body Provides Two (2) Levels of Protection from Infectious Diseases:

30. Distinguishing Innate and Adaptive Immunity
No. Characteristics INNATE IMMUNITY ADAPTIVE IMMUNITY
1. Recognition Broad specific- recognition of
conserved molecular patterns
Highly Specific- recognition of
specific antigen determinants
2. Diversity Limited Large
3. Immunogenic Memory None Present
4. Self-Foreign
Discrimination
Present Present
5. Genes of Receptor No rearrangement required Rearrangement required
6. Response Rapid ( minutes) Delayed ( usually days)
7. Components
Mechanical and Chemical barriers,
phagocytes, natural killer cells,
complement, acute-phase
proteins,
Antibodies, T and B –lymphocytes,
antigen-presenting cells, etc.

32. In general, most pathogens encountered by a healthy individual
are rapidly cleared within a few days of their entry into the host
body by the Non-specific defence of the host, much before the full
force of the Adaptive Immune Response is unleashed.
THE COMPONENTS OF THE IMMUNITY
i.e., Most MO’s are quickly cleared within a few days by
innate immunity – before adaptive immunities are activated

33. 1.4. The Immune System
Immune System
Innate
(Nonspecific)
Adaptive
(Specific)
Cellular
Components
Humoral
Components
Cell-Mediated
Humoral
(Ab)

34. THE INNATE IMMUNITY
 The Non- specific component of immunity, also known as
innate immunity is not directed against any particular pathogen
but is a general defence mechanism as the human body must
constantly defend itself from microbial invasion.
 The specificity of innate immunity is very relatively low as it
lacks the ability to distinguish one microbes from the another.
 The principal components of innate immunity are: a)
Mechanical and Chemical barriers, b) Phagocytosis, b)
Fever, d) Inflammation and e) Acute- phase proteins

36.  4 barriers to infection:
Anatomic
Physiologic
Phagocytic
Inflammatory
•1st
line of defense:
•includes chemicals, structure of
skin/other epithelia, and mechanisms
as well as cells – mainly neutrophils
and macrophage
1) Anatomic
skin -> epidermis w/ keratin
mucus memb. ->inner surfaces
2) Physiological
temperature, pH, soluble subst.
3) Phagocytes
blood monocytes, tissue MØ, and
neutrophils
4) Inflammatory response
triggered by wound/foreign particle
5 Cardinal signs reflect 3 major events of
inflam response:
-vasodilation
- >capillary permeability
-influx of phagocytes

37. The Mechanical or Physical Barriers
 It refers to the various physical hindrances blocking the
entry of microbes into the host body; these include the
Skin and the Mucous membrane
 The Skin: consist of two distinct layers –
the thinner outer Epidermis and the thicker inner
Dermis
 The Epidermis consist of several layers of tightly
packed epithelial cell. Its outer layer is coated with a
tough protein called Keratin that does not support viral
replication or penetration by bacteria

38.  The intact surface of a healthy epidermis provides an excellent
defence against penetration by bacteria or viruses.
 The epidermis of the skin is constantly shed off, resulting in
the continual removal of any clinging pathogens
 Any break in the integrity of the skin facilitates the entry of
pathogens
 The Dermis – is the inner layer of the skin which contains most
of the skin’s living structures such as blood vessels, nerve
endings, elastic fibres, sweat glands, and sebaceous glands
The Mechanical or Physical Barriers

39.  Any break into the dermis introduces bacteria that are most
likely to cause dermal infections, under such conditions are
those that infect hair follicles, eg: Staphylococci
 Viruses, such as Papillomaviruses, which produce human
warts, enter the skin at the sites where cuts and abrasions
have resulted in the loss of epithelial integrity.
 The skin is also penetrated by insect bites ( mosquitoes,
ticks, fleas and flies) Pathogen infected arthropods
introduce the pathogen into the host
The Mechanical or Physical Barriers

40. • Plasmodium, the causative agent of malaria, is introduced into the
human body by mosquito bites. Similarly, viruses such as human
papillomaviruses, myxomaviruses and flaviviruses are introduced
into the host by arthropod vectors during feeding
 The Mucous Membrane: Regions of the body that are not protected
by intact skin are lined by the mucous membrane. These include the
gastrointestinal tract, respiratory tract, urogenital tract, and
conjunctiva
The Mechanical or Physical Barriers

41. • The mucous membrane protects the human body in several ways:
• In the respiratory tract Goblet cells secret mucous that entraps
dusts and microbes, and is propelled by the action of ciliated
epithelial cells, thereby clearing foreign material from the respiratory
tract; same happens in the gastrointestinal tract.
The Mechanical or Physical Barriers

42.  Some factors that assist in protecting the mucous membrane
include; and not limited to:
---------------------------------------------------------------------------
• The lavaging action of physiological fluids; tears and saliva that
assist in flushing microbes from the body
• The trapping action of mucous-coated hair in the anterior
chambers of the nose
• The expulsive effects of coughing and sneezing, which protect
the respiratory and gastrointestinal tracts
• The cool temperature of the upper respiratory tract which
inhibits replication by many viruses
The Mechanical or Physical Barriers

43. Some factors that assist in Protecting the Mucous Membrane
SNEEZING
COUGHING
Mucous-coated hair

44. The Chemical Barriers
 Mechanical barriers alone can not account for the remarkable
resistance provided by the innate defence mechanism to
pathogenic invasion.
• The host body has several chemical/physiological barriers that
contribute to innate immunity; namely:
 Low pH of the skin, gastric and duodenal enzymes, antibodies
and inhibitors, interferons, complements proteins and anti-
microbial peptides.

46.  Low pH of the Skin:
• Sebum, secreted by the sebaceous glands present in the dermis,
contains organic acids. These organic acids maintain the pH of the
skin in the range of 3-5. The low pH inhabits or retards the growth
of most microorganisms present on the surface of the skin.
 Acidic Gastric Secretions:
• The physiochemical environment in the stomach appears to be
extremely inhospitable to invading pathogens. The secretion of
hydrochloric acid by gastric parietal cells maintains the pH of the
stomach at 2.0, which kills most microorganisms.
( except some resistance ones; Hepatitis A virus, Picornavirus and
typhoid bacilli)

47.  Lysozymes:
• It is a hydrolytic enzyme present in all mucous secretions, including
tears, saliva and nasal secretion. It can Lyse Gram-positive bacteria
by cleaving the peptidoglycan layer found in the bacterial cell wall
 Gastric and duodenal Enzymes:
• These include proteases and lipases, digests a verity of structural and
metabolic chemical components of pathogens.
• Rhinovirus for example, are easily inactivated by gastric acids, in rare
cases, the infectivity of the pathogen is increased by the acidity
(eg: Coronavirus)

48.  Antibodies and Inhibitors:
• The mucous secreted by gastric and intestinal cells usually
contains IgA molecules as well as Non- specific inhibitors of viral
infections.
• Sialic acid found in mucous inhibits the attachment of influenza
virus particles to cells.
• Antibodies (IgA) are also found in tears and saliva
• Secretory IgA protects the body surface against invading
pathogenic microbes

49.  Interferons:
• The name interferons refers to a group of proteins produced by
virus-infected cells that induce a generalized antiviral state in
neighbouring un-infected cells.
• These proteins also augment innate immunity
 Anti-Microbial Peptide:
• All insects and mammals, including humans, secrete a number of
antimicrobial peptides, such as Defensins, for their protection.
• The human body is protected by 1 um thick biofilm of Defensins that
protects the external surface of the body from microbial assaults.

50. The Complementary Proteins:
 Complement Proteins:
• These are a group of serum proteins that circulate in an inactive
state in the plasma,
• They become activated by a verity of specific and non-specific
mechanism
• The activated forms of these proteins damage the invading
pathogen.

51.  Phagocytosis:
• It is another important innate defence mechanism for
invading microorganisms
• It can be define as ligand-induced uptake of particulate
material of 150-200 nm diameter or more; such as cell
debris and microbial cells
 When bacteria or invading parasites penetrate the skin or
the mucous membrane, phagocytes (Neutrophils, Blood
monocytes, and tissue microphages) surge upwards the
site of infection

52. • These phagocytes engulf the bacteria to form a large vesicle,
called Phagosome, containing the bacteria
• Then the involuntary guest trapped within the phagosome is
destroyed by fusing it with ‘ granules’ (lysosomes‘ granules’ (lysosomes)) found in the
cytoplasm of the phagocytes.
• These granules discharge their contents ( enzymes and reactive
oxygen species) inside the phagocytic vacuole, thereby degrading
the bacteria, the insoluble remnants of degradation in the
phagocytic vacuole are egested from the phagocyte

53.  Phagocytosis, which is non-specific, is different from specific
receptor mediated Endocytosis wherein extracellular molecules are
ingested after they bind to specific cellular receptors
 Phagocytosis is also different from Pinocytosis - the mechanism
by which cell take up fluids ( dissolved solutes) from the
surrounding.
 Phagocytes must be selective of cells and materials they
phagocytose, otherwise, normal cellular structures would be
ingested

54. The occurrence of phagocytosis depends on the following
factors:
 Presence of Strong Electric Charge:
 Dead tissue or foreign particles ( bacteria) that have a strong
electric charge on their surface are ideal for phagocytosis
 Presence of antibodies and Complement Component on the
Cell Surface:
 The immune system develops antibodies against invading
pathogens (bacteria) that adhere to the bacterial membrane

55. These antibodies are recognized by the receptors present on
phagocytes, which binds them, making the bacteria susceptible to
phagocytosis
Surface of the Particle:
The surface of the particle should be rough.
This is best exemplified by the fact that phagocytosis works more
effectively for non-encapsulated bacteria, but less so for
encapsulated bacteria which have a relatively smooth surface

56.  To phagocytose such resistant encapsulated bacteria, the
immune system uses antibodies that binds the capsule on
the bacteria, enabling the phagocytic cells ingest such
microbes using their Fc receptors

57. Phagocytosis
 Phagocytic cells Chemotaxins such as
 Complement components
 Coagulation cascade proteins
 Bacterial and viral products
 Attract phagocytic cells including:
 Mast cell, lymphocyte, macrophage, neutrophil products
 Physical contact between phagocytic cell and foreign object results in
 Formation of phagosome
 Formation of phagolysosome
 Digestion
 Release of debris

58.  Phagocytosis
 Is a form of endocytosis.
 Important body defense mechanism is process in which
specialized cells engulf and destroy foreign particles
such as microorganisms or damaged cells.
 Macrophages and segmented Neutrophiils are the
most important phagocytic cells.
cont…

59.  Can be divided in to several stages:
 Chemotaxis – attraction of leukocytes or other cells by
chemicals
 Movement of neutraphils is influenced by chemotaxins –
chemical messangers
 Complement, proteins from coagulation,
 Products from bacteria and viruses,
 Secretions from mast cells, lymphocytes,
macrophages, and other neutraphils
cont…

60.  Phagocytosis ...
 Adherence – binding of organism to the surface of
phagocytic cell.
 Engulfment:- is the injestion of m/os and formation of
phagosomes.
 Digestion – after the foreign particle or m/os is
ingested, cytoplasm lysosome fuse with phagosome
The enzymes of lysosome then contribute to microbial
killing and lysis.
cont…

61. Phagocytosis ...
cont…
Source: Kuby immunology 2007, 5th
ed

62.  Fever:
• The condition of an abnormally high body temperature,
companied by increased pulse rate and dry skin
• It provides a Non-specific defence against diseases
• It is a physiological response to infection

63.  Many proteins, and breakdown products of proteins, toxins, and
lipopolysaccharides ( particularly from Gram- negative bacteria),
released by microbes can affect the endothelial cells of the
hypothalamus to raise the body temperature from its ‘ set point’
of 36.5 degree Celsius
 Such substances that can increase the body temperature are
called Pyrogens.
 The Gram-negative bacteria release a class of very potent
endotoxins called Endogenous pyrogens ( namograms or
endogenous pyrogens) which causes high fever.

64.  This class of molecule is released when either the bacteria or its
breakdown products bind to macrophages and neutrophils
 These cells then release several cytokines that act on the
hypothalamus to produce fever.
 Fever is beneficial to the host because it inhibits the growth of
temperature-sensitive pathogens.
• Also, increased cell metabolism encourages rapid tissue repair
and phagocytosis

65.  Inflammation:
• It is the reaction of living tissue to either an injury or infection.
• It is characterized by heat (calor), redness ( rubor), swelling
( tumor) and pain ( dolor)
• It is a non-specific response to the body injury
 This tissue injury could be cause by either Mechanical agents
(such as cut or pinprick) or Chemical agents ( such as bee
venom, acid or alkali).
 Physical agents ( such as heat or ultraviolet radiation) and
infectious agents ( such as bacteria and pathogens can also
induce inflammation

66.  The process of inflammation may be triggered or initiated by a
verity of tissue products such as Histamine, Bradykinin, Serotonin
and Prostaglandins released by a number of cells ( such as Mast
cells and basophils, found in most tissues)
 The mediators released by damaged cells, chemicals released by
invading microorganisms, products of complement system and
reaction products of blood-clotting system also triggered the
process of inflammation.

67. • The inflammatory response occurs in several different ways:
 Attack by Tissue Macrophages:
• Macrophages are already present in the tissues – The alveolar
macrophages ( in lungs), Histocytes ( in subcutaneous tissue),
Kupffer cells ( in liver) Microglia ( in brain).
 However, tissue macrophages are present in small numbers
initially. In the case of inflammation, these macrophages
immediately proceed towards the injury site to begin their
phagocytic action. They serve as the FIRST LINE OF DEFENCE
AGAINST INFECTION.

68.  The Next Step In Inflammation is the Redirection Of Blood
Phagocytes Towards The Lesion Site, which is facilitated by
Vasodilation of blood vessels and capillaries at he site of injury.
• The increase in the diameter of blood vessels I brought about by
chemical mediators like histamine and bradykinins
• These mediators bind to the receptors on the nearby capillaries
and vessels, causing Vasodilation
• The engorged capillaries are responsible for increase blood
accumulation and the redness of the inflamed tissue (Erythema)

69. • The increased permeability of the capillaries permits the flux of
fluid from the engorged capillaries into the site of irritation or injury
• The accumulation of the fluid at the site of irritation results in
tissue swelling ( Oedema)
 Margination and Diapedesis:
• The products released from the inflamed area also cause
phagocytes ( mainly Neutrophils,) to move towards the inflamed
area, a process facilitated by vasodilation and increased capillary
permeability

70. • The emigration of phagocytes involves the adherence of the cells
to the capillary walls, a process called Margination
• The adhered phagocytes then pass from the blood vessels into
tissue spaces through the spaces between capillary endothelial
cells, a process termed as Diapedesis; once in the tissue space,
the phagocytes migrate towards the injured site
• Once phagocytes engulf the invading bacteria and the necrotic
tissue, many phagocytes eventually die.
• However, some enzymes may leak out into the extracellular
environment from the neutrophils before the phagosome closes,
this process termed sloppy eatingsloppy eating, damages healthy cells

71. • After a few days, a cavity containing necrotic tissue, dead bacteria
and dead phagocytes is formed at the site of inflammation, this fluid
mixture is often called PUS; pus formation continues until all
infection is supressed.
 Pus: thick yellowish or greenish
Opaque liquid produced in infected
tissue, consisting of dead white blood
cells and bacteria with tissue
debris and serum.

72. • The blood clotting system is also activated in the inflamed
region which result sin the deposition of insoluble strands of
fibrin.
• This seals off the injured area from the rest of the body, thereby
preventing the spread of infection
• This pus, enclosed in a wall of fibrin, usually forms an opening on
the surface of body, from where it empties out.
• The fibrin clot dissolves, tissue repair occurs and scar tissue is
formed.

73. 1.5 THE INNATE IMMUNITY
SUMMARIZED
Natural Immune System (Innate Immunity)
 Non – specific
 First line of defense
 Repeated exposure - no augmentation
 Components
 Biochemical
 Physical
 Cells

74. 1. Components
a. Biochemical
 enzymes, C’, etc.
 secretions
 pH
a. Physical
 skin
 cilia
a. Cells
 Phagocytes, NK
2. Example
a. Burn response
b. Inflammation
Lysozymes
Mucus
Sebaceous glands
Skin
Cilia: trachea
Acid in
stomach
Commensal
organisms in
gut & vagina
Spermine in semen
cont…

75.  Overall non-specific reaction of body to injury or invasion – starts
immediately with infection or trauma
 Reactants may initiate, expand, or sustain the response
 Can be acute (short duration) or become chronic (prolonged
duration)
 Has 4 cardinal signs: heat, pain, redness, loss of function resulting
from:
cont…

76.  Increased blood and plasma flow to the area
 Increased capillary permeability by retraction of
endothelial cells
 Mediated by vaso active agents such as histamine
and prostaglandins.
 derived from injured cells and later from cells that
infiltrate the area.
 Migration of leucocytes, particularly Neutrophils and
macrophages, from the capillaries to the site of injury is
due to a process called Chemotaxis.

77.  Migration of white cells, especially early migration of
neutrophils then macrophages to the area
 Increased release of mediators such as histamine from
damaged mast cells – furthering capillary dilation
 Increased concentration of acute phase reactants that
can amplify and/or control the response
 Complement – a series of enzymes normally circulating in an
inactive form may be activated resulting in lysis or
enhanced phagocytosis of cells
cont…

78. 1.4.1 External Innate Defense Systems
Prevent entrance:
 Structural barriers – effective with most
microorganisms
 Skin - epidermis = layers of tightly packed
epithelial cells. Outer layer is dead cells and
keratin, waterproofing protein
 Inner layer skin - dermis = blood vessels, hair
follicles, sweat glands, and sebaceous glands
that produce an oily secretion called sebum
 Cilia and cough reflex – helps expel microbe
containing mucous
 Sneeze
cont…

79. 1.4.1 External Innate Defense Systems
Mucus - conjunctivae, alimentary, respiratory, and urogenital
tracts
• saliva, tears, and mucous secretions wash away
invaders and contain antibacterial or antiviral
substances.
• acidity (pH 5.6) of sweat, sebaceous glands, vagina
(pH 5) and stomach (pH 1) – unfriendly to many
microorganisms
 enzymes present in the skin and stomach, tears
Normal flora - out compete pathogens for attachment sites
on the epithelial cell surface and for necessary nutrients.
cont…

80. 1.4.2 Internal Innate Defense System
To prevent expansion of penetration
 Recognize carbohydrates not normally present on cells
such as mannose
 May cause nonspecific activation of white cells
 Phagocytosis – by neutraphils, eosinophils,
basophils, or macrophages, mast cells, and dendritic
cells
 Clotting mechanism which entraps organisms in fibrin
clots
 Complement System can lyse cells or enhance
phagocytosis
cont…

81. Physiologic Barriers
 Soluble factors contribute to innate immunity, they are
collectively known as acute phase reactants.
 Normal serum components, non-specific responders to
inflammation
 Increase because of infection, injury, trauma
 Produced mostly by liver in response to inflammation
and cytokine stimulation
 Cytokines: IL-1, IL-6 and TNF alpha which are produced by
macrophages and monocytes at inflammatory site are activators
cont…

82.  Acute phase reactants are chemically varied and include:
 C-reactive protein,
 serum amyloid A,
 mannose binding protein,
 alpha-1 anti-trypsin,
 haptoglobulin,
 fibrinogen,
 ceruloplasmin,
 alpha-1 acid glycoprotein
 Complement
cont…

83.  Complement – a series of enzymes normally circulating
in an inactive form
 May be activated by the classical or alternate
pathways
 Can result in lysis or enhanced phagocytosis of cells
 Lysozyme, a hydrolytic enzyme in mucous secretions
and in tears, can cleave the peptidoglycan layer of
bacterial cell wall.
 Interferon, proteins produced by virus-infected cells.
Has many functions including ability to bind to nearby
cells and induce a generalized antiviral state.
cont…

84. C-Reactive Protein
 Normally trace levels in serum
 Early acute inflammation indicator:
 increases within 4-6 hrs of infection or trauma
 100 to 1000 fold increase serum concentration
 concentration drops rapidly in serum when stimulus
removed
 Enhances opsonization, agglutination,
precipitation, and classical pathway complement
activation – enhances removal of irritant
cont…

85. 1.5. THE ADAPTIVE IMMUNE SYSTEM
Immune System
Innate
(Nonspecific)
Adaptive
(Specific)
Cellular
Components
Humoral
Components
Cell-Mediated
Humoral
(Ab)

86. Adaptive Immunity
 In contrast to innate immunity, adaptive immunity is a more evolved
and Specific Defence Mechanism
• Its characteristics are exquisitely antigenic specificity and the
ability to ‘ remember’ different types of antigens
• It is activated by only against invading foreign material and never
against its own molecules ( except in autoimmune diseases)
• Thus, it has the ability to distinguish between self and non-self
 Since it can differentiate verity of different antigens, invading
pathogens and self-antigens, and induce different types of immune
response, adaptive immunity is often called SPECIFIC IMMUNITY

87. 1.5. The adaptive Immune System

88. 1.5. Adaptive Immunity:
 Specific
 Second line of defense
 Repeated exposure - augmented – memory
 Faster response
 More vigorous response
 Longer lasting response
 Anamnestic
Components:
Classic Immune System
 Cells (Cell mediated) =CMI
 Soluble Factors (Humoral immunity) = HI
1.5. The Adaptive Immune System

89.  Capable of recognizing and selectively eliminating specific foreign
microorganisms and molecules(i.e., foreign antigens).
 Unlike innate immune responses, adaptive immune responses are
reactions to specific antigenic challenges
 Different populations of lymphocytes and their products are the major
actors together with accessory cells – Antigen presenting cells (APCs)
 Cardinal features are :
 Specificity
 Diversity , Memory,
1.5. THE ADAPTIVE IMMUNE SYSTEM

90. Cardinal Features of adaptive Immune Responses
 Specificity –
 specific for distinct antigen, and
 for different structural components of a single complex protein,
polysaccharide, or other macromolecules.
 Portions of such antigens recognized by individual lymphocytes are
called determinants or epitopes.
 This fine specificity exists because individual lymphocyte express
membrane receptors able to distinguish subtle (slight) differences in
structure between distinct antigens.
1.5. THE ADAPTIVE IMMUNE SYSTEM

91.  Diversity- total number of antigenic specificities of the lymphocytes
in an individual, called the lymphocyte repertoire, is extremely large.
 Estimated mammalian immune system can discriminate 109
to
1011
distinct antigenic date ruminants.
 This property of the lymphocyte repertoire is called diversity. It is
the result of variability in the structures of antigen- binding sites
of lymphocyte receptors for antigens.
1.5. THE ADAPTIVE IMMUNE SYSTEM

92.  Memory- Exposure of the immune system to foreign
antigen:
 Enhances its ability to respond again to that antigen.
 Responses to second and subsequent exposure to
the same antigen, called secondary immune
responses, are usually more rapid and larger than the
first or primary immune response.
1.5. THE ADAPTIVE IMMUNE SYSTEM

93.  An effective immune response involves three major groups of cells:
Cellular Immunity (T lymphocytes), Humoral Immunity (B cells), and
Accessory cells (antigen-presenting cells).
 The two major populations of lymphocytes—B lymphocytes (B
cells) of Humoral immunity and T lymphocytes (T cells) of
Cellular Immunity provide us with our specific adaptive
immunity
1.5. THE ADAPTIVE IMMUNE SYSTEM

94.  Specialization –the immune system responds in distinct and special
ways to different microbes, maximizing the efficiency of antimicrobial
defense mechanisms. Thus, humoral immunity and cell mediated
immunity are elicited by different classes of microbes or by the same
microbe at different stages of infection (extra cellular & intra cellular)
 Self –limitation- All normal immune responses returning the immune
system to its resting or basal state with time after antigen stimulations,
process called homeostasis.
1.5. THE ADAPTIVE IMMUNE SYSTEM

95. Innate Immunity Adaptive Immunity
Comparison of Innate and Adaptive Immunity
• No memory
• No time lag
• Not antigen specific
• A lag period
• Antigen specific
• Development
of memory
Summary of innate and adaptive immunity

96. Adaptive and Innate - Interactions
InfectiousInfectious
ExposureExposure
Innate ImmunityInnate Immunity
holdsholds
Innate ImmunityInnate Immunity
FailsFails
DiseaseDisease
AdaptiveAdaptive
Immune systemImmune system
RecoveryRecovery
Second InfectiousSecond Infectious
ExposureExposure
Same organismSame organism
Adaptive ImmunityAdaptive Immunity
Specific memorySpecific memory
NoNo
DiseaseDisease
Summary of innate and adaptive immunity

98. This is the end of chapter I
and
The next chapter will be:
THE CELLS AND ORGANS OF IMMUNE SYSTEM
Next

99. Review Questions:
1. Define the term immunity and immunology?
2. Describe the historical events of immunology and its
development.
3. What is the difference between innate and adaptive
immunity in terms of components and type of immune
response.
4. Explain major defense mechanism of innate immunity
and adaptive immune system

100. Reference:
 THE ELEMENTS OF IMMUNOLOGY; FAHIM HALIM KHAN
1. Kuby; Goldsby et. al. Immunology. 2007 (5th
ed)
2. Tizard. Immunology an introduction,4th
edition ,Saunders publishing,1994
3. Naville J. Bryant Laboratory Immunology and Serology 3rd
edition. Serological services
Ltd.Toronto,Ontario,Canada,1992
4. Abul K. Abbas and Andrew H. Lichtman. Cellular And Molecular Immunology 2008, 5th
edition
5. Mary T. Keogan, Eleanor M. Wallace and Paula O’Leary Concise clinical immunology for
health professionals , 2006; Ivan M. Roitt and Peter J. Delves Essential immunology
2001, 3rd
ed.