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Immunology
Life Science
Noem Dawood
Lecturer ION,DUHS.
Teaching objectives
 To recognize the significance of the
immune system in combating infection
and disease.
 To distinguish between the innate and
adaptive immunity
 To know the humoral and cellular
components of innate immunity.
RS 2
• The Perfect
World
• The Real World
COL
D
FLU
CHICKEN
POX
STOMAC
H UPSET
HELP
ME !
HELP !
HELP
ME!
Anatomy of the immune system
 Immune system comprises cell and
moclecules with specilaized role in
defending against infection and
invasion by other organisms.
 Major components include the bone
marrow, and the lymphoid tissues.
 Lymphoid tissue include : thymus
gland, spleen, lymph node , tonsile
etc.
RS 4
RS 5
Immunity
 The term immunity has come to mean the
protection from disease and, more specifically,
infectious disease. The collective, coordinated
response of the cells and molecules of the
immune system is called the immune response.
 The system in the body responsible for
maintaining homeostasis (inner environment) by
recognizing harmful from nonharmful
organisms and produces an appropriate
response.
RS 6
Immunity
 The immune system is clearly essential for
survival. It constantly defends the body
against bacteria, viruses, and other foreign
substances it encounters.
 It also defends against abnormal cells and
molecules that periodically develop in the
body, such as cancer cells.
RS 7
leukocytes
 Important function in defense and
immunity
 Leukocytes are the largest blood cells.
 They contain nuclei and some have
granules in their cytoplasm.
 Two main types;
◦ Granulocytes (polymorphonuclear)
◦ -neutrophils, eosinophils and basophils
◦ Agranulocytes
◦ -monocytes and Lymphocytes
Granulocytes
(Polymorphonuclear leukocytes
PMNs)
 During granulopoiesis.
 They follow a common line of
development through myeloblast to
myelocyte before differentiating into
three types
 All granulocytes have multilobed
nuclei in their cytoplasm.
RS 9
Neutrophils PMNs
 Small, fast and active scavengers
protect the body against bacterial
invasion, and remove dead cells and
debris from damaged tissue.
 Highly mobile, and squeeze through
the capillary wall in the affected area.
 Nuclei are characteristically complex.
 Live on average 6- 9 hours in the
blood stream.
 Professional phagocytes.
Eosinophils
 Eosinophils are less active than
neutophils .
 Specialized role appears to be in the
elimination of parasites(worms)
 Certain toxic chemicals stored in their
granules.
 Often found at site of allergic
inflammation ( asthmatic airway and
skin allergies.)
RS 11
Basophils
 Closely associated with
allergic reactions and
 Inflammation .
 Granules packed with heparin and
histamine that increase capillary
permeability during inflammation.
 MAST Cell are similar in appearance
and function to basophils.
RS 12
Agranulocytes
 Monocytes and lymphocytes make up
25 to 50% of the total leukocyte count.
 Have a large nucleus and no
cytoplasmic granules.
RS 13
Monocytes
 Largest of the white blood cells.
 Actively motile and phagocytic
 Some circulate in the blood other
migrate into the tissue where they
develop into the macrophages
 Both types of cell produce
interleukin 1.
 Which act ………………………..cont.
RS 14
monocytes
 Act on hypothalamus,
 Rise in body temperature
 Stimulates the production of some
globulins by liver.
 Enhances the production of activated
T-lymphocytes
RS 15
The monocytes-macrophages
system.
 Some macrophages are mobile,
whereas others are fixed, providing
effective defense at key body location.
 Langerhans cells in the skin
 Microglia in the brain
 Kupffer cell in the liver
 Alveolar macrophages in the lungs
 Osteoclasts in bone.
RS 16
Lymphocytes
 Lymphocytes are smaller than
monocytes and have large nuclei
 Lymphocytes develop from pluripotent
stem cell in red bone marrow.
 Circulate in the blood
 Great number in lymphoid tissue
RS 17
RS 18
NK Cells
 Natural killer cells do not attack invading microbes
dierectly. they kill cells of the body that have been
infected with viruses. They kill not by phagocytosis,
but rather by creating a hole in the plasma
membrane of the target cell Proteins,
 perforins, are released from the natural killer cells
and insert into the membrane of the target cell,
forming a pore. This pore allows water to rush into
the target cell, which then swells and bursts.
RS 19
NK Cells
RS 20
Proteins that kill invading
microbes
 Complement system is the major humoral
non-specific defense mechanism
 Approximately 20 different proteins that
circulate freely in the blood plasma
 Aggregate to form a membrane attack
complex
 Forming a pore like produced by NK
 Water enter through this pore, causing the
cell to swell and brust.
RS 21
RS 22
 Dendritic cells (DCs) are antigen-presenting
cells, Their main function is to process antigen
material and present it on the cell surface to
the T cells of the immune system. They act as
messengers between the innate and the
adaptive immune systems.
 Dendritic cells are present in those tissues that
are in contact with the external environment,
such as the skin ( Langerhans cell) and the
inner lining of the nose, lungs, stomach and
intestines.
 Once activated, they migrate to the lymph
nodes where they interact with T cells and B
cells to initiate and shape the adaptive immune
response. RS 23
Dendritic cell
Overview of the immune system
 The immune system is composed of
two major subdivision.
 Innate or non specific
 Adaptive or specific
 Innate immune system is our first line
of defense against invading organisms
 Adaptive immune act as a second line
of defense and also protection against
re-exposure of the same pathogen.
RS 25
Overview of the immune system
 Each of the major subdivision of the
immune system has both;
 Cellular and humoral
 Innate immune system also has anatomical
features that function as barriers to
infection.
 Innate and adaptive immune systems both
function to protect against invading
organisms.
 Differ in a number of way.
RS 26
 Adaptive immune system require some time
to react to an invading organism.
 Innate immunity constitutively present and
ready to be mobilized upon infection.
 Adaptive immune is antigen specific
 Innate system is not antigen specific and
equally well to a variety of organisms.
 Adaptive demonstrates immunological
memory
 Innate immune does not demonstrate
immunological memory.
RS 27
RS 28
Characteristics of Innate and
Adaptive Immunity
No Immunologic
memory
Antigen independent
No time lag
Not antigen specific
Antigen dependent
A lag period
Antigen specific
Development
of memory
Innate Immunity Adaptive Immunity
28
RS 29
Non- specific defense
 There are five main non- specific
defence mechanisms.
 Defence at body surfaces
 Phagocytosis
 Natural antimicrobial substances
 The inflammatory response
 Immunological survellance
RS 30
Innate and Adaptive Defenses
Anatomical barriers to infection
- 1. Mechanical Factors
- Acts as our first line defense
against invading organisms.
- The epithelial surfaces form a
physical barrier
- Impermeable to most
infectious agents.
RS 32
RS 33
1. Mechanical factors
ANATOMICAL BARRIER TO INFECTION
 Movement due to cilia or peristalsis
help to keep air passages and the
gastrointestinal tract free from
microbes.
 Flushing action of tears and saliva
helps prevent infection of the eye and
mouth.
 The trapping action of mucus protect
the lungs.
RS 34
2. Chemical factors
ANATOMICAL BARRIER TO INFECTION
RS 35
 Fatty acids sweat inhibit the growth of
bacteria.
 Lysozyme and phospholipase found in
tear, saliva and nasal secretion can
breakdown the cell wall of bacteria
and destabilize bacterial membranes.
 Low PH of sweat and gastric secretion
prevent growth of bacteria.
3. Biological factors
ANATOMICAL BARRIERS TO INFECTION
 The normal flora of the skin and the
GIT can prevent the colonization of
pathogenic bacteria.
RS 36
RS 37
Second-Line Defenses
If a pathogen is able to get past the
body's first line of defense, and an
infection starts, the body can rely on
it's second line of defense.
37
RS 38
Second Line of Defense
Nonspecific Immune Response
These defenses include:
Fever:
◦ Caused by IL1 . The fever (high temp) kills
invaders by denaturing their proteins. Heat
– Increased temperature inhibits the growth
of antigens or microbial proliferation.
Pain:
◦ Due mainly to tissue destruction and, to a
lesser extent, swelling.
.
38
RS 39
Inflammation:
 Damage tissue release histamine from
leukocytes –inflammation cause rednes - due
to capillary dilatition resulting in increase
blood Flow. Histamine cause capillaries to
leak, releasing phagocytes and clotting factors
into the wound. phagocytes engulf bacteria
,dead cell and cellular debris. Platelet move
out of capillary to seal the wounded area.
 Swelling – due to passage of plasma from the
blood stream into the damaged tissue.
Second Line of Defense
39
RS 40
Second Line of Defense
 Inflammatory response: Prevents spread of
harmful agents to adjacent tissues; promotes
tissue repair; release chemical mediators to
attract phagocytes and stimulate third line of
immune response.
◦ Phagocytes: Engulf pathogens and
contributes immune response
◦ Phagocytosis – Done by Macrophages
◦ Macrophage:A phagocytic cell found in the
liver, spleen, brain and lungs. Travels to all
areas of the body to find and eat pathogens.
40
RS 41
Second Line of defense
 Antimicrobial proteins:
Interferon:
 Proteins released by virus infected cells
that protect uninfected cells from viral
overtake.
Complement:
 Lyses microbes, enhances phagocytosis
by opsonization, and intensifies
inflammatory and immune responses.
41
Antimicrobial substances
 Iron binding protein
◦ Lactoferrin found in saliva, mucus and
milk
◦ Transferrin found in blood and tissue,
LYSOZYME:
Enzymes that degrades peptidoglycan (
found in tears, saliva and mucus.
Also found in phagocytic cell
Primarilly effective against Gram- positive
bacteria.
DEFENSINS;
RS 42
phagocytosis
 Macrophages and neutrophils migrate
to site of inflammation
 Phagocytosis occurs in five phases:
chemotaxis, adherence,ingestion,
digestion, and killing
RS 43
44
Phagocytosis
44
45
Figure 21.2b
(b)
Lysosome
Microbe adheres to phagocyte.
Phagocyte forms pseudopods that
eventually engulf the particle.
Phagocytic vesicle is
fused with a lysosome.
Microbe in fused vesicle
is killed and digested by
lysosomal enzymes within
the phagolysosome, leaving
a residual body.
Indigestible and
residual material
is removed by
exocytosis.
Phagocytic vesicle
containing antigen
(phagosome).
Residual body
Acid
hydrolase
enzymes
Phagolysosome
4
3
2
1
5
45
RS 46
Figure 21.2b
(b)
Microbe adheres to phagocyte.
1
46
RS 47
Figure 21.2b
(b)
Microbe adheres to phagocyte.
Phagocyte forms pseudopods that
eventually engulf the particle.
2
1
47
RS 48
Figure 21.2b
(b)
Lysosome
Microbe adheres to phagocyte.
Phagocyte forms pseudopods that
eventually engulf the particle.
Phagocytic vesicle
containing antigen
(phagosome).
2
1
48
RS 49
Figure 21.2b
(b)
Lysosome
Microbe adheres to phagocyte.
Phagocyte forms pseudopods that
eventually engulf the particle.
Phagocytic vesicle is
fused with a lysosome.
Phagocytic vesicle
containing antigen
(phagosome).
Acid
hydrolase
enzymes
Phagolysosome
3
2
1
49
50
Figure 21.2b
(b)
Lysosome
Microbe adheres to phagocyte.
Phagocyte forms pseudopods that
eventually engulf the particle.
Phagocytic vesicle is
fused with a lysosome.
Microbe in fused vesicle
is killed and digested by
lysosomal enzymes within
the phagolysosome, leaving
a residual body.
Phagocytic vesicle
containing antigen
(phagosome).
Residual body
Acid
hydrolase
enzymes
Phagolysosome
4
3
2
1
50
51
Figure 21.2b
(b)
Lysosome
Microbe adheres to phagocyte.
Phagocyte forms pseudopods that
eventually engulf the particle.
Phagocytic vesicle is
fused with a lysosome.
Microbe in fused vesicle
is killed and digested by
lysosomal enzymes within
the phagolysosome, leaving
a residual body.
Indigestible and
residual material
is removed by
exocytosis.
Phagocytic vesicle
containing antigen
(phagosome).
Residual body
Acid
hydrolase
enzymes
Phagolysosome
4
3
2
1
5
52
52
Key concepts of specific
immunity
Antigen
 Antigen , or immunogens are substance
foreign to the host that can stimulate an
immune response.
 These foreign molecules are recognized by
receptor on immune cells /protein called
antibodies or immunoglobulins.
 Most antigens are macro- molecules.
 Immunologically active sites on antigen are
called antigenic determinants, or eiptopes
53
Antigens
Epitope:
u Small part of an antigen that
interacts with an antibody.
u Any given antigen may have
several epitopes.
u Each epitope is recognized by a
different antibody.
54
55
Antigenic Determinants
RS 56
Hapten:
 A substance of low molecular weight that is not
antigenic itself except when combined with a
carrier/protein. E.g. Penicillin drug.
 Small molecules, such as peptides, nucleotides,
and many hormones, that are not immunogenic
but are reactive when attached to protein carriers
How Do B Cells Produce
Antibodies?
◦ B cells develop from stem cells in the bone
marrow of adults (liver of fetuses).
◦ After maturation B cells migrate to lymphoid
organs (lymph node or spleen).
◦ Clonal Selection: When a B cell encounters
an antigen it recognizes, it is stimulated and
divides into many clones called plasma cells,
which actively secrete antibodies.
◦ Each B cell produces antibodies that will
recognize only one antigenic determinant.
RS 57
RS 58
Primary Response
(initial encounter
with antigen)
Antigen
Antigen binding
to a receptor on a
specific B lymphocyte
(B lymphocytes with
non-complementary
receptors remain
inactive)
RS 59
Primary Response
(initial encounter
with antigen)
Antigen
Antigen binding
to a receptor on a
specific B lymphocyte
(B lymphocytes with
non-complementary
receptors remain
inactive)
Proliferation to
form a clone
B lymphoblasts
RS 60
Plasma
cells
Secreted
antibody
molecules
Memory
B cell
Primary Response
(initial encounter
with antigen)
Antigen
Antigen binding
to a receptor on a
specific B lymphocyte
(B lymphocytes with
non-complementary
receptors remain
inactive)
Proliferation to
form a clone
B lymphoblasts
RS 61
Plasma
cells
Secreted
antibody
molecules
Clone of cells
identical to
ancestral cells
Subsequent
challenge by
same antigen
Memory
B cell
Secondary Response
(can be years later)
Primary Response
(initial encounter
with antigen)
Antigen
Antigen binding
to a receptor on a
specific B lymphocyte
(B lymphocytes with
non-complementary
receptors remain
inactive)
Proliferation to
form a clone
B lymphoblasts
RS 62
Plasma
cells
Secreted
antibody
molecules
Clone of cells
identical to
ancestral cells
Subsequent
challenge by
same antigen
Memory
B cell
Memory
B cells
Plasma
cells
Secreted
antibody
molecules
Secondary Response
(can be years later)
Primary Response
(initial encounter
with antigen)
Antigen
Antigen binding
to a receptor on a
specific B lymphocyte
(B lymphocytes with
non-complementary
receptors remain
inactive)
Proliferation to
form a clone
B lymphoblasts
RS 63
5 main Classes of Immunoglobulins (Ig)
IgA
 5-10% of serum antibody.
 Most common in fluids like saliva , tears
and breast milk (helps keep baby safe
while it develops its own immune system)
 Respiratory (bronchi) and intestinal
mucous (gut) Prevent attachment of
viruses and/or bacteria to mucosal
surfaces.
63
RS 64
IgD
 0.2%, found on surface of B cells and act
as antigen receptors (no known function
in serum)
 It is protein that is present in normal
human serum in very small amount . The
function of IgD is unknown except
antigen receptor.
64
RS 65
IgG
 80% of all serum antibody, cross blood
vessel walls and enter tissue fluids
◦ Cross placenta to protect fetus.
◦ It possess immunity in infants prior to
birth.
◦ Protect against circulating bacteria,
viruses, neutralize toxin, trigger
complement, and enhance phagocytic
cells.
◦ Each molecule of igG has two antigen-
binding site
65
RS 66
IgE
 0.002% of serum antibody, that binds to mast
cells and basophils (allergic reactions).
◦ Increases during parasite or allergy
 It is produced by the cell of the liver ,
respiratory and intestinal tract.
IgM
 5-10% of serum antibody.
◦ First respond to initial antigen exposure.
◦ Valuable in diagnosis because it is early to
respond.
◦ Larger than IgG -10 antigen binding sites.
66
RS 67
Third Line of defense
 It’s response is antigen specific means
differentiate pathogens.
 Third line of defense consists of humoral
and cell mediated immune response.
 They fight off pathogens and provide long
term immunity by keeping record of the
antigen into its memory.
 Secondary response is thus relatively rapid
and stronger than the primary response.
67
RS 68
68
RS 69
Active and Passive Immunity
 Acquired immunity can be acquired
passively or actively
 Active or passive can be acquired
naturally or artificially
Natural active immunity - acquired due to
infection exposure to antigens (you get
sick and recover)- long lived
69
RS 70
Artificial active immunity – Vaccination
 Takes time for enough B and T cells to be
produced to mount an effective response.
 Gets a vaccination which introduces
specially prepared antigens into the body
 Doesn’t cause disease but stimulates your
immune response.
70
RS 71
Passive immunity
 Individual is given antibody by someone
else.
B and T cells are not activated and plasma
cells have not produced antibodies.
The antigen doesn’t have to be encountered
for the body to make the antibodies.
Antibodies appear immediately in blood
but protection is only temporary.
71
RS 72
Artificial passive immunity
 Used when a very rapid immune response
is needed e.g. after infection with
tetanus.
 Human antibodies are injected. In the
case of tetanus these are antitoxin
antibodies.
 Antibodies come from blood donors who
have recently had the tetanus vaccination.
 Only provides short term protection ,
destroyed by phagocytes in spleen and
liver. introduces antibodies or antitoxin
into the body.
72
RS 73
Natural passive immunity
 A mother’s antibodies pass across the
placenta to the foetus and remain for
several months.
 Colostrums' (the first breast milk)
contains lots of IgA which remain on
surface of the baby’s gut wall and pass
into blood.
 (breast feeding and in uterus)-this is
short lived.
73
RS 74
Passive .vs. Active Immunity
1. Active Immunity
This is immunity where the body is “actively” producing
antibodies to fight infection.
You have a throat infection and you are actively creating
antibodies to fight it.
2. Passive Immunity
This is immunity where antibodies are given to a
person from the blood of another person or animal.
This immunity only lasts for a short period of time.
Breastfeeding mothers pass antibodies to their children
through the milk.
74
RS 75
IMMUNITY
Natural
Defence mechanisms
IMMUNITY
Passive
Immunogl
obulin
serum
with
antibodie
s
Cell
mediated
,T
lymphocyte
s
Humoral
immunity ,B
Lymphocyte
.
Non –specific
mechanisms
Primary and secondary
response
NOEM
DAWOOD
Vaccine
Specific defence
mechanism
Anti body production following
immunization
Acquired immunity
Active
Clinical
disease
,infection
artificial
From
mother
Natural artificial
75
RS 76
References
 Kathleen Talaro ,Aurthur Talaro ,
Foudations in microbiology 2nd edition
G1-G11
 www.ivcc.edu/.../microbiology_pow
erpoint_presenta.htm
 Vivien A.stuke ,microbiology for
nurses ,7th edition pp 58-91
 Ross and Wilson ,anatomy and
physiology in health and illness 8th
edition, pp 64-67
76

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Immunity 1,2,3 line.ppt

  • 2. Teaching objectives  To recognize the significance of the immune system in combating infection and disease.  To distinguish between the innate and adaptive immunity  To know the humoral and cellular components of innate immunity. RS 2
  • 3. • The Perfect World • The Real World COL D FLU CHICKEN POX STOMAC H UPSET HELP ME ! HELP ! HELP ME!
  • 4. Anatomy of the immune system  Immune system comprises cell and moclecules with specilaized role in defending against infection and invasion by other organisms.  Major components include the bone marrow, and the lymphoid tissues.  Lymphoid tissue include : thymus gland, spleen, lymph node , tonsile etc. RS 4
  • 6. Immunity  The term immunity has come to mean the protection from disease and, more specifically, infectious disease. The collective, coordinated response of the cells and molecules of the immune system is called the immune response.  The system in the body responsible for maintaining homeostasis (inner environment) by recognizing harmful from nonharmful organisms and produces an appropriate response. RS 6
  • 7. Immunity  The immune system is clearly essential for survival. It constantly defends the body against bacteria, viruses, and other foreign substances it encounters.  It also defends against abnormal cells and molecules that periodically develop in the body, such as cancer cells. RS 7
  • 8. leukocytes  Important function in defense and immunity  Leukocytes are the largest blood cells.  They contain nuclei and some have granules in their cytoplasm.  Two main types; ◦ Granulocytes (polymorphonuclear) ◦ -neutrophils, eosinophils and basophils ◦ Agranulocytes ◦ -monocytes and Lymphocytes
  • 9. Granulocytes (Polymorphonuclear leukocytes PMNs)  During granulopoiesis.  They follow a common line of development through myeloblast to myelocyte before differentiating into three types  All granulocytes have multilobed nuclei in their cytoplasm. RS 9
  • 10. Neutrophils PMNs  Small, fast and active scavengers protect the body against bacterial invasion, and remove dead cells and debris from damaged tissue.  Highly mobile, and squeeze through the capillary wall in the affected area.  Nuclei are characteristically complex.  Live on average 6- 9 hours in the blood stream.  Professional phagocytes.
  • 11. Eosinophils  Eosinophils are less active than neutophils .  Specialized role appears to be in the elimination of parasites(worms)  Certain toxic chemicals stored in their granules.  Often found at site of allergic inflammation ( asthmatic airway and skin allergies.) RS 11
  • 12. Basophils  Closely associated with allergic reactions and  Inflammation .  Granules packed with heparin and histamine that increase capillary permeability during inflammation.  MAST Cell are similar in appearance and function to basophils. RS 12
  • 13. Agranulocytes  Monocytes and lymphocytes make up 25 to 50% of the total leukocyte count.  Have a large nucleus and no cytoplasmic granules. RS 13
  • 14. Monocytes  Largest of the white blood cells.  Actively motile and phagocytic  Some circulate in the blood other migrate into the tissue where they develop into the macrophages  Both types of cell produce interleukin 1.  Which act ………………………..cont. RS 14
  • 15. monocytes  Act on hypothalamus,  Rise in body temperature  Stimulates the production of some globulins by liver.  Enhances the production of activated T-lymphocytes RS 15
  • 16. The monocytes-macrophages system.  Some macrophages are mobile, whereas others are fixed, providing effective defense at key body location.  Langerhans cells in the skin  Microglia in the brain  Kupffer cell in the liver  Alveolar macrophages in the lungs  Osteoclasts in bone. RS 16
  • 17. Lymphocytes  Lymphocytes are smaller than monocytes and have large nuclei  Lymphocytes develop from pluripotent stem cell in red bone marrow.  Circulate in the blood  Great number in lymphoid tissue RS 17
  • 18. RS 18
  • 19. NK Cells  Natural killer cells do not attack invading microbes dierectly. they kill cells of the body that have been infected with viruses. They kill not by phagocytosis, but rather by creating a hole in the plasma membrane of the target cell Proteins,  perforins, are released from the natural killer cells and insert into the membrane of the target cell, forming a pore. This pore allows water to rush into the target cell, which then swells and bursts. RS 19
  • 21. Proteins that kill invading microbes  Complement system is the major humoral non-specific defense mechanism  Approximately 20 different proteins that circulate freely in the blood plasma  Aggregate to form a membrane attack complex  Forming a pore like produced by NK  Water enter through this pore, causing the cell to swell and brust. RS 21
  • 22. RS 22
  • 23.  Dendritic cells (DCs) are antigen-presenting cells, Their main function is to process antigen material and present it on the cell surface to the T cells of the immune system. They act as messengers between the innate and the adaptive immune systems.  Dendritic cells are present in those tissues that are in contact with the external environment, such as the skin ( Langerhans cell) and the inner lining of the nose, lungs, stomach and intestines.  Once activated, they migrate to the lymph nodes where they interact with T cells and B cells to initiate and shape the adaptive immune response. RS 23
  • 25. Overview of the immune system  The immune system is composed of two major subdivision.  Innate or non specific  Adaptive or specific  Innate immune system is our first line of defense against invading organisms  Adaptive immune act as a second line of defense and also protection against re-exposure of the same pathogen. RS 25
  • 26. Overview of the immune system  Each of the major subdivision of the immune system has both;  Cellular and humoral  Innate immune system also has anatomical features that function as barriers to infection.  Innate and adaptive immune systems both function to protect against invading organisms.  Differ in a number of way. RS 26
  • 27.  Adaptive immune system require some time to react to an invading organism.  Innate immunity constitutively present and ready to be mobilized upon infection.  Adaptive immune is antigen specific  Innate system is not antigen specific and equally well to a variety of organisms.  Adaptive demonstrates immunological memory  Innate immune does not demonstrate immunological memory. RS 27
  • 28. RS 28 Characteristics of Innate and Adaptive Immunity No Immunologic memory Antigen independent No time lag Not antigen specific Antigen dependent A lag period Antigen specific Development of memory Innate Immunity Adaptive Immunity 28
  • 29. RS 29
  • 30. Non- specific defense  There are five main non- specific defence mechanisms.  Defence at body surfaces  Phagocytosis  Natural antimicrobial substances  The inflammatory response  Immunological survellance RS 30
  • 32. Anatomical barriers to infection - 1. Mechanical Factors - Acts as our first line defense against invading organisms. - The epithelial surfaces form a physical barrier - Impermeable to most infectious agents. RS 32
  • 33. RS 33
  • 34. 1. Mechanical factors ANATOMICAL BARRIER TO INFECTION  Movement due to cilia or peristalsis help to keep air passages and the gastrointestinal tract free from microbes.  Flushing action of tears and saliva helps prevent infection of the eye and mouth.  The trapping action of mucus protect the lungs. RS 34
  • 35. 2. Chemical factors ANATOMICAL BARRIER TO INFECTION RS 35  Fatty acids sweat inhibit the growth of bacteria.  Lysozyme and phospholipase found in tear, saliva and nasal secretion can breakdown the cell wall of bacteria and destabilize bacterial membranes.  Low PH of sweat and gastric secretion prevent growth of bacteria.
  • 36. 3. Biological factors ANATOMICAL BARRIERS TO INFECTION  The normal flora of the skin and the GIT can prevent the colonization of pathogenic bacteria. RS 36
  • 37. RS 37 Second-Line Defenses If a pathogen is able to get past the body's first line of defense, and an infection starts, the body can rely on it's second line of defense. 37
  • 38. RS 38 Second Line of Defense Nonspecific Immune Response These defenses include: Fever: ◦ Caused by IL1 . The fever (high temp) kills invaders by denaturing their proteins. Heat – Increased temperature inhibits the growth of antigens or microbial proliferation. Pain: ◦ Due mainly to tissue destruction and, to a lesser extent, swelling. . 38
  • 39. RS 39 Inflammation:  Damage tissue release histamine from leukocytes –inflammation cause rednes - due to capillary dilatition resulting in increase blood Flow. Histamine cause capillaries to leak, releasing phagocytes and clotting factors into the wound. phagocytes engulf bacteria ,dead cell and cellular debris. Platelet move out of capillary to seal the wounded area.  Swelling – due to passage of plasma from the blood stream into the damaged tissue. Second Line of Defense 39
  • 40. RS 40 Second Line of Defense  Inflammatory response: Prevents spread of harmful agents to adjacent tissues; promotes tissue repair; release chemical mediators to attract phagocytes and stimulate third line of immune response. ◦ Phagocytes: Engulf pathogens and contributes immune response ◦ Phagocytosis – Done by Macrophages ◦ Macrophage:A phagocytic cell found in the liver, spleen, brain and lungs. Travels to all areas of the body to find and eat pathogens. 40
  • 41. RS 41 Second Line of defense  Antimicrobial proteins: Interferon:  Proteins released by virus infected cells that protect uninfected cells from viral overtake. Complement:  Lyses microbes, enhances phagocytosis by opsonization, and intensifies inflammatory and immune responses. 41
  • 42. Antimicrobial substances  Iron binding protein ◦ Lactoferrin found in saliva, mucus and milk ◦ Transferrin found in blood and tissue, LYSOZYME: Enzymes that degrades peptidoglycan ( found in tears, saliva and mucus. Also found in phagocytic cell Primarilly effective against Gram- positive bacteria. DEFENSINS; RS 42
  • 43. phagocytosis  Macrophages and neutrophils migrate to site of inflammation  Phagocytosis occurs in five phases: chemotaxis, adherence,ingestion, digestion, and killing RS 43
  • 45. 45 Figure 21.2b (b) Lysosome Microbe adheres to phagocyte. Phagocyte forms pseudopods that eventually engulf the particle. Phagocytic vesicle is fused with a lysosome. Microbe in fused vesicle is killed and digested by lysosomal enzymes within the phagolysosome, leaving a residual body. Indigestible and residual material is removed by exocytosis. Phagocytic vesicle containing antigen (phagosome). Residual body Acid hydrolase enzymes Phagolysosome 4 3 2 1 5 45
  • 46. RS 46 Figure 21.2b (b) Microbe adheres to phagocyte. 1 46
  • 47. RS 47 Figure 21.2b (b) Microbe adheres to phagocyte. Phagocyte forms pseudopods that eventually engulf the particle. 2 1 47
  • 48. RS 48 Figure 21.2b (b) Lysosome Microbe adheres to phagocyte. Phagocyte forms pseudopods that eventually engulf the particle. Phagocytic vesicle containing antigen (phagosome). 2 1 48
  • 49. RS 49 Figure 21.2b (b) Lysosome Microbe adheres to phagocyte. Phagocyte forms pseudopods that eventually engulf the particle. Phagocytic vesicle is fused with a lysosome. Phagocytic vesicle containing antigen (phagosome). Acid hydrolase enzymes Phagolysosome 3 2 1 49
  • 50. 50 Figure 21.2b (b) Lysosome Microbe adheres to phagocyte. Phagocyte forms pseudopods that eventually engulf the particle. Phagocytic vesicle is fused with a lysosome. Microbe in fused vesicle is killed and digested by lysosomal enzymes within the phagolysosome, leaving a residual body. Phagocytic vesicle containing antigen (phagosome). Residual body Acid hydrolase enzymes Phagolysosome 4 3 2 1 50
  • 51. 51 Figure 21.2b (b) Lysosome Microbe adheres to phagocyte. Phagocyte forms pseudopods that eventually engulf the particle. Phagocytic vesicle is fused with a lysosome. Microbe in fused vesicle is killed and digested by lysosomal enzymes within the phagolysosome, leaving a residual body. Indigestible and residual material is removed by exocytosis. Phagocytic vesicle containing antigen (phagosome). Residual body Acid hydrolase enzymes Phagolysosome 4 3 2 1 5
  • 52. 52 52
  • 53. Key concepts of specific immunity Antigen  Antigen , or immunogens are substance foreign to the host that can stimulate an immune response.  These foreign molecules are recognized by receptor on immune cells /protein called antibodies or immunoglobulins.  Most antigens are macro- molecules.  Immunologically active sites on antigen are called antigenic determinants, or eiptopes 53
  • 54. Antigens Epitope: u Small part of an antigen that interacts with an antibody. u Any given antigen may have several epitopes. u Each epitope is recognized by a different antibody. 54
  • 56. RS 56 Hapten:  A substance of low molecular weight that is not antigenic itself except when combined with a carrier/protein. E.g. Penicillin drug.  Small molecules, such as peptides, nucleotides, and many hormones, that are not immunogenic but are reactive when attached to protein carriers
  • 57. How Do B Cells Produce Antibodies? ◦ B cells develop from stem cells in the bone marrow of adults (liver of fetuses). ◦ After maturation B cells migrate to lymphoid organs (lymph node or spleen). ◦ Clonal Selection: When a B cell encounters an antigen it recognizes, it is stimulated and divides into many clones called plasma cells, which actively secrete antibodies. ◦ Each B cell produces antibodies that will recognize only one antigenic determinant. RS 57
  • 58. RS 58 Primary Response (initial encounter with antigen) Antigen Antigen binding to a receptor on a specific B lymphocyte (B lymphocytes with non-complementary receptors remain inactive)
  • 59. RS 59 Primary Response (initial encounter with antigen) Antigen Antigen binding to a receptor on a specific B lymphocyte (B lymphocytes with non-complementary receptors remain inactive) Proliferation to form a clone B lymphoblasts
  • 60. RS 60 Plasma cells Secreted antibody molecules Memory B cell Primary Response (initial encounter with antigen) Antigen Antigen binding to a receptor on a specific B lymphocyte (B lymphocytes with non-complementary receptors remain inactive) Proliferation to form a clone B lymphoblasts
  • 61. RS 61 Plasma cells Secreted antibody molecules Clone of cells identical to ancestral cells Subsequent challenge by same antigen Memory B cell Secondary Response (can be years later) Primary Response (initial encounter with antigen) Antigen Antigen binding to a receptor on a specific B lymphocyte (B lymphocytes with non-complementary receptors remain inactive) Proliferation to form a clone B lymphoblasts
  • 62. RS 62 Plasma cells Secreted antibody molecules Clone of cells identical to ancestral cells Subsequent challenge by same antigen Memory B cell Memory B cells Plasma cells Secreted antibody molecules Secondary Response (can be years later) Primary Response (initial encounter with antigen) Antigen Antigen binding to a receptor on a specific B lymphocyte (B lymphocytes with non-complementary receptors remain inactive) Proliferation to form a clone B lymphoblasts
  • 63. RS 63 5 main Classes of Immunoglobulins (Ig) IgA  5-10% of serum antibody.  Most common in fluids like saliva , tears and breast milk (helps keep baby safe while it develops its own immune system)  Respiratory (bronchi) and intestinal mucous (gut) Prevent attachment of viruses and/or bacteria to mucosal surfaces. 63
  • 64. RS 64 IgD  0.2%, found on surface of B cells and act as antigen receptors (no known function in serum)  It is protein that is present in normal human serum in very small amount . The function of IgD is unknown except antigen receptor. 64
  • 65. RS 65 IgG  80% of all serum antibody, cross blood vessel walls and enter tissue fluids ◦ Cross placenta to protect fetus. ◦ It possess immunity in infants prior to birth. ◦ Protect against circulating bacteria, viruses, neutralize toxin, trigger complement, and enhance phagocytic cells. ◦ Each molecule of igG has two antigen- binding site 65
  • 66. RS 66 IgE  0.002% of serum antibody, that binds to mast cells and basophils (allergic reactions). ◦ Increases during parasite or allergy  It is produced by the cell of the liver , respiratory and intestinal tract. IgM  5-10% of serum antibody. ◦ First respond to initial antigen exposure. ◦ Valuable in diagnosis because it is early to respond. ◦ Larger than IgG -10 antigen binding sites. 66
  • 67. RS 67 Third Line of defense  It’s response is antigen specific means differentiate pathogens.  Third line of defense consists of humoral and cell mediated immune response.  They fight off pathogens and provide long term immunity by keeping record of the antigen into its memory.  Secondary response is thus relatively rapid and stronger than the primary response. 67
  • 69. RS 69 Active and Passive Immunity  Acquired immunity can be acquired passively or actively  Active or passive can be acquired naturally or artificially Natural active immunity - acquired due to infection exposure to antigens (you get sick and recover)- long lived 69
  • 70. RS 70 Artificial active immunity – Vaccination  Takes time for enough B and T cells to be produced to mount an effective response.  Gets a vaccination which introduces specially prepared antigens into the body  Doesn’t cause disease but stimulates your immune response. 70
  • 71. RS 71 Passive immunity  Individual is given antibody by someone else. B and T cells are not activated and plasma cells have not produced antibodies. The antigen doesn’t have to be encountered for the body to make the antibodies. Antibodies appear immediately in blood but protection is only temporary. 71
  • 72. RS 72 Artificial passive immunity  Used when a very rapid immune response is needed e.g. after infection with tetanus.  Human antibodies are injected. In the case of tetanus these are antitoxin antibodies.  Antibodies come from blood donors who have recently had the tetanus vaccination.  Only provides short term protection , destroyed by phagocytes in spleen and liver. introduces antibodies or antitoxin into the body. 72
  • 73. RS 73 Natural passive immunity  A mother’s antibodies pass across the placenta to the foetus and remain for several months.  Colostrums' (the first breast milk) contains lots of IgA which remain on surface of the baby’s gut wall and pass into blood.  (breast feeding and in uterus)-this is short lived. 73
  • 74. RS 74 Passive .vs. Active Immunity 1. Active Immunity This is immunity where the body is “actively” producing antibodies to fight infection. You have a throat infection and you are actively creating antibodies to fight it. 2. Passive Immunity This is immunity where antibodies are given to a person from the blood of another person or animal. This immunity only lasts for a short period of time. Breastfeeding mothers pass antibodies to their children through the milk. 74
  • 75. RS 75 IMMUNITY Natural Defence mechanisms IMMUNITY Passive Immunogl obulin serum with antibodie s Cell mediated ,T lymphocyte s Humoral immunity ,B Lymphocyte . Non –specific mechanisms Primary and secondary response NOEM DAWOOD Vaccine Specific defence mechanism Anti body production following immunization Acquired immunity Active Clinical disease ,infection artificial From mother Natural artificial 75
  • 76. RS 76 References  Kathleen Talaro ,Aurthur Talaro , Foudations in microbiology 2nd edition G1-G11  www.ivcc.edu/.../microbiology_pow erpoint_presenta.htm  Vivien A.stuke ,microbiology for nurses ,7th edition pp 58-91  Ross and Wilson ,anatomy and physiology in health and illness 8th edition, pp 64-67 76