1. The Immune System: Innate and Adaptive Body Defenses: Part A21
The Immune System: Innate and Adaptive Body Defenses: Part A

2. Immunity Resistance to disease Immune system Two intrinsic systems
Innate (nonspecific) defense system
Adaptive (specific) defense system
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3. Figure 21.1 Overview of innate and adaptive defenses.
Surface barriers
• Skin
• Mucous membranes
Innate
Defenses-
NONSpecific
Internal defenses
• Phagocytes
• Natural killer cells
• Inflammation
• Antimicrobial proteins
• Fever
Humoral immunity
• B cells
Adaptive
Defenses
SPECIFIC
Cellular immunity
• T cells
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4. 1st line of defense-BARRIERS
NonSpecific Defenses
1st line of defense-BARRIERS
Skin, mucous membranes, and their secretions
Oils, sweat, tears, mucus, stomach acids
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5. Surface Barriers
Protective chemicals inhibit or destroy microorganisms
Acidity of skin , oil, sweat
Enzymes - lysozyme of saliva, respiratory mucus, and lacrimal fluid (tears) – kill many microorganisms
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6. Internal Defenses: Cells and Chemicals
Surface barriers breached by nicks or cuts - second line of defense must protect deeper tissues
Phagocytes
Natural killer (NK) cells
Antimicrobial proteins (interferons and complement proteins)
Fever
Inflammatory response (macrophages, mast cells, WBCs, and inflammatory chemicals)
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7. Phagocytes Neutrophils most abundant but die fighting
Monocytes-macrophages
Eosinophils-parasites
Basophils-blood anticoagulant
Lymphocytes-lymph glands-antibodies
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8. Events of phagocytosis.
Figure 21.2b Phagocytosis.
Slide 1
Phagocyte
adheres to
pathogens or debris. 1
Phagocyte forms
pseudopods that
eventually engulf the
particles, forming a
phagosome. 2
Phagosome
(phagocytic
vesicle)
Lysosome
Lysosome fuses
with the phagocytic
vesicle, forming a
phagolysosome. 3
Acid
hydrolase
enzymes
Lysosomal
enzymes digest the
particles, leaving a
residual body. 4
Exocytosis of the
vesicle removes
indigestible and
residual material. 5
Events of phagocytosis.
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9. Natural Killer (NK) Cells
Nonphagocytic large granular lymphocytes
Attack cells that lack "self" cell-surface receptors
Induce apoptosis in cancer cells and virus-infected cells
Secrete potent chemicals that enhance inflammatory response
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10. Inflammatory Response
Triggered by injury
Prevents spread of damaging agents
Disposes of cell debris and pathogens
Alerts adaptive immune system
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11. Inflammatory Response
Cardinal signs of acute inflammation:
Redness
Heat
Swelling
Pain
(Sometimes 5. Impairment of function)
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12. © 2013 Pearson Education, Inc.

13. Inflammatory Response
Inflammatory mediators
Kinins,
Dilate local arterioles
Causes redness and heat of inflamed region
Make capillaries leaky
Many attract leukocytes to area
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14. Inflammatory Response
Fibrinogen form fibrin mesh
Scaffold for repair
Isolates injured area so invaders cannot spread
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15. Figure 21.3 Inflammation: flowchart of events.
Innate defenses
Internal defenses
Initial stimulus
Physiological response
Signs of inflammation
Tissue injury
Result
Release of inflammatory chemicals
(histamine, complement,
kinins, prostaglandins, etc.)
Release of leukocytosis-
inducing factor
Leukocytosis
(increased numbers of white
blood cells in bloodstream)
Arterioles
dilate
Increased capillary
permeability
Attract neutrophils,
monocytes, and
lymphocytes to
area (chemotaxis)
Leukocytes migrate to
injured area
Local hyperemia
(increased blood
flow to area)
Capillaries
leak fluid
(exudate formation)
Margination
(leukocytes cling to
capillary walls)
Diapedesis
(leukocytes pass through
capillary walls)
Leaked protein-rich
fluid in tissue spaces
Leaked clotting
proteins form interstitial
clots that wall off area
to prevent injury to
surrounding tissue
Phagocytosis of pathogens
and dead tissue cells
(by neutrophils, short-term;
by macrophages, long-term)
Heat
Redness
Pain
Swelling
Locally increased
temperature increases
metabolic rate of cells
Possible temporary
impairment of
function
Temporary fibrin
patch forms
scaffolding for repair
Pus may form
Area cleared of debris
Healing
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16. Figure 21.4 Phagocyte mobilization.
Slide 1
Innate defenses
Internal defenses
Opsonization-marked for destruction
Inflammatory
chemicals
diffusing
from the
inflamed
site act as
chemotactic
agents.
Chemotaxis.
Neutrophils follow
chemical trail. 4
Capillary wall
Basement
membrane
Endothelium
Leukocytosis.
Neutrophils enter
blood from bone
marrow. 1
Margination.
Neutrophils cling
to capillary wall. 2
Diapedesis.
Neutrophils flatten
and squeeze out of
capillaries. 3
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17. Antimicrobial Proteins
Include interferons (interfere with viral reproduction)
and complement proteins
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18. Figure 21.5 The interferon mechanism against viruses.
Slide 1
Innate defenses
Internal defenses
Virus
Viral nucleic acid 1
Virus
enters cell.
New viruses
Antiviral
proteins
block viral
reproduction. 5
Antiviral
mRNA
Interferon
genes switch
on. 2
DNA
Nucleus
mRNA for
interferon
Interferon binding stimulates cell to
turn on genes for antiviral proteins. 4 3
Cell produces
interferon molecules.
Interferon
receptor
Interferon
Host cell 2
Host cell 1
Binds interferon
from cell 1; interferon
induces synthesis of
protective proteins
Infected by virus;
makes interferon;
is killed by virus
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19. Complement
Unleashes inflammatory chemicals that amplify all aspects of inflammatory response
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20. Abnormally high body temperature
Fever
Abnormally high body temperature
Systemic response to invading microorganisms
Leukocytes and macrophages exposed to foreign substances secrete pyrogens
Pyrogens act on body's thermostat in hypothalamus, raising body temperature
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21. Benefits of moderate fever
Causes liver and spleen to sequester iron and zinc (needed by microorganisms)
Increases metabolic rate  faster repair
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22. Targets of all adaptive immune responses nonself
Antigens
Substances that can mobilize adaptive defenses and provoke an immune response
Targets of all adaptive immune responses
nonself
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23. Cells of the Adaptive Immune System
Three types of cells
Two types of lymphocytes
B lymphocytes (B cells)—humoral immunity
T lymphocytes (T cells)—cellular immunity
Antigen-presenting cells (APCs)
Do not respond to specific antigens
Play essential auxiliary roles in immunity
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24. Table 21.3 Overview of B and T Lymphocytes
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25. Figure 21.11a Clonal selection of a B cell.
Adaptive defenses
Humoral immunity
Antigen
Primary response
(initial encounter
with antigen)
Antigen binding
to a receptor on a
specific B lymphocyte
(B lymphocytes with
noncomplementary
receptors remain
inactive)
Proliferation to
form a clone
Activated B cells
Plasma cells
(effector B cells)
Memory B cell—
primed to respond
to same antigen
Secreted
antibody
molecules
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26. Active Humoral Immunity-ALL ABOUT YOU
When B cells encounter antigens and produce specific antibodies against them
Two types of active humoral immunity:
Naturally acquired—response to bacterial or viral infection (you get it and get over it)
Artificially acquired—response to vaccine of dead or attenuated pathogens
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27. Passive Humoral Immunity- SOMEONE or thing PASSES these on to you
Two types
Naturally acquired—antibodies delivered to fetus via placenta or to infant through milk
Artificially acquired—injection of serum, such as gamma globulin
Protection immediate but ends when antibodies naturally degrade in body
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28. Figure 21.13 Active and passive humoral immunity.
Naturally
acquired
Infection;
contact
with
pathogen
Artificially
Vaccine;
dead or
attenuated
pathogens
Antibodies
passed from
mother to
fetus via
placenta; or
to infant in
her milk
Injection of
exogenous
antibodies
(gamma
globulin)
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