Transcript B cells - Humble ISD

PowerPoint® Lecture Slides
prepared by
Barbara Heard,
Atlantic Cape Community
College
CHAPTER
21
The Immune
System: Innate
and Adaptive
Body Defenses:
Part A
© Annie Leibovitz/Contact Press Images
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Immunity
• Resistance to disease
• Immune system
– Two intrinsic systems
• Innate (nonspecific) defense system
• Adaptive (specific) defense system
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Figure 21.1 Overview of innate and adaptive defenses.
Surface barriers
• Skin
• Mucous membranes
Innate
DefensesNONSpecific
Adaptive
Defenses
SPECIFIC
Internal defenses
• Phagocytes
• Natural killer cells
• Inflammation
• Antimicrobial proteins
• Fever
Humoral immunity
• B cells
Cellular immunity
• T cells
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NonSpecific Defenses
• 1st line of defense-BARRIERS
• Skin, mucous membranes, and their
secretions
• Oils, sweat, tears, mucus, stomach acids
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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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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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Phagocytes
•
•
•
•
•
Neutrophils most abundant but die fighting
Monocytes-macrophages
Eosinophils-parasites
Basophils-blood anticoagulant
Lymphocytes-lymph glands-antibodies
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Figure 21.2b Phagocytosis.
1 Phagocyte
adheres to
pathogens or debris.
Phagosome
(phagocytic
vesicle)
Lysosome
Acid
hydrolase
enzymes
2 Phagocyte forms
pseudopods that
eventually engulf the
particles, forming a
phagosome.
3 Lysosome fuses
with the phagocytic
vesicle, forming a
phagolysosome.
4 Lysosomal
enzymes digest the
particles, leaving a
residual body.
5 Exocytosis of the
vesicle removes
indigestible and
residual material.
Events of phagocytosis.
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Slide 1
Natural Killer (NK) Cells
• Nonphagocytic large granular lymphocytes
• Attack cells that lack "self" cell-surface
receptors
– Induce apoptosis in cancer cells and virusinfected cells
• Secrete potent chemicals that enhance
inflammatory response
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Inflammatory Response
•
•
•
•
Triggered by injury
Prevents spread of damaging agents
Disposes of cell debris and pathogens
Alerts adaptive immune system
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Inflammatory Response
• Cardinal signs of acute inflammation:
1. Redness
2. Heat
3. Swelling
4. Pain
(Sometimes 5. Impairment of function)
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•
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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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Inflammatory Response
• Fibrinogen form fibrin mesh
– Scaffold for repair
– Isolates injured area so invaders cannot
spread
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Figure 21.3 Inflammation: flowchart of events.
Innate defenses
Internal defenses
Initial stimulus
Physiological response
Tissue injury
Release of inflammatory chemicals
(histamine, complement,
kinins, prostaglandins, etc.)
Signs of inflammation
Result
Release of leukocytosisinducing factor
Leukocytosis
(increased numbers of white
blood cells in bloodstream)
Arterioles
dilate
Increased capillary
permeability
Local hyperemia
(increased blood
flow to area)
Capillaries
leak fluid
(exudate formation)
Leaked protein-rich
fluid in tissue spaces
Heat
Redness
Locally increased
temperature increases
metabolic rate of cells
Pain
Attract neutrophils,
monocytes, and
lymphocytes to
area (chemotaxis)
Margination
(leukocytes cling to
capillary walls)
Leaked clotting
proteins form interstitial
clots that wall off area
to prevent injury to
surrounding tissue
Swelling
Possible temporary
impairment of
function
Temporary fibrin
patch forms
scaffolding for repair
Healing
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Leukocytes migrate to
injured area
Diapedesis
(leukocytes pass through
capillary walls)
Phagocytosis of pathogens
and dead tissue cells
(by neutrophils, short-term;
by macrophages, long-term)
Pus may form
Area cleared of debris
Figure 21.4 Phagocyte mobilization.
Innate defenses
Slide 1
Internal defenses
Opsonizationmarked for
destruction
Inflammatory
chemicals
diffusing
from the
inflamed
site act as
chemotactic
agents.
1 Leukocytosis.
Neutrophils enter
blood from bone
marrow.
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2 Margination.
Neutrophils cling
to capillary wall.
4 Chemotaxis.
Neutrophils follow
chemical trail.
Capillary wall
Basement
membrane
Endothelium
3 Diapedesis.
Neutrophils flatten
and squeeze out of
capillaries.
Antimicrobial Proteins
• Include interferons (interfere with viral
reproduction)
• and complement proteins
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Figure 21.5 The interferon mechanism against viruses.
Innate defenses
Slide 1
Internal defenses
Virus
Viral nucleic acid
1 Virus
New viruses
enters cell.
2 Interferon
genes switch
on.
5 Antiviral
proteins
block viral
reproduction.
Antiviral
mRNA
DNA
Nucleus
mRNA for
interferon
3 Cell
produces
interferon
molecules.
Interferon
receptor
Host cell 1
Infected by virus;
makes interferon;
is killed by virus
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Interferon
Host cell 2
Binds interferon
from cell 1; interferon
induces synthesis of
protective proteins
4 Interferon binding
stimulates cell to
turn on genes for
antiviral proteins.
Complement
• Unleashes inflammatory chemicals that
amplify all aspects of inflammatory
response
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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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Fever
• 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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Antigens
• Substances that can mobilize adaptive
defenses and provoke an immune
response
• Targets of all adaptive immune responses
• nonself
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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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Table 21.3 Overview of B and T Lymphocytes
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Figure 21.11a Clonal selection of a B cell.
Adaptive defenses
Humoral immunity
Primary response
(initial encounter
with antigen)
Activated B cells
Plasma cells
(effector B cells)
Secreted
antibody
molecules
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Proliferation to
form a clone
Antigen
Antigen binding
to a receptor on a
specific B lymphocyte
(B lymphocytes with
noncomplementary
receptors remain
inactive)
Memory B cell—
primed to respond
to same antigen
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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Passive Humoral Immunity- SOMEONE or
thing PASSES these on to you
•
Two types
1. Naturally acquired—antibodies delivered to
fetus via placenta or to infant through milk
2. Artificially acquired—injection of serum,
such as gamma globulin
•
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Protection immediate but ends when antibodies
naturally degrade in body
Figure 21.13 Active and passive humoral immunity.
Humoral
immunity
Active
Naturally
acquired
Infection;
contact
with
pathogen
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Artificially
acquired
Vaccine;
dead or
attenuated
pathogens
Passive
Naturally
acquired
Antibodies
passed from
mother to
fetus via
placenta; or
to infant in
her milk
Artificially
acquired
Injection of
exogenous
antibodies
(gamma
globulin)