Transcript Adv Phys Immune System

ADVANCED
PHYSIOLOGY
IMMUNE
SYSTEM
Instructor Terry Wiseth
IMMUNE SYSTEM
Two major categories of immune mechanisms
Nonspecific immunity
Specific immunity
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Nonspecific Immunity
includes mechanisms that resist a variety of
threatening agents or conditions
Nonspecific Immunity means that these
immune mechanisms do not act on one or two
specific invaders, but rather provide a more
general defense by simply acting against any
thing recognized as not self
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Specific Immunity
involves mechanisms that recognize specific
threatening agents and respond by targeting
their activity against these specific agents
These mechanisms often take some time to
recognize their targets and react with
sufficient force to overcome the threat
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Cells of Nonspecific
Immunity
Natural-Killer (NK) cells
Neutrophils
Monocytes
Macrophages
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Nonspecific Immunity
Skin and mucous membranes
Antimicrobial substances
Natural Killer Cells (NK)
Phagocytosis
Inflammation
Fever
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Nonspecific Immunity
Skin and mucous membranes
Antimicrobial substances
Natural Killer Cells (NK)
Phagocytosis
Inflammation
Fever
7
Skin and Mucous
Membranes
Internal environment of the human body is
protected by a continuous mechanical barrier
formed by the cutaneous membrane (skin) and
mucous membranes
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Skin and Mucous
Membranes
Often called the first line of defense
Besides forming a protective wall, the skin
and mucous membranes operate various
additional immune mechanisms
Mechanical barriers
Chemical barriers
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Mechanical and
Chemical Barriers
Sebum
Contains pathogen-inhibiting agents
Mucus
Pathogens may stick and be swept away
Viscosity inhibits microbe movements
Enzymes
May hydrolyze pathogens
Lysozymes
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Mechanical and
Chemical Barriers
Hydrochloric acid
May destroy pathogens
Sweat, tears, saliva
Dilution and washing action
Also contain enzymes which inhibit
microbial growth
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Nonspecific Immunity
Skin and mucous membranes
Antimicrobial substances
Natural Killer Cells (NK)
Phagocytosis
Inflammation
Fever
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Antimicrobial
Substances
2nd line of defense
Contained within blood and interstitial fluid
Transferrins
Interferons
Complement
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Transferrins
Fe++ binding proteins in blood
Inhibit microbial growth by binding free Fe++ in
blood
++
Fe
Transferrin
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Interferons
Stimulates phagocytosis
Inhibits viral replication
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Interferon
Cells invaded by viruses may respond
rapidly by synthesizing the protein
interferon and releasing it into
circulation
Interferon interferes with the ability of
viruses to cause disease by preventing
the viruses from multiplying in the cell
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Interferon
Interferon is produced within a cell that has
been invaded by a virus
Virus
Anti viral protein
Interferon
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Interferon
 Intron A
Kaposis sarcoma
Genital herpes
Hepatitis B and C
Betaseron
Slows progression of MS
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Complement
Is the name given to
each of a group of
about twenty (20)
inactive enzymes in
the plasma
activated in a
cascade of chemical
reactions triggered by
either specific or
nonspecific
mechanisms
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Complement
Complement or
enhance immune,
allergic and
inflammatory
reactions
The complement
cascade causes
lysis of the foreign
cell that triggered it
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Complement
Proteins are given names C1 through C9, B, D, P
C3 activation is the key to the complement
cascade
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Complement
C3 activation may occur in two ways
Classical pathway
Alternative pathway
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Classical Pathway
Complexes formed between antibodies and
antigens of microbes
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Classical Pathway
Complexes formed between antibodies and
antigens of microbes
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Classical Pathway
Complexes formed between antibodies and
antigens of microbes
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Alternative Pathway
Polysaccharides on microbes can directly
trigger C3
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Complement and
Alzheimer’s Disease
Beta-amyloid is a peptide that is the major
component of senile plaques within
Alzheimer's disease brains
May trigger an immune response that
significantly contributes to the disease
process
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Complement and
Alzheimer’s Disease
Beta-amyloid binds very specifically to a
protein which is part of the complementary
protein group and activates the protein
There is clear evidence of activated
complement proteins near senile plaques
and on damaged neurons in Alzheimer's
disease, and it appears that beta-amyloid
triggers this response by its binding to
complementary proteins
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Complement and
Alzheimer’s Disease
Complement proteins are usually released
from liver cells but appear to originate in
Alzheimer's disease brain from glial cells that
surround senile plaques
It is possible to inhibit the activation of
complement by beta-amyloid without
affecting the ability of
complement to respond
in the rest of the body
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Complement and
Alzheimer’s Disease
The results suggest that it may be possible to
develop drugs which specifically inhibit
complement activation in the Alzheimer's
disease brain without causing general immune
suppression
There is increasing evidence that much of
the neuropathology seen in the
Alzheimer's disease brain
results from a chronic
immunoinflammatory
reaction to senile plaques
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Complement
Activated C3 will cascade the complement
resulting in:
Activation of the inflammatory response
Opsonization
Cytolysis
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Activation of
Inflammatory Response
Arteriole dilation
Cells release histamine
Increases capillary permeability
Enhances WBC mobility
Complements act as chemostatic agents
attracting other WBC
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Opsonization
C3 coats the microbes and promotes
phagocytosis
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Opsonization
C3 coats the microbes and promotes
phagocytosis
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Cytolysis
Numerous complement proteins form a
membrane attack complex (MAC)
Punches hole in the microbial membrane
Microbe ruptures
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Nonspecific Immunity
Skin and mucous membranes
Antimicrobial substances
Natural Killer Cells (NK)
Phagocytosis
Inflammation
Fever
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Natural Killer Cells (NK)
3rd line of defense
a group of lymphocytes that kill many types of
tumor cells and cells infected by different
kinds of viruses
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Natural Killer Cells (NK)
Found in the spleen, lymph nodes, red marrow
Lack antigen receptors
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Natural Killer Cells (NK)
Release interferons
Release perforins which cause cytolysis of the
microbe
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Natural Killer Cells (NK)
Attack cells which lack MHC antigens
NK cells are decreased in AIDS victims
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Nonspecific Immunity
Skin and mucous membranes
Antimicrobial substances
Natural Killer Cells (NK)
Phagocytosis
Inflammation
Fever
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Phagocytosis
Is the ingestion and destruction of
microorganisms or other small particles by
phagocytes
Neutrophils (phagocytes)
Macrophage (scavenger)
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Phagocytosis
Macrophages are phagocytic monocytes that
have grown to several times their normal size
after migrating out of the blood stream
Digestion and killing
Fuses lysozyme vesicles with engulfed
microbes in cytoplasm
Release defensins
Active against bacteria, fungi, viruses
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Phagocytosis
Three phases to phagocytosis
Chemotaxis
Adherence
Ingestion
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Chemotaxis
Kinins, microbial products
Chemical attraction
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Adherence
Attachment
Opsonization by complement assists
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Ingestion
Engulf bacteria or antigen
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Phagocytosis
Some microbes are ingested but not killed
Staphylococcus produce toxins which kill
phagocytes
TB multiply within the phagocytes
Tularemia and brucellosis may lie dormant
for months to years
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Phagocytes
The densest populations of phagocytes occur
in the bone marrow, thymus gland, lymph
nodes, and spleen
From these structures, lymphocytes enter the
blood and distribute themselves throughout
the tissues of the body
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Phagocytes
After wandering throughout
the tissue spaces, they
eventually make their way
into lymphatic tissues
Lymph flow transports the
lymphocytes through a
succession of lymph nodes
and lymph vessels and
empties them into veins
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Nonspecific Immunity
Skin and mucous membranes
Antimicrobial substances
Natural Killer Cells (NK)
Phagocytosis
Inflammation
Fever
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Inflammatory Response
tissue damage elicits many responses that
counteract the injury and promote a return to
normal
Bacteria cause tissue damages
triggers the release of mediators from cells
such as mast cells found in connective
tissue
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Inflammation
Response to stress of tissue damage
Symptoms include:
Loss of function in injured area
Redness
Pain
Heat
Swelling
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Inflammation
Inflammation helps to restore homeostasis
Stages of inflammation
1) vasodilation
2) phagocyte migration
3) tissue repair
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Vasodilation
Blood vessels
Become more permeable
Dilate
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Vasodilation
Increased
blood flow
Allows
defensive
mediators to
leave blood
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Inflammation
Defensive mediators
Clot-forming chemicals
Antibodies
Phagocytes
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Inflammation
Histamine released by injured cells brings on
vasodilation
Also attract phagocytes
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Inflammation
Kinines,
prostaglandins,
leukotrienes and
complement promote
actions of histamine
Kinins and
prostaglandins induce
pain associated with
inflammation
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Cytokines
Small protein homones
Stimulate or inhibit growth or differentiation of
cells
Secreted by lymphocytes, APC, fibroblast,
endothelial cells, monocytes
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Cytokine Function
Chemotactic factors
attracts macrophages causing hundreds of
then to migrate into the vicinity of the
antigen bound, sensitized T-cells
Macrophage activating factor
causes the macrophages to destroy
antigens by phagocytosing them at a rapid
rate
Lymphotoxin
powerful poison that acts more directly,
quickly killing any cell it attacks
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Inflammation
Pus
Collection of dead cells, fluids
Abscess develops when pus cannot drain
away
Pimples, boils
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Inflammation
Phagocytes arrive about 1 hour after
inflammation
Neutrophils
Arrive first
Die quickly
Monocytes
Arrive after neutrophils
Modify into macrophages
More powerful and longer lived than
neutrophils
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Atopic Dermatitis (Eczema)
A skin disease characterized by itchy, red,
inflammed portions of the skin
Scientists have found that people with atopic
dermatitis have a low level of a cytokine (a
protein) that is essential to the healthy
function of the body's immune system and a
high level of other cytokines that lead to
allergic reactions
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Nonspecific Immunity
Skin and mucous membranes
Antimicrobial substances
Natural Killer Cells (NK)
Phagocytosis
Inflammation
Fever
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Fever
Abnormally high body temperature
Bacterial toxins trigger release of interleukin
Interleukins
Reset body thermostats
Intensify effects of interferons
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Interleukin
Causes fever
Stimulates proliferation and activation of:
Helper T-cells
Killer T-cells
B-cells
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Specific Immune System
The various types of specific immune
mechanisms attack specific agents that the
body recognizes as "not self"
Antigens
Substances that are recognized as
foreign and invoke an immune response
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Specific Immune System
Two types of
specific immune
responses are
mediated by two
different types of
cells
The two types of
immune responses
are:
1) Antibody mediated
2) Cell mediated
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Specific Immune System
Specific immunity is orchestrated by two
different classes of lymphocytes
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Cells of Specific
Immunity
Lymphocytes are formed in red
bone marrow and are derived
from primitive cells called stem
cells
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Cells of Specific
Immunity
Stem cells destined to become lymphocytes
follow two developmental paths and
differentiate into two major classes of
lymphocytes
B-lymphocytes or B-cells
T-lymphocytes or T-cells
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B Cells
Originate, mature and develop in bone marrow
B-cells do not attack pathogens
Produce antibodies that attack pathogens or
direct other cells, such as phagocytes, to
attack them
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B Cells
B-cell mechanisms are often classified as
antibody-mediated-immunity (AMI) or humoral
immunity
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T Cells
Originate in bone
marrow
Mature and develop in
the thymus
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T Cells
Proliferate into “killer” T-cells and “helper”
T-cells
Attack pathogens more directly
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T Cells
T-cell immune mechanisms are classified as
cell-mediated-immunity (CMI)
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TWO
TYPES OF
SPECIFIC
IMMUNE
RESPONSE
78
TWO
TYPES OF
SPECIFIC
IMMUNE
RESPONSE
79
Antibody Mediated
Immunity
Functions in defense against:
Dissolved antigens
Extracellular pathogens
Bacteria
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Humoral Response
Antibody Mediated
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Humoral Response
Antibody Mediated
82
Cell Mediated Immunity
Functions in defense against:
Intracellular pathogens
Fungi, parasites, virus
Cancer cells
Foreign tissues
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Cell Mediated Immunity
84
Specific Immune
Response
Antibody mediated and Cell mediated immune
responses are very complex in how they
function
Both responses involve common or similar
process and factors
Antigens
Cytokines
Antibodies
Epitopes
Interleukins
B-cells
MHC
Interferons
T-cells
APC
Perforins
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Antigens
Substances which provoke the immune
system
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Antigens
May consist of:
1) Microbes or parts of microbes
2) Bacterial toxins
3) Allergens
pollen, egg white, etc
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Antigens
4) Transplanted tissue cells
5) Large complex molecules
proteins, glycoproteins, lipoproteins
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Antigens
6) Some smaller substances can act as
antigens if combined with a body protein
Ex. Lipid toxin can combine with body
protein to form a complex which initiates
immune response
Poison ivy
Allergic reactions to drugs
Penicillin
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Antigens
7) Allergic
reactions to
chemicals in the
environment
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Non-antigenic
Large molecules that have simple repeating
units are not antigenic (cellulose, plastics)
That is why plastics work as artificial hearts
and joints
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Epitopes
Specific portions of antigens trigger immune
responses
Immune system capable of recognizing at
least a billion epitopes
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Epitopes
Receptor molecules complementary to
antigen epitopes are located on cell
membrane of T-cells and B-cells
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MHC Antigens
Major histocompatibility complex antigens are
found on body cells
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MHC Antigens
Unique to the individual
Number in the thousands
Mark body cells as “self”
Help T-cells recognize foreign invaders
Found on cell membranes
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MHC –I
Markers of “self”
Alert killer T-cells to presence of body cells
that have changed due to viral infection or
transformed to cancer cells
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MHC-II
B-cells, macrophages
MHC-II is combined with ingested antigens
and presented as a complex on the B-cell
membrane to T-cells
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Antigen
If foreign antigen is detected by B-cells and T-
cells the immune response is initiated
B-cells can recognize and bind to antigens
in extracellular fluids
T-cells can recognize fragments of antigen
only if presented in association with MHC by
antigen presenting cells (APC)
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Antigen
Epitope binding and presentation
of viral epitope on MHC-1
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Antigen
T-cell binding to MHC-1 molecule
100
Antigen
T-cell recognition of MHC-2
molecule
101
Antigen
B-cell activated antibody
production
102
APC (Macrophages)
After macrophages engulf antigen, pieces of
antigen are associated with MHC and
subsequently presented as MHC-antigen
complex on cell membrane
103
APC
After antigen processing, APC cells migrate to
lymphatic tissue and present MHC-antigen
complex to T-cells
APC cells located in
Skin
Respiratory
Urinary
Reproductive tracts
Lymph nodes
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T-cells
T-cells with correctly shaped receptors that
match the presented MHC-antigen complex
trigger:
1) Cell-mediated immune response (CMI)
2) Antibody-mediated immune response (AMI)
105
Immune Activation
106
Antibodies
Antibodies are glycoproteins of the family
called immunoglobulins (Igs)
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Antibodies
Each immunoglobulin molecule consists of
four polypeptide chains joined together by
disulfide bonds (S-S)
108
Antibodies
Each polypeptide chain is folded to form
globular regions that are joined together in
such a way that the whole molecule is Yshaped
109
Antibodies
Each of us is thought
normally to have millions
of different kinds of
antibody molecules in our
bodies
Each of these has its
own uniquely shaped
combining sites
Antigen binding sites
are in variable regions
110
Antibodies
It is this structural feature that enables
antibodies to recognize and combine with
specific antigens
both of which are crucial first steps in the
body's defense against microbes and other
foreign cells
111
Functions of Antibodies
The function of antibody molecules is to
produce antibody-mediated immunity
This type of immunity is also called humoral
immunity because it occurs within the
plasma
112
Antibodies
Antibodies function to:
1) Neutralize toxins, viral attachments
2) Immobilization of bacteria, flagella, cilia
3) Agglutination, clumping of bacteria, cells
4) Activation of complement, classical
pathway
5) Enhancing phagocytosis (opsinization)
6) Provide fetal newborn immunity
113
Antibody Function
114
Antigen-Antibody
Reactions
Antibodies fight disease by distinguishing
non-self antigens from self antigens
Recognition occurs when an antigen's
epitopes fit into and bind to an antibody
molecule's antigen-binding sites
115
Antigen-Antibody
Reactions
The binding forms an antibody-antigen
complex that may produce one or more effects
It transforms antigens that are toxins into
harmless substances
It agglutinates antigens that are molecules
on the surface of microorganisms which
makes them stick together so phagocytes
can engulf them
116
Antigen-Antibody
Reactions
Neutralization of bacteria by antigen-antibody
reactions
117
Classes of Antibodies
There are five (5) classes of antibodies
identified by letter names as immunoglobulins
M
G
A
E
D
118
Ig M (Immunoglobulin M)
5-10 % of Igs
Activate complement
Is the antibody that
immature B cells synthesize
and insert into their plasma
membranes
Is the predominate class of
antibody produced after
initial contact with an
antigen in the blood
119
Ig G (Immunoglobulin G)
Most abundant circulating
antibody
Normally makes up about
75% of the antibodies in
the blood
Enhances phagocytosis
Able to pass the placenta
from mother to fetus
Confers immune
protection to newborn
120
Ig A (Immunoglobulin A)
Constitutes about 15%
Major class of antibody present in the mucous
membranes of the body, in saliva, sweat, milk
and in tears
121
Ig E (Immunoglobulin E)
Minor in amount (less than 0.1%)
Can produce harmful effects such as those
associated with allergies and hypersensitivity
122
Ig D (Immunoglobulin D)
Constitutes less than 1%
Activates B-cells
Protects against parasitic worms
123
B-Cells and AntibodyMediated Immunity
B-cells start their development in the
embryonic yolk sac, then the red marrow or
fetal liver
By the time a human infant is a few months
old, its pre-B-cells have completed the first
stage of development
Are then known as
inactive B-cells
124
B-Cells and AntibodyMediated Immunity
 Inactive B-cells synthesize antibody molecules but
secrete few if any of them
Instead, they insert on the surface of their plasma
membranes perhaps 100,000 antibody molecules
The combining sites of these surface antibody
molecules are now ready to serve as receptors
for a specific antigen if it comes by
125
B-Cell Activation
126
B-Cells and AntibodyMediated Immunity
After being released from the bone marrow,
inactive B-cells circulate to the lymph nodes,
spleen, and other lymphoid structures
Occurs when the inactive B-cells become
activated
127
B-Cells and AntibodyMediated Immunity
Activation of a B-cell
must be initiated by an
encounter between an
inactive B-cell and its
specific antigen
The antigen binds to
these antibodies on
the B-cell's surface
128
B-Cells and AntibodyMediated Immunity
Antigen-antibody binding activates the B-cell
triggering a rapid series of mitotic divisions
129
B-Cells and AntibodyMediated Immunity
 By dividing rapidly, a single B-cell produces a clone mass
Some of them become differentiated to form plasma
cells
Others do not differentiate completely and remain in
lymphatic tissue as memory B-cells
130
Plasma B-Cells
Plasma cells synthesize and secrete large
amounts of antibody
2000 molecules/sec for 4-5 days or until
plasma cell dies
131
Memory
B-Cells
 Memory B-cells do not
themselves secrete
antibodies
 if they are later exposed to
the antigen that triggered
their formation
memory B-cells become
plasma cells and the
plasma cells secrete
antibodies that can
combine with the
initiating antigen
132
Memory B-Cells
The ultimate function of B-cells is to serve as
ancestors of antibody-secreting plasma cells
133
Humoral
Immunity
134
Humoral Immunity
135
Humoral Immunity
136
Humoral Immunity
137
Humoral Immunity
138
T-Cells and CellMediated Immunity
T-cells are lymphocytes that have made a
detour through the thymus gland before
migrating to the lymph nodes and spleen
During their residence in the thymus, pre-Tcells develop into thymocytes
139
T-Cells and CellMediated Immunity
Thymocytes divide up to
three times/day and their
numbers increase
enormously in a relatively
short period of time
They leave the thymus and
move into the blood and
take up residence in lymph
nodes and spleen
now are known as T-cells
140
Activation and Function
of T-Cells
Each T-cell, like each B-cell, displays unique
antigen receptors in its surface membrane
When an antigen (preprocessed and
presented by macrophages) encounters a Tcell whose surface receptors fit the antigen's
epitopes, the antigen binds to the T-cell's
receptors
141
Activation and Function
of T-Cells
An antigen bound T-Cell activates or
sensitizes the T-cell, causing it to divide
repeatedly to form a clone of sensitized T-cells
The sensitized T-cells then travel to the site
where the antigen originally entered the body
142
Activation and Function
of T-Cells
There in inflamed tissue,
the sensitized T-cells bind
to antigens of the same
kind that led to their
formation
T-cells will bind to their
specific antigen only if
the antigen is presented
by a macrophage
143
Activation and Function
of T-Cells
The antigen-bound sensitized T-cells then
release chemical messengers into the
inflamed tissues called cytokines
144
Types of T-cells
Helper T-cells
Killer T-cells
Suppressor T-cells
Memory T-cells
145
Helper T-cells
 TH
Cooperate with B-cell to amplify antibody
production by plasma cells
Secrete interleukins which stimulates
proliferation of T and B cells
146
Helper T-cells
 TH
Cooperate with B-cell to amplify antibody
production by plasma cells
Secrete interleukins which stimulates
proliferation of T and B cells
147
Killer T-Cells
 TC
Cytotoxic , Killer T-cells
148
Killer T-Cells
Recognize foreign antigens presented by:
1) body cells infected by virus
2) some tumor cells
3) cell of tissue transplant
Requires Helper T-cells to be activated
Sensitized T-cells then release lymphotoxin
which kill target cells
149
Suppressor T-Cells
 TS
Inhibit proliferation of T-cells
Dampens immune response
150
Memory T-Cells
Programmed to recognize original invading
antigens
Able to initiate a swift reaction on subsequent
infections
151
T-Cell Summary
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152
Types of Specific
Immunity
Inherited immunity
Immunity to certain diseases develops
before birth
Acquired immunity
Exposure to the causative agent is not
deliberate
Natural
Artificial
153
Natural Acquired
Immunity
Active
A child develops measles and acquires an
immunity to subsequent infection
Passive
A fetus receives
protection from the
mother through the
placenta, or an infant
receives protection by
way of the mother's milk
154
Artificial Acquired
Immunity
Exposure is deliberate
Active
Injection of the causative agent, such
as vaccination against polio, confers
immunity
Passive
Injection of immunoglobulins
(antibodies) that were developed by
another individual's immune system
155
Disorders of the Immune
System
 AIDS
 Chronic Fatigue Syndrome
 Severe Combined Immunodeficiency (SCID)
 Allergy
 Tissue Rejection
 Hodgkin’s Disease
 Autoimmune Disease
Lupus
Multiple Sclerosis
Myasthenia Gravis
Graves Disease
156
AIDS
HIV attack T-cells
157
Chronic Fatigue
Syndrome
Extreme fatigue
Lowered levels of corticotropin releasing
hormone and cortisol
158
Severe Combined
Immunodeficiency
Both B-cells and T-cells are missing or
inactive
Caused by mutated genes
Infusions of red marrow from sibling provide
normal stem cells
David “bubble boy”
159
Allergy
Overly reactive to
antigen that is
tolerated by most
others
160
Type I Allergies
Anaphylaxis
Most common allergic reaction
Cells release histamine which causes
bronchiole constriction
Bee sting
Treated with epinephrine
161
Type II Allergies
Cytotoxic
Cells damaged by lysis
Incompatible transfusion reactions
162
Type III Allergies
Immune complex
Complexes of antigen-antibody which are
small and escape phagocytosis
Accumulate in blood vessel lining causing
inflammation
Rheumatoid arthritis, systemic lupus,
glomerulonephritis
163
Type IV Allergies
Delayed type hypersensitivity
Carried by macrophages which have been
activated by T-cells
Symptoms occur 12-72 hours after exposure
Skin tests for TB
164
Tissue Rejection
Immune system recognizes transplanted
tissues as antigens
Immunosuppressive drugs suppress entire
immune system
Cyclosporin
Inhibits secretion of
interleukins by Helper
T-cells but does not
impact B-cells
165
Hodgkin’s Disease
Cancer usually arising in lymph nodes
Considered a curable disease
Lymph node
Malignant cells
166
Autoimmune Disease
Lupus
Multiple Sclerosis
Myasthenia Gravis
Grave’s Disease
167
Lupus
Inflammatory, non-contagious
disease of connective tissue
Blood vessel damage results in
release of chemicals causing
inflammation
Skin lesions, rashes
168
Multiple Sclerosis
immune cells mistake myelin as a foreign
invader and attack it
the protective coating on nerve fibers (myelin)
becomes detached and eventually destroyed
MS can affect vision, sensation, coordination,
movement and bladder and bowel control
169
Myasthenia Gravis
Disease affecting the neuromuscular junction
and producing weakness of voluntary muscles
Receptors for acetylcholine at the muscle
surface are destroyed
Healthy
Ach
receptors
Destroyed
Ach
receptors
170
Myasthenia Gravis
Voluntary muscles of the eyes are commonly
affected
Three different serial pictures to demonstrate fatigue
of eyelid muscles as the patient keeps looking up
After a few minutes of rest, the eyelids have returned to
near-normal position
171
Grave’s Disease
Antibodies are produced against certain
proteins on the surface of thyroid cells
Stimulating those cells to overproduce thyroid
hormones
Results in an overactive thyroid
172
Grave’s Disease
The immune system also attacks the tissue
behind the eyes and the skin of the lower legs
Tissues behind the eye attract and hold water
When this happens, the tissues and muscles
swell, causing the eyeball to move forward in
the orbit
173
End
Immune System