Download Body Defenses

4/2/13
Lymphoid Organs
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Body Defenses
Lymphoid tissues and organs –
provide defense against disease by:
  Housing and facilitating the
maturation of lymphocytes
  Cleansing the lymph of
pathogens
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Keri Muma
Bio 6
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Body Defenses
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Body Defenses
Body defense mechanisms are aimed at
eliminating abnormal cells or any foreign
materials that are not self
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Invading pathogens (viruses, bacteria, ect.)
Removal of worn out cells, damaged tissue
Identification and destruction of abnormal or
cancerous cells
Rejection of foreign tissue
Inappropriate responses can lead to allergies or
autoimmune diseases
Innate (nonspecific) system responds quickly
and consists of:
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First line of defense – physical barriers; intact skin
and mucosa prevent entry of microorganisms
Second line of defense – antimicrobial proteins,
phagocytes, and other cells
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Inhibit spread of invaders throughout the body
Inflammation is its hallmark and most important
mechanism
The body has two defense systems – that
differ in timing and specificity yet are interactive
and interdependent
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Body Defenses
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Lymph nodes
Tonsils
MALTs (mucus associated lymph
tissue)
Spleen
Thymus
Bone Marrow
Innate immunity
Adaptive or Acquired immunity
Engulfing and Destroying Pathogens
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Neutrophil and
macrophage destruction
of bacteria
Phagocytosis:
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Engulfs foreign material
into a vacuole
Enzymes from lysosomes
digest the material
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Innate Immunity
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The inflammatory response is triggered
whenever body tissues are injured physically
or by infection
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Prevents the spread of damaging agents to
nearby tissues
Disposes of cell debris and pathogens
Sets the stage for repair processes
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Inflammation is mediated by phagocytes
Toll-like receptors (TLRs) present on phagocytes recognize
and bind to foreign microbes and those that have been
marked by an opsonin (complement protein or antibody)
Activated TLRs triggers the phagocyte to:
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Engulf and destroy the pathogen
And/or release chemicals that promote inflammation
The four cardinal signs of acute inflammation
are redness, heat, swelling, and pain
Inflammatory Response
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Inflammation
Inflammatory chemicals are released into the
extracellular fluid by injured tissue,
phagocytes, lymphocytes, and mast cells
Inflammatory chemicals:
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Include kinins, histamine, prostaglandin,
complement, and cytokines.
  Cause local blood vessels to dilate, resulting in
hyperemia (heat and redness)
  Capillaries become “leaky” (edema and pain)
  Attract other WBCs to the area
Mobilization
of WBC
Inflammatory Response
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Mobilization of WBC – leukocytes emigrate
from the blood into the tissues
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Additional neutrophils are released from the bone
marrow in response to leukocytosis-inducing
factors released by injured cells
Margination – neutrophils cling to the walls of
capillaries in the injured area
Diapedesis – neutrophils squeeze through
capillary walls
Chemotaxis – inflammatory chemicals attract
neutrophils to the injury site and they begin
phagocytosis
Inflammation
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Other Secreted Chemicals
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Pyrogens – secreted by macrophages
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Cause hypothalamus to elevate the body’s set
temperature (fever)
Moderate fever can be beneficial, as it causes:
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Antimicrobial Proteins
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Enhance the innate defenses by:
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The liver and spleen to sequester iron and zinc
(needed by microorganisms to grow and divide)
Increase rate of chemical reactions which speeds
up tissue repair
Antimicrobial proteins
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Innate Immunity
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Attacking microorganisms directly
Hindering microorganisms’ ability to reproduce
The most important antimicrobial proteins are:
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Interferon
Complement proteins
Defense Cells
Interferon
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Released by virus infected
cells and binds to receptors
on neighboring healthy cells
Interferon protects these
neighbors by activating genes
for PKR (an antiviral protein)
PKR nonspecifically blocks
viral reproduction in the cell if
it becomes infected
Also slows division of tumor
cells
Enhances natural killer cells
Antimicrobial Proteins
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Natural killer cells
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Lyse and kill cancer cells and virus- infected cells
on first exposure to them
Immediate and nonspecific response
Immunosurveillance
Body Defenses
Complement
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25 or so proteins that circulate in the blood in an inactive form
Forms membrane attacking complex that punch holes in foreign
cell’s membrane
Also act as opsonins and chemotaxins
Activated by:
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Exposure to carbohydrate chains on the surface of micro-organisms
Exposure to antibodies produced by the adaptive immune response
against the micro-organism
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Adaptive (specific) defense system
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Third line of defense – mounts attack against
particular foreign substances
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Takes longer to react than the innate system
Targets invaders that the body has previously been
exposed to
Involves lymphocytes
Works in conjunction with the innate system
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Characteristics of Adaptive Immunity
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The adaptive immune system is:
antigen-specific - requires the production of specific
lymphocytes and antibodies against a specific antigen
systemic - not restricted to the initial infection site
has memory -second encounter causes a more rapid and
vigorous response
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Antigens - any substance capable of provoking an
immune response
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Adaptive Immunity
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Antigens include foreign protein, nucleic acid, some lipids,
and large polysaccharides
It has two separate but overlapping
branches:
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Lymphocytes - originate from stem cells in
the red bone marrow
Each lymphocyte is equipped with:
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Immunocompetent – cells display a unique type
of receptor that responds to a distinct antigen
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Become immunocompetent before they encounter
antigens they may later attack
Are exported to secondary lymphoid tissue where
encounters with antigens occur
Mature into fully functional antigen-activated cells
upon binding with their recognized antigen
a unique receptor that binds a specific antigen
and a MHC receptor that distinguishes and
recognizes “self”
Cells of the Immune System
Immunocompetent B or T cells
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Humoral, or antibody-mediated immunity
Cellular, or cell-mediated immunity
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B lymphocytes become immunocompetent
in the bone marrow
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Responsible for antibody-mediated immunity
Defend against extracellular pathogens by
producing antibodies
T lymphocytes become immunocompetent
in the thymus
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Responsible for cell-mediated immunity
Defend against intracellular pathogens and cancer
Maturation of T Cells
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T cells mature in the thymus under negative
and positive selection pressures
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Negative selection – eliminates T cells that are
strongly anti-self
Positive selection – selects T cells with a weak
response to self-antigens, which thus become
both immunocompetent and self-tolerant
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T Cell Selection in the Thymus
Antibody-Mediated Response
B-cells with specific receptors bind to a
specific antigen
The binding event activates the lymphocyte
to multiply (clonal selection)
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Most B cells become plasma cells that produce
antibodies to destroy antigens
Some B cells become long-lived memory cells
that will remain in the body to respond to the
antigen if exposed again
Figure 21.7
Antibody-Mediated Response
Antibodies (immunoglobulins)
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Antibodies – proteins that travel in the plasma
and combine with a specific antigen
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Example: blood types
Mark the antigens for destruction by specific or
nonspecific mechanisms
Y shaped molecules with variable region on the tips of
each arm that binds a specific antigen
Antibody Function
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Antibodies inactivate antigens in a number of
ways:
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Complement fixation – bind and lyse cell
Opsonization – mark antigen for phagocytosis
Neutralization – block harmful effects of toxins
Agglutination – clumping of foreign cells
Precipitation – clumping of antigens
Attract natural killer cells
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Antibody
Function
Cell Mediated Response
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Cell Mediated Response
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T cells can recognize and
bind antigens that are
presented to them by
antigen presenting cells
(macrophages)
APCs are macrophages
that engulf pathogens
and then present pieces
of the antigen to
lymphocytes.
Mechanisms of Cytotoxic T cells
Antigens must be presented by APC to a THelper cell
which triggers the cell to release cytokines that
stimulate division of various cells:
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Enhances proliferation of B-cells
and Cytotoxic T-cells which specialize in killing cancer
and virus infected cells
Mechanisms of Cytotoxic T cell
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Cytotoxic T cells bind to virus infected and
cancerous cells and destroy them by releasing:
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Perforins that punch holes in the target cells
membrane
Granzymes that cause the cell to undergo
apoptosis
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Immunological Memory
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Immunity – ability to defend against specific
invaders
Primary immune response – cellular
differentiation and proliferation, which occurs
on the first exposure to a specific antigen
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Immunological Memory
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Lag period: 3 to 6 days after antigen challenge
Peak levels of plasma antibody are achieved in 10
days
Antibody levels then decline
Primary and Secondary Responses
Secondary immune response – re-exposure
to the same antigen
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Sensitized memory cells respond within hours
Antibody levels peak in 2 to 3 days at much higher
levels than in the primary response
Antibodies bind with greater affinity, and their
levels in the blood can remain high for weeks to
months
Figure 21.10
Immunological Memory
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Active Immunity - B cells encounter
antigens and produce antibodies against
them
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Naturally acquired – response to a bacterial or
viral infection
Artificially acquired – response to a vaccine of
dead or attenuated pathogens
  Vaccines – spare us the symptoms of disease,
and their weakened antigens provide antigenic
determinants that build our immunity
Immunological Memory
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Passive Immunity -differs from active
immunity in that:
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B cells are not challenged by antigens
Immunological memory does not occur
Protection ends when antigens naturally degrade
in the body
Naturally acquired – from the mother to her fetus
via the placenta or IgA antibodies in breast milk
Artificially acquired – from the injection of serum
that contains the immunoglobulins
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Acquired Immunity
Immune Disorders
Hypersensitivity
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Allergies
Hypersensitivity - abnormal, vigorous immune
responses (overzealous immune system)
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Immediate hypersensitivity – occurs within seconds to 20
minutes
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Allergies and Asthma
  Plasma cells produce IgE antibodies which attach
to mast cells
  Mast cells release histamine – which causes
inflammation and itching
  Also releases a leukotriene called slow reactive
substance – causes smooth muscle contraction in
air ways
  Treated with anti-histamines and newer drugs that
block leukotrienes such as Singular
Hypersensitivity
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that is life-threatening
  Allergen directly enters blood
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Systemic histamine and SRS releases may result in:
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Immunodeficiencies
Anaphylactic Shock - systemic allergic response
Constriction of bronchioles
Sudden vasodilation and fluid loss from the bloodstream
Hypotensive shock and death
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Immunodeficiency - production or function of
immune cells is lacking or abnormal
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Treated with epinephrine
Delayed hypersensitivity - symptoms appear
after 1-3 days
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Severe combined immunodeficiency disease
(SCID)
  Deficiency of B and T-cells
Acquired Immune Deficiency Syndrome
  HIV destroys THelper cells
Inflammation caused by cytotoxic T-cells release of
lymphokines
Treated with corticosteroids
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Autoimmune Diseases
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Autoimmune - the immune system does not
distinguish between self and non-self
The body produces antibodies and cytotoxic
T-cells that attack its own tissues
Possible causes:
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Inefficient lymphocyte programming
Appearance of new self-antigens
Antibodies produced against foreign antigens
react with self-antigens (example: streptococcus
and rheumatic fever)
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