KEY CONCEPT
The immune systems
consists of organs, cells,
and molecules that fight
infections.
Immunology- Three lines
of defense
Barriers, Nonspecific responses,
specific-targeted response
First line of defense-Barriers
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Physical and chemical barriers
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Nonspecific-doesn’t distinguish, same for all
invaders
Skin-outer layer of tough,dead cells
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Mechanical barrier
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Constantly shedding
Bacteria can’t enter.
Sweat and oil glands- chemical barrier
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secrete acids
Sweat has lysozyme- breaks down cell walls.
Barriers continued
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Mucous membranes
Mechanical barrier
 Mucous traps pathogens
 Cilia moves trapped particles out of body
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Secretions
Saliva and tears
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washing action
Lysozyme enzymes breaks down cell walls.
Stomach acids, enzymes
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Destroy pathogens
Microorganisms in foods,drinks
Second line of defense
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Nonspecific- doesn’t single out a specific
pathogen.
When pathogens get through primary first
line of defense.
Includes
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Pathogen destroying white blood cells
Inflammatory response
Specialized proteins
White Blood Cells-wbcs
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bloodstream, interstitial fluid, and
lymphatic system
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attacking invaders
Macrophages ( big eaters) mainly in
interstitial fluid.
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macrophage engulfs the organism.
the pathogen is drawn into the macrophage,
where enzymes such as lysozyme kill the
pathogen.
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Neutrophiles-smaller and more numerous
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60-70% of wbcs.
Multilobed- PMNs
Neutrophils also kill by phagocytosis
neutrophil releases chemicals - kill the invading
pathogen. Chemicals also kill the neutrophil.
White blood cells can identify certain proteins and
carbohydrates on the surface of an invading
pathogen. These "foreign" molecules triggers the
cells' responses.
Pus- fluid containing wbcs and debri from dead tissue

Natural killer cell (NK)
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Do not kill pathogens directly
Recognize body cells that have become
infected by a virus
Release chemicals to break infected cell’s
membrane
Also attack cancer cells/ abnormal cells before
a tumor is formed.
Inflammatory Response
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Nonspecific defense characterized by 6 characteristics
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redness, heat, swelling, pain, fever phagocytosis.
mast cells release histamine
nearby blood vessels to dilate (expand).
Increases the volume of blood flowing to the injured
tissue.
Other chemicals attract additional phagocytes and other
white blood cells to the area, where they pass through
the leaky blood vessel walls into the interstitial fluid
Local increase of blood flow, fluid, and white blood cells
produces the redness, heat, swelling, and pain at the
injured area.

In fever, body temperature increases.
– Low fevers stimulate white blood cells to mature.
– High fevers can cause seizure, brain damage, and even
death.
During an inflammatory response, chemical signals trigger
changes in blood vessels and attract white blood cells that help
destroy the invaders.
Specialized Proteins
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Interferon
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a family of proteins produced by T-cells or virusinfected cells.
The infected cell may die, but its interferon reaches
healthy cells in the area, stimulating them to produce
proteins that interfere with virus reproduction.
Interferon is effective against many viruses and is
therefore nonspecific. Interferon seems to be
effective against viruses that cause the flu and the
common cold.
Genetically engineered
Infected cells produce interferon, which
stimulates non-infected cells to manufacture
substances that block virus reproduction.
Third line of defense
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Immune system
Specific
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Recognizes specific pathogens, cancer cells,certain
chemicals
Immune system must recognize self from
nonself.
Cells of the immune system
produce specific responses.
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Specific immune responses begin with the
detection of antigens.
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Antigens are surface proteins on pathogens.
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Means antibody generating.
Each pathogen has a different antigen.
antigens
virus
There are two specific immune responses.
1. Humoral immunity - B cells to produce antibodies.
antibodies
B cell
pathogen
T cell
memory B cells
activated B cells
2. Cellular immunity -T cells -destroys infected body
cells.
pathogen
antigens
antigens
T cell
receptors
memory T cells
activated T cells
Both responses produce memory cells.
B cell
T cell
– specialized T and B cells
– provide acquired (active) immunity
Immunity

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Resistance to a pathogen that causes
disease.
Antigens- large molecules of protein or
polysaccharides that induce a specific
response.
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Rarely can be lipids or nucleic acids
Small molecules are poor antigens
They are not attracted to macrophages.
Examples of antigens
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Bacterial capsules
Lipopolysaccharides of gram neg. bacteria
Glycoproteins in cell membranes
Attachment sites on viruses that interact
with mammalian cells.
Soluble bacterial toxins,venoms
Pollens, food, house dust
Properties of antigens
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Foreign to host
Capable of inducing an antibody response
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Large
Antibody must bind to the antigen
Epitope- Specific location on antigen that
combines with antibody
Hapten- if molecule is too small to induce an
antibody response by itself it combines with a
carrier molecule (protein). Ex. penicillin
Antibodies
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Antibodies- proteins found on the surface
of certain white blood cells, or in blood
plasma, that attach to particular antigens.
Also known as immunoglobulins- Ig
Specific B-Cell Receptor:
Immunoglobulin
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Composed of 4 polypeptide chains:
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Y shaped arrangement –
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2 identical heavy chains (H)
2 identical light chains (L)
ends of the forks formed by light and heavy chains
contain a wide range of variable antigen binding
sites
Variable regions
Constant regions
T-Cell Receptors for Antigen
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Formed by genetic recombination, with
variable and constant regions
2 parallel polypeptide chains
small, without humoral functions
Classes of Immunoglobulins
5 classes of Immunoglobulins (Ig):
1. IgG - long term immunity- crosses
placenta
2. IgA – secretory antibody- mucous
3. IgM – immediate response
4. IgD – receptor on B cells
5. IgE – allergic response
Classes of Antibodies(Ab)
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IgG
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2 antigen binding sites
Crosses placenta
80% of all immunoglobulins
IgM
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5 or more binding sites
Largest
Found in plasma
1st Ab after injection of antigen
Especially effective against gram negative bacteria
Immunity Titers
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IgA
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IgD
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Secretions of exocrine glands- mother’s milk
Saliva, tears
Effective against bacteria and viruses
2 sites
On B cells that recognizes antigens
Function difficult to determine
IgE
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Least amount
In allergic reactions
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Allergen- IgE- mast cells- histamine.
Lymphocytes
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Lymphocytes- special wbcs that recognize specific
invaders.
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In bone marrow, lymphocytic stem cells
differentiate into
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either T or B lymphocytic cells.
B cells mature in the bone marrow
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B- bursa of birds
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T cells migrate to thymus gland to mature.
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Mature T and B cells migrate to lymph nodes and
other parts of the lymphatic system.
All lymphocytes begin development in the bone marrow. B cells complete their
development there (think "B for bone"). T cells are transported to the thymus gland
where they mature (think "T for thymus").
B Cells and Humoral Immunity
Antibody proteins on the surface of B cells
act as specific receptors for antigens.
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~ 100 million different B cell surfaces
B Cells act primarily against bacteria and
viruses in body fluids outside of cells.
Humoral Immunity
Figure 31-12
A particular type of antigen activates a specific B cell. The activated B cell
produces a clone of millions of plasma cells that produce antibodies to the
specific antigen.
Steps:
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Activation occurs: B cell with matching antigen
receptor binds to the antigens of the pathogen.
B cell grows and clones itself, forming millions of
identical cells.
Each cell can become a plasma cell, which
produces and secretes antibodies specific to the
original antigen that activated the original B cell.
Plasma cells are carried by lymph and blood to
sites of infection in the body.
Termed humoral immunity since antibodies
travel in the blood and other body fluids once
called “humors”.
T cells and Cell-Mediated Immunity
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T cells directly attack infected host cells that
contain bacteria or viruses.
Each T cell has a receptor for a specific antigen.
Steps:
1. The infecting pathogen’s antigens are displayed on
the host body cell.
2. Activation occurs- the antigens on the host body cell
bind to receptors on the matching T cell, activating the T
cell.
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3. Activated T cell divides producing clones.
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4. T cell clones become cytotoxic T cells-
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5. Cytotoxic T cells attack infected cells.
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bind to infected cell membranes
secrete perforin - pokes holes in the membrane-leakage and
cell death.
Macrophages display the antigens of pathogens they have "eaten." This display
activates a specific version of helper T cells. The activated helper T cells in turn
stimulate cytotoxic T cells and B cells.
Role of Helper T Cells
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Role in both humoral and cellular
immunity.
Helper T cells are activated by binding to
macrophages that display antigens of a
pathogen.
Helper T cells then secrete chemicals that
activate both cytotoxic T cells and B cells
How the Immune System Remembers Pathogens

Memory B and T cells
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The first formation of T and B cells is called the
primary immune response.
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After the first exposure of a pathogen some of the B
and T cells remain in your body.
A slower and weaker response- requires time
Second exposure to the same pathogenSecondary immune response.
Quicker and stronger response- don’t develop
symptoms
Memory T cells produce cytotoxic T cells
Memory B cells produce plasma cells that secrete Ab
Passive and Active Immunity

Passive immunity- receive antibodies from another
source
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Antibodies to fetus from mother.
Travelers receive antibodies rather than antigens.
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hepatitis A
Lasts a short time- weeks or months
Active Immunity- your body produces antibodies
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Get disease.
Vaccines Heat killed dose of pathogen (antigen)
 Attenuated (very low, nonvirulent) dose of pathogen
 Booster shot- tetanus- additional dose of antigenneeded because initial memory cells have died
A vaccine stimulates the production of antibodies and memory cells that
protect against future exposure to the pathogen.