Transcript Immune System

By : Pooja Patel & Sarah Gianopoulos
Innate immunity—nonspecific, used against
many organisms:
 First line of defense includes barriers, such
as skin and molecules toxic to invaders
 Second line of defense includes phagocytic
cells, which ingest foreign cells and particles
 Most animals use innate immunity
Adaptive Immmunity—specific, used to
distinguish between substances that were made by
the organism or if they are foreign substances:
 Uses antibody proteins to recognize, bind to,
assist in destroying specific bacteria and viruses
 Adaptive immunity is slow to develop and long
lasting
 Innate immunity is much quicker to develop (096 hours)
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Phagocytes
 Large cells that engulf pathogens
and harmful substances
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Lymphocytes
 Include B and T cells
 B Lymphocytes differentiate and form antibody
producing cells and memory cells
 T Lymphocytes kill the virus infected cells and
regulate white blood cell activity
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Cytokines bind to cell surface receptors and
alter the behavior of their target cells
 Some can activate or inactivate B and T cells and
macrophages
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Antibodies are proteins, produced by B cells
that bind specifically to nonself substances
 Acts as a flag to make it easier for the immune system
cells to attack the invader
 Destruction done by inactivating/destroying harmful
pathogens, toxins and other microorganisms
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Major histocompatibility
complex (MHC)
• MHC proteins are important self-
identifying labels that make sure
the appropriate type of T cell binds
during immune responses.
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T cell receptors are integral
membrane proteins on T cells,
recognize and bind to nonself
molecules
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Skin
 Rarely penetrated by bacteria
 Skin’s saltiness is not an ideal environment for
bacterial growth
 Both harmless and helpful bacteria will have to
compete for space and nutrients on the skin
against pathogens and harmful substances
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Mucus
 Traps microorganisms and pathogens and is
carried away by cilia
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Lysozome (enzyme)
 Produced by mucus membranes and cleaves on
the cell walls of the bacteria, thus making the
harmful cell ‘lyse’
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Use of internal substances
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Defensins (peptides)
 Made by mucus membranes
 Hydrophobic and toxic to
several other pathogens
 Insert themselves into the
plasma membrane to make the
it permeable to water and
solutes, thus killing the harmful
substances
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Phagocytes ingest the harmful substance and
destroy it by 1 of 2 ways:
 Hydrolysis within
lysosomes
 Defensins
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Natural Killer Cells
 Distinguishing between healthy
and unhealthy cells
▪ Apoptosis for cancerous cells
▪ For other cells, Innate and Adaptive
defenses combine by lysing
antibody –labeled target cells
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Complement Proteins
 A system that activates several proteins in
sequence in order to lyse the invaded cell
▪ One complement protein acts as a flag to the
phagocytes as it binds to the invaded cells
▪ Next protein is activated to initiate the inflammation
response and signals to the phagocytes to the infection
site
▪ Then many other proteins now lyse the invaded cell
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Interferons
 Proteins that help increase resistance of
neighboring cells to infection
▪ Bind to receptors on the plasma membranes of the
uninfected cells to stimulate a pathway that inhibits viral
reproduction the other cells become infected
Inflammation
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Isolates the infected area to stop spreading
the damage
Brings in cells and molecules to kill off any
remaining pathogens and initiates the
healing process
Mast cells are cells adhering to skin and organ
linings; release chemical signals.
Tumor necrosis factor—cytokine that kills
target cells and activates immune cells
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Adaptive Immunity is:
 Specific
 Diverse
 Can distinguish between self and nonself
substances
▪ Clonal deletion
 Has immunological memory
Specificity:
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T cell receptors and antibodies
bind to specific nonself
molecules (antigens).
Specific sites on the antigens
are called antigenic
determinants.
The host responds to an
antigen’s presence with
highly specific defenses using
T cell receptors and
antibodies.
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Lymphocytes are usually activated by binding
to antigens to induce production of clones of
B Cells and T Cells-clonal selection.
To protect Self substances:
 Clonal deletion—Any immature B and T cells that
show the potential to mount an immune response
to self antigens undergo apoptosis.
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Primary Immune
Response
 Memory Cells
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Secondary Immune
Response
 Produces a quicker and
more powerful response
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Recognition phase—the organism
discriminates between self and nonself to
detect a pathogen.
Activation phase—the recognition event
leads to a mobilization of cells and molecules
to fight the invader.
Effector phase—the mobilized cells and
molecules destroy the invader.
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Cytotoxic T (TC) cells power the cellular
immune response.
An antigen is inserted into the membrane of
an antigen-presenting cell.
The antigen is recognized by a T-helper (TH)
cell, with a specific T cell receptor protein.
TH cell binding to the antigen-presenting cell
causes cytokine release.
Cytokines stimulate TC cells to divide.
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Humoral immune response involves B cells
that make antibodies.
Antigen is recognized when the it binds to a B
cell that has an antibody specific to that
antigen.
Antigen binding readies a B cell for division.
The TH cell bound to the B cell secretes
cytokines that stimulate the B cell to divide
and form a clone.
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The result of both types of immunities:
• A clone of B cells that can produce antibodies
specific for the antigen
• A clone of TC cells that express a T cell receptor
that can bind to any cell expressing the antigen on
its surface
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In the effector phase, B clone cells produce
antibodies that bind to free antigen— results
in inactivation and destruction of the antigen.
TC clone cells bind to cells bearing the antigen
and destroy them.
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B cells give rise to clones of plasma and
memory cells upon activation.
Plasma cells and B Cells secrete antibodies
into the blood stream.
• Some bind to the antigen on surface of a
pathogen.
• Some may use cross-linking function to form large
complexes to be destroyed by phagocytes.
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Antibodies all contain a tetramer of four
polypeptides.
In each molecule are two light chains and two
heavy chains, held together by disulfide bonds.
Each polypeptide chain has a constant region
and a variable region.
The constant region determines the general
structure and function of an immunoglobulin.
The variable region is different for each specific
immunoglobulin—responsible for antibody
specificity.
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IgG is secreted by B cells and constitutes
about 80 percent of circulating antibodies.
IgD is the cell surface receptor on a B cell.
IgM is the initial surface and circulating
antibody released by a B cell.
IgA protects mucosa on epithelia exposed to
the environment.
IgE binds to mast cells and is involved with
inflammation.
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Each mature B cell can produce only one
specific antibody with a specific amino acid
sequence.
The B cell genome:
• Each gene encoding an antibody is a supergene
assembled from many smaller genes.
 During B cell development the genes are cut out
and rearranged.
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DNA is rearranged or mutated to create high
diversity of antibodies.
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Cellular immune response involves:
• T-helper cells (TH)
• Cytotoxic T cells (TC)
• Histocompatibility proteins (MHC) proteins
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T cells have specific membrane receptors—
glycoproteins, with two polypeptide chains.
Each chain is encoded by a different gene
T cell receptors can bind a piece or fragment
of an antigen, on the surface of an antigenpresenting cell.
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TC cells bind to cells carrying the antigen–
MHC I protein complex.
When bound, the TC cells do two things to
eliminate the antigen-carrying cell:
• They produce perforin, which lyses the bound
target cell.
• They stimulate apoptosis in the target cell.
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Regulatory T cells (Tregs) regulate the
immune response.
Tregs recognize and mediate tolerance to self
antigens—when activated they release the
cytokine interleukin 10.
This blocks T cell activation and leads to
apoptosis of TC and TH cells bound to the
same antigen.
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Immune deficiency disorders can be inherited
or acquired.
T or B cells may never form, or B cells lose
their ability to give rise to plasma cells
Acquired immune deficiency syndrome
(AIDS) results from infection by human
immunodeficiency virus (HIV).
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HIV initially infects TH cells, macrophages,
and antigen-presenting dendritic cells.
Numbers of TH cells decline after infection.
HIV-infected cells activate the humoral
immune system and symptoms abate.
During the dormant period, people with HIV
feel fine.
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Eventually more TH cells are destroyed and
the person is susceptible to opportunistic
infections:
• Pneumonia
• Lymphoma tumors
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Drug treatments for HIV are focused on
inhibiting processes necessary for viral entry,
assembly, and replication.