Non-specific defenses

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Transcript Non-specific defenses

Immune System
Chapter 14
Humans have two major types of defense mechanisms:
Non-specific defenses & Specific defenses
 Non-specific defenses
 do not distinguish between one threat and
another
 are present at birth
 include: physical barriers (e.g. skin), phagocytic
cells, inflammation, fevers, etc.
 provides body with “non-specific resistance”
 Specific defenses
 protect against specifically identified threats
(i.e. may defend against one particular bacterial
infection but not a different one)
 most develop after birth upon exposure to an
antigen (Ag); an antigen can be a pathogen
(disease-causing organism), foreign protein (e.g.
toxin), abnormal or infected body cell, foreign
tissue transplant
 specific defenses produce a state of long-term
protection known as “specific resistance” or
“Immunity”
Immunity
 depends on coordinated activity of T & B
lymphocytes
 T cells- involved in “cell-mediated (aka cellular)
immunity”; defense against abnormal cells &
intracellular pathogens
 B cells- involved in “antibody-mediated (aka
humoral) immunity”; defense against pathogens
(Ag’s) in body fluids (blood/lymph)
Overview of Immunity
Fig. 14-11)
Immunity is either “innate” or “acquired”
Innate Immunity
 present at birth
 independent of previous
exposure to Ag
 genetically determined
 species dependent
Acquired Immunity
 arises throughout life by active or passive means
Active immunity – development of resistance (i.e.
antibody (Ab) production) to specific disease
secondary to exposure to specific Ag (pathogen)
 naturally acquired active immunity – natural exposure
results in immune response & development of long term
immunity
 induced (artificial) active immunity – deliberate “artificial”
exposure to Ag (i.e. vaccine/immunization)
Passive immunity – development of immunity due to
transfer of “pre-made” antibodies
 naturally acquired passive immunity – Ab’s transferred from
mom  baby across placenta or in breast-milk
 induced (artificial) passive immunity – administration of Ab’s
to fight disease after exposure to pathogen
Properties of Immunity
Immunity has four general properties:
 Specificity
 Versatility
 Memory
 Tolerance
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
Properties of Immunity
 Specificity – T & B cells have specific receptors that will
allow them to only recognize & target a specific Ag; this
process is known as “antigen recognition”
 Versatility – millions of different lymphocyte populations,
each with specific Ag recognizing receptors; allows for
“anticipation” of potential Ag’s
 Memory – after initial exposure, long term acquired
immunity occurs through the production of memory cells;
secondary exposure results in stronger faster response to
previously recognized Ag
 Tolerance – immune cells recognize self-antigens &
“tolerate” (ignore) them, only going after foreign (non-self)
Ag’s
Overview of the immune response
 The
purpose of the immune response is to inactivate or
destroy pathogens, abnormal cells & foreign molecules (such
as toxins)
 In order for the response to occur, lymphocytes must be
“activated” by the process of antigen recognition
 T cells are usually activated first, & then B cells. T cells mainly
rely on activation by phagocytic cells collectively known as
“antigen presenting cells (APC’s)” (ie. Macrophages, dendritic
cells)
 Once activated, T cells both attack the invader, & stimulate
the activation of B cells
 Activated B cells mature into “plasma cells” which produce
specific antibodies designed to destroy the particular antigen.
Cell Mediated (a.k.a. Cellular) Immunity
 In order for T cells to respond, they must first be activated by
exposure to an antigen
 antigen is bound to membrane receptors of phagocytic antigen
presenting cells (APC’s) (“antigen recognition”)
 These membrane receptors on cells are called “MHC proteins”
(major histocompatibility complex proteins), & are genetically
determined (i.e. differ among individuals)
 Antigens bound to MHC proteins “tell” the T lymphocyte what the
specific foreign invader is (i.e. a specific bacteria) so that the
lymphocytes can mount a cellular defense
Cell Mediated (a.k.a. Cellular) Immunity
Once a T cell is activated by the presentation of the
combined MHC/Ag, it will clone (by mitosis) &
differentiate into:
 cytotoxic T cells
 helper T cells
 memory T cells
 suppressor T cells
Cell Mediated (a.k.a. Cellular) Immunity
 cytotoxic T cells – seek out the specific
pathogen/infected cell that contains the targeted Ag &
destroys it by secreting various chemicals
 helper T cells – necessary for coordination of both
specific & non-specific defenses, as well as for stimulating
both cell-mediated & antibody-mediated immunity.
 In cell-mediated immunity they release chemicals
(cytokines) that strengthen the activity of cytotoxic T
cells.
 In antibody-mediated immunity they release
cytokines that stimulate activated B cell division &
differentiation into plasma cells
Cell Mediated (a.k.a. Cellular) Immunity
 memory T cells – remain “in reserve” so if same Ag
appears, these cells can immediately differentiate into
cytotoxic & helper T cells, causing a swift secondary
response to the invasion
 suppressor T cells – activated more slowly than the other T
cells; inhibit the response of the immune cells to prevent
potential “autoimmune” response
Activated T cells clone &
differentiate into:
 Cytotoxic T cellsstimulate
 Helper T cells
 Memory T cells
 Suppressor T cells
Direct physical &
chemical attack
Antigens
Remain in
reserve
B cell
activation
Prevent
autoimmune
response
CELL MEDIATED IMMUNITY
bacteria
ANTIGENS
viruses
bacteria
viruses
SPECIFIC
DEFENSES
(Immune
response)
APC’s phagocytize Ag & activate T
cells
Antibody Mediated (Humoral) Immunity
The body has millions of different B
cell populations, each B cell has its
own particular antibody (Ab) molecule
(transmembrane protein) within its cell
membrane
 When the corresponding Ag invades
the interstitial fluid surrounding the B
cell, the Ag binds to the Ab molecule, &
is taken into the cell, eventually being
displayed on the B cell’s MHC protein.
The B cell is now “sensitized”
Antibody Mediated (Humoral) Immunity
 Helper T cells (that had been
previously activated to the same Ag)
then attach to the sensitized B cells &
activate them by secreting chemicals
(cytokines)
 Cytokine secretion results in B cell
cloning & differentiation into plasma
cells & memory cells
Antibody Mediated (Humoral) Immunity
 Plasma cells produce millions of
copies of antibodies which are
released into the blood & lymph
 Antibodies seek out & bind to the
Ag forming an “Ab-Ag complex”,
eventually leading to the elimination
of the antigen by various means
 Memory cells remain in reserve to
respond to any subsequent
exposure by the same Ag. Upon
secondary exposure, memory B
cells quickly differentiate into Ab
producing plasma cells
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A46_2a.htm
Antibody Mediated (Humoral) Immunity
Review of Immune Response