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133 Cards in this Set

  • Front
  • Back
1st line of defense mechanisms against
infection
Innate Immunity
Fast response, non-specific, no memory
Innate Immunity
May not effectively contain or eradicate
infection
Innate Immunity
can engulf and phagocytize
microbial cells, viruses or inert particles
Phagocytic cells
recognize damaged or altered cells
of the body, such as virally infected cells or
tumor cells
NK cells
Produce large quantities of interferon-γ
NK cells
Mediate cytotoxicity via apoptosis
NK cells
remove apoptotic bodies from
the body
Phagocytic cells
Capillary permeability increases allowing __
to enter the damaged
tissue
exudate and cells
The accumulation of exudate in the tissue
results in
edema
Exudate is rich in
complement
enter the damaged tissue
surveying for possible microbial invasion
(infection)
Phagocytic cells
controlled by cytokines produced
locally that enter the bloodstream
The Acute Phase Response
regulates body temperature
Hypothalamus
responsible for replacement of complement proteins
and production of acute phase proteins such
as C-reactive protein
Liver
Develops only after invasion of foreign
material
Acquired Immunity
Slow response initially, highly specific,
can result in memory
Acquired Immunity
Fast response with subsequent infection
with the same organism
Acquired Immunity
Specialized antigen presenting cells
• Tissue associated macrophage network
• Blood monocytes are converted in tissue to macrophages
Reticuloendothelial System (RES)
Mononuclear Phagocytic System
macrophages in the liver
Kupffer cells
macrophages in the spleen
denritic cells
macrophages in the skin
Langerhan cells
macrophages in the brain
microglial cells
are present on
almost all cell types in the body and thereby
can present Ag of intracellular origin to
CD8 cells for destruction
MHC class I molecules
are only on
specialized antigen presenting cells and
present Ag of extracellular origin to CD4
cells (helper cells)
MHC class II molecules
T-cells can only recognize Ag when bound
to
an MHC molecule
activate tissue macrophages and enhance
phagocytosis and cell mediated immunity
TH1
stimulate B-cells to make Ab which bind
extracellular bacteria and viral particles
TH2
Naïve T-cell encounters an antigen for the
first time and is stimulated to
differentiate
into an effector T-cell.
Present throughout the cortex of lymph nodes,
connective tissues, spleen and epithelial tissues
dendritic cells
Most potent and dedicated solely to presenting
antigens to T-cells
dendritic cells
Present throughout lymph nodes and in most
tissues in the body and body cavities
macrophages
Present in the follicle of lymph nodes and blood
b-cells
Primary function is to make immunoglobulins
b-cells
controls the differentiation of
activated T-cells
Interleukin-2
triggers cell division
IL-2 binds to the IL-2 receptor on T-cells
are known as cytotoxic
T-cells
Activated CD8 cells
kill infected or
abnormal cells
Cytotoxic CD8 T-cells
Killing is not by lysis but rather apoptosis
or programmed cell death
Cytotoxic CD8 T-cells
results
when microbes resist the
cidal effects of the
activated macrophages
and chronic infection
with inflammation sets in
Granuloma
Consists of infected
macrophages in the center,
surrounded by activated
T-cells
Granuloma
Means of communication between activated
cells of the immune system
cytokines
– Inflammation
– Differentiation of T-cells and their function
– Control of Cell Mediated Immunity
– Control of Humoral Immunity
– Control of Cellular and Tissue Development
cytokines!!
Produced primarily by macrophages but
also can be produced by other immune cells
cytokines
Essential for the innate immune response
and primes immune cells to better respond
with an acquired immune response
cytokines
leads to
– Tissue necrosis
– Shock
– Death
overproduction of cytokines
mediates or promotes:
– IL-6 production
IL-1
is a mediator of the acute-phase
response primarily in the liver
IL-6
mediates or promotes or activates:
– B-cell growth and differentiation
IL-6
Augments NK-cell activity
IL-6
Activates mononuclear phagocytes
INF-γ
Induces the differentiation of monocytes into
activated macrophages
INF-γ
Promotes T- and B-cell differentiation
INF-γ
Activates neutrophils and NK cells
INF-γ
Enhancement of cell adhesion molecules
promoting cell-cell interaction and
inflammatory cell extravasation
all mentioned cytokines except 1L-6
at high concentrations it enters the
blood and acts more like IL-1
TNF-α
- Acts as a pyrogen
– Stimulates acute-phase response from the liver
– Disseminated intravascular coagulation (DIC)
TNF-α
most important of the cytokines that drive TH1 and therefore cell-mediated
immunity
IL-2
most important of the cytokines that drive TH2 and therefore humoral
immunity
IL-4
is a multi-lineage colony stimulating
factor
IL-3
promotes expansion of number of bone
marrow progenitor cells
IL-3
promotes the
development of secondary lymphoid tissues
LT (formerly TNF-β)
can kill T cells, fibroblasts, and some
tumor cells
LT
can inhibit B-cell activity, and activate
phagocytic cells
LT
Primary function is to attract neutrophils to the
area
IL-8
Lymphocytes, basophils, and eosinophils are
attracted but to a lesser extent than neutrophils
IL-8
First antibodies made are always
IgM
converted into plasma cells which
produce very large quantities of Ig
B-cells
predominantly in secretory fluids
IgA
on surface of B cells function unknown
IgD
predominantly on surface of mast cells
– Allergic response and some parasitic infections
IgE
predominant antibody in blood & body
IgG
– 4 subclasses
– longest t1/2 ~ 3 weeks
– crosses placenta
IgG
1st to respond to a new antigen
IgM
1st antibody produced in the fetus
IgM
tags microorganisms for
destruction
Complement
One of the major defenses against bacterial
infections
Complement
Individual must 1st be sensitized to an
allergen before a reaction can occur
Type 1 Hypersensitivity
First exposure results in no symptoms
Type 1 Hypersensitivity
Most common form of the allergic reaction
Type 1 Hypersensitivity
Ranges from uncomfortable but harmless
symptoms such as runny nose or itchy eyes
to life-threatening symptoms such as
swelling of the airway
Type 1 Hypersensitivity
IgE production is dependent upon
TH2 cells
will
inhibit IgE production
TH1 cell production or stimulation
Both are dependent upon IL-4
IgE and IgG4
can be produced in response to an
allergen but does not generate an allergic
response but elicits tolerance to the allergen
IgG4
key to production of IgG4 versus IgE
IL-10
can bind Ag but is not bound to a mast cell; is free-floating and does not ellicit a response
IgG4
in mast cells and eosinophils only
Histamine
– activation of kinins and complement
– Increase bronchial mucus secretions
– Degradation of blood vessel basement membrane
proteases
Type 1 Mediators –
Newly-synthesized
phospholipase A2
Leukotrienes
Platelet activating factor
responsible for Systemic anaphylaxis
IL-1, TNF-α
Stimulates mast cell growth and histamine
secretion
IL-3
– Stimulates mast cell growth
– Induces activated B-cells to switch to IgG1 and
IgE production
IL-4
Promotes growth and differentiation of
eosinophils
IL-5
Chemotactically attracts monocytes and
macrophages
TGF-β
histamine does not cause
airway inflammation
Leukotrienes, PAF and ECF-A all cause
airway inflammation
An antigen specific immune reaction
mediated primarily by IgE resulting in vasodilation and constriction of smooth muscle
anaphylaxis
may cause degranulation without
involving IgE or Fcε-receptors
Drugs
is released within seconds to 15
minutes of allergen exposure and only
accounts for a small portion of the disease
acutely
Histamine
Goal is to increase IgG antibodies to allergen
thereby preventing the binding of the allergen
to mast cell associated IgE
Desensitization to Allergens
Bind up histamine but no effect on leukotrienes; would have no effect on airway inflammation
Antihistamines
drugs which cause Bronchodilation & smooth muscle
relaxation, mast cell stabilization
Inhaled β agonists (selective β2 preferred)
Inhaled β agonists (selective β2 preferred) treat only
bronchospasm
EPI treats only
bronchospasm
Stabilize mast cells against degranulation
Cromolyn
Promotes inhibition of phospholipase A2,
therefore, decreases arachidonic acid
Corticosteroids
Decreases in leukotrienes, prostaglandins,
thromboxanes
Corticosteroids
Inhibits influx of eosinophils, basophils, and
lymphocytes into local sites
Corticosteroids
Prevent eosinophil production in BM, and
rapidly decrease circulating eosinophils
Corticosteroids
Inhibit production of many cytokines, TNFα,
some chemokines
Corticosteroids
treat all sx of type one hypersensitivity
Corticosteroids
Mediated by IgG and IgM antibodies
binding to specific cells or tissues bearing
a specific antigen
Type II Hypersensitivity
Occur most prevalently with erythrocytes
ABO and Rhesus incompatibility
Type II Hypersensitivity
Transfusion reactions are a type of
Type II Hypersensitivity
Hemolytic disease of the newborn is a type of
Type II Hypersensitivity
Univsersal blook acceptor
AB - no Ab
Drugs or their metabolites can cause __, although this is rare
type II
reactions
Immune-complex hypersensitivity
Type III Hypersensitivity
initial step is formation of soluble
antibody-antigen complexes
Type III
Low-grade persistent infection with weak
immune response causes chronic immunecomplex
formation which eventually deposit
in the tissues
Type III Hypersensitivity
Leprosy, malaria, dengue hemorrhagic fever,
viral hepatitis
Type III Hypersensitivity
As the number of complexes in the blood
increase the mononuclear phagocytosis,
erythrocytes, or complement responsible for
clearing them are overloaded
Type III Hypersensitivity
Mould or plant spores, occupational hazards
complex with IgG and can precipitate in the
lungs
Type III Hypersensitivity
Serum Sickness relates to this type
Type III Hypersensitivity
Circulating immune complexes deposit in the
blood vessel walls and tissues causing increased
vascular permeability and can result in
inflammatory diseases such as arthritis and
glomerulonephritis
Serum Sickness
Drugs associated with type III
monoclonal antibodies & cytokines,
β-lactams, sulfa-drugs
Cell-mediated delayed hypersensitivity
reaction
Type IV Hypersensitivity
Takes 12-48 hours to develop symptoms
Type IV Hypersensitivity
Does not involve antibodies
Type IV Hypersensitivity
The reaction is mediated by interleukins
secreted from T-lymphocytes and
macrophages in response to antigen
challenge (cell-mediated immunity)
Type IV Hypersensitivity
– Contact dermatitis
– PPD skin test for tuberculosis
– Organ transplant rejection
– Killing of viruses, fungi, and tumor cells
Type IV Hypersensitivity
tumor-like mass or nodule of
granulation tissue, with actively growing
fibroblasts and capillary bud
Granuloma