Immunology Exam One
Terms
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1st line of defense mechanisms against
infection - Innate Immunity
- Fast response, non-specific, no memory
- Innate Immunity
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May not effectively contain or eradicate
infection - Innate Immunity
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can engulf and phagocytize
microbial cells, viruses or inert particles - Phagocytic cells
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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
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remove apoptotic bodies from
the body - Phagocytic cells
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Capillary permeability increases allowing __
to enter the damaged
tissue - exudate and cells
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The accumulation of exudate in the tissue
results in - edema
- Exudate is rich in
- complement
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enter the damaged tissue
surveying for possible microbial invasion
(infection) - Phagocytic cells
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controlled by cytokines produced
locally that enter the bloodstream - The Acute Phase Response
- regulates body temperature
- Hypothalamus
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responsible for replacement of complement proteins
and production of acute phase proteins such
as C-reactive protein - Liver
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Develops only after invasion of foreign
material - Acquired Immunity
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Slow response initially, highly specific,
can result in memory - Acquired Immunity
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Fast response with subsequent infection
with the same organism - Acquired Immunity
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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
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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
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are only on
specialized antigen presenting cells and
present Ag of extracellular origin to CD4
cells (helper cells) - MHC class II molecules
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T-cells can only recognize Ag when bound
to - an MHC molecule
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activate tissue macrophages and enhance
phagocytosis and cell mediated immunity - TH1
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stimulate B-cells to make Ab which bind
extracellular bacteria and viral particles - TH2
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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
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Most potent and dedicated solely to presenting
antigens to T-cells - dendritic cells
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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
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controls the differentiation of
activated T-cells - Interleukin-2
- triggers cell division
- IL-2 binds to the IL-2 receptor on T-cells
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are known as cytotoxic
T-cells - Activated CD8 cells
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kill infected or
abnormal cells - Cytotoxic CD8 T-cells
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Killing is not by lysis but rather apoptosis
or programmed cell death - Cytotoxic CD8 T-cells
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results
when microbes resist the
cidal effects of the
activated macrophages
and chronic infection
with inflammation sets in - Granuloma
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Consists of infected
macrophages in the center,
surrounded by activated
T-cells - Granuloma
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Means of communication between activated
cells of the immune system - cytokines
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– Inflammation
– Differentiation of T-cells and their function
– Control of Cell Mediated Immunity
– Control of Humoral Immunity
– Control of Cellular and Tissue Development - cytokines!!
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Produced primarily by macrophages but
also can be produced by other immune cells - cytokines
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Essential for the innate immune response
and primes immune cells to better respond
with an acquired immune response - cytokines
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leads to
– Tissue necrosis
– Shock
– Death - overproduction of cytokines
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mediates or promotes:
– IL-6 production - IL-1
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is a mediator of the acute-phase
response primarily in the liver - IL-6
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mediates or promotes or activates:
– B-cell growth and differentiation - IL-6
- Augments NK-cell activity
- IL-6
- Activates mononuclear phagocytes
- INF-γ
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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
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Enhancement of cell adhesion molecules
promoting cell-cell interaction and
inflammatory cell extravasation - all mentioned cytokines except 1L-6
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at high concentrations it enters the
blood and acts more like IL-1 - TNF-α
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- Acts as a pyrogen
– Stimulates acute-phase response from the liver
– Disseminated intravascular coagulation (DIC) - TNF-α
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most important of the cytokines that drive TH1 and therefore cell-mediated
immunity - IL-2
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most important of the cytokines that drive TH2 and therefore humoral
immunity - IL-4
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is a multi-lineage colony stimulating
factor - IL-3
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promotes expansion of number of bone
marrow progenitor cells - IL-3
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promotes the
development of secondary lymphoid tissues - LT (formerly TNF-β)
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can kill T cells, fibroblasts, and some
tumor cells - LT
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can inhibit B-cell activity, and activate
phagocytic cells - LT
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Primary function is to attract neutrophils to the
area - IL-8
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Lymphocytes, basophils, and eosinophils are
attracted but to a lesser extent than neutrophils - IL-8
- First antibodies made are always
- IgM
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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
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predominantly on surface of mast cells
– Allergic response and some parasitic infections - IgE
- predominant antibody in blood & body
- IgG
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– 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
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tags microorganisms for
destruction - Complement
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One of the major defenses against bacterial
infections - Complement
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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
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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
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will
inhibit IgE production - TH1 cell production or stimulation
- Both are dependent upon IL-4
- IgE and IgG4
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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
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– activation of kinins and complement
– Increase bronchial mucus secretions
– Degradation of blood vessel basement membrane - proteases
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Type 1 Mediators –
Newly-synthesized -
phospholipase A2
Leukotrienes
Platelet activating factor - responsible for Systemic anaphylaxis
- IL-1, TNF-α
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Stimulates mast cell growth and histamine
secretion - IL-3
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– Stimulates mast cell growth
– Induces activated B-cells to switch to IgG1 and
IgE production - IL-4
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Promotes growth and differentiation of
eosinophils - IL-5
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Chemotactically attracts monocytes and
macrophages - TGF-β
- histamine does not cause
- airway inflammation
- Leukotrienes, PAF and ECF-A all cause
- airway inflammation
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An antigen specific immune reaction
mediated primarily by IgE resulting in vasodilation and constriction of smooth muscle - anaphylaxis
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may cause degranulation without
involving IgE or Fcε-receptors - Drugs
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is released within seconds to 15
minutes of allergen exposure and only
accounts for a small portion of the disease
acutely - Histamine
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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
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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
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Promotes inhibition of phospholipase A2,
therefore, decreases arachidonic acid - Corticosteroids
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Decreases in leukotrienes, prostaglandins,
thromboxanes - Corticosteroids
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Inhibits influx of eosinophils, basophils, and
lymphocytes into local sites - Corticosteroids
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Prevent eosinophil production in BM, and
rapidly decrease circulating eosinophils - Corticosteroids
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Inhibit production of many cytokines, TNFα,
some chemokines - Corticosteroids
- treat all sx of type one hypersensitivity
- Corticosteroids
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Mediated by IgG and IgM antibodies
binding to specific cells or tissues bearing
a specific antigen - Type II Hypersensitivity
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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
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type II
reactions - Immune-complex hypersensitivity
- Type III Hypersensitivity
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initial step is formation of soluble
antibody-antigen complexes - Type III
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Low-grade persistent infection with weak
immune response causes chronic immunecomplex
formation which eventually deposit
in the tissues - Type III Hypersensitivity
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Leprosy, malaria, dengue hemorrhagic fever,
viral hepatitis - Type III Hypersensitivity
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As the number of complexes in the blood
increase the mononuclear phagocytosis,
erythrocytes, or complement responsible for
clearing them are overloaded - Type III Hypersensitivity
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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
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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
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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
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The reaction is mediated by interleukins
secreted from T-lymphocytes and
macrophages in response to antigen
challenge (cell-mediated immunity) - Type IV Hypersensitivity
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– Contact dermatitis
– PPD skin test for tuberculosis
– Organ transplant rejection
– Killing of viruses, fungi, and tumor cells - Type IV Hypersensitivity
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tumor-like mass or nodule of
granulation tissue, with actively growing
fibroblasts and capillary bud - Granuloma