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Hypersensitivity:
Immediate
Hypersensitivity
Group 5:
Garcia, Vixienne Geia
Natividad, Justine
Lorenz
Nicdao, Jan Kevin
BSMT III-A
Overview
Type I hypersensitivity
reactions result from the
binding of antigen to
antigen-specific IgE bound
to its Fcreceptor,
principally on mast cells.
This interaction causes the
degranulationof mast cells
and the release of
inflammatory mediators.
Overview
Type I reactions are
commonly caused by
inhaled particulate
antigens, of which plant
pollens are good
examples. Type I reactions
have effects on varying
severity, ranging from a
running nose to breathing
difficulties and even death
by asphyxiation.
Overview
. Type I hypersensitivity
reactions are also
described as immediate
hypersensitivity because
they occur immediately on
exposure to antigen.
Type 1
Hypersensitivity
Allergens
Substances that can give
rise to wheal and flare
responses in the skin and
to the symptoms of allergic
disease are derived from
many different sources.
Almost all are protiens
10 000 to 40 000 Daltons
freely soluble in aqueous
solution
Allergens
Biological functions
(digestive enzymes, carrier
proteins, calycins and
pollen recognition
proteins)
Classified by:
• Source
• Route of Exposure
• Nature of Specific Protein
•
Common sources of allergens
Inhaled Materials
Plant pollens
Dander of domesticated animals
Mold spores
Feces of very small animals
e.g., house dust mites
Injected Materials
Insect venoms
Vaccines
Drugs
Therapeutic proteins
Ingested Materials
Food
Orally administered drugs
Contacted Materials
Plant leaves
Industrial products made from plants
Synthetic chemicals in industrial
products
Metals
Allergens
Atopy
• a hereditary
predisposition to the
development of the
immediate
hypersensitivity
reactions against
common
environmental
antigens
Immunoglobulin E
The B-cell response leading
to production of IgEoccurs
in 2 stages. In the first
stage, a resting B-cell
switches from IgD/IgM
production to
IgEproduction under the
influence of IL-4. Th2 cells
produce IL-4 and Th1 cells
produce IFN-y, which has
an opposing effect.
Immunoglobulin E
The ratio of Th1 to Th2 cells
engaged in an immune
response probably
determines the level of
IgEproduced. The second
stage of IgE response
proceeds when an IgE-
producing B cell develops
into a plasma cell. This is
controlled by cell surface
protein called Fc€RII or
CD23. Fc€RII links the B-cells
to dendritic cells and so
prevents their destruction by
apoptosis.
Immunoglobulin E
They are thus free to
differentiate into
plasma cells. Fc€RII
expression is
regulated by the
presence of IL-4,
which stimulates its
production, and by
IgE, which suppress
its production.
Mast Cells
There are two
populations of mast
cells in rodents and
humans: connective
tissue mast cells and
mucosal mast cells.
Mast Cells
Connective tissue mast cells
arise from precursors in
fetal liver and bone
marrow.
Connective tissue mast cells
contain many uniform
granules and are rich in
histamine and heparin.
•
Mast Cells
Mucosal mast cells have
abundant chondroitin
sulphate and little
histamine in their
granules.
Mucosal mast cell proliferate
in response to IL-3
produced by Tcells.
•
Basophil
Peripheral blood
basophilsshould not be
considered simply as
circulating mast cells.
They may, however, be
passively sensitized with
IgE, and they will respond
to antigen in a manner
apparently similar to that
of mast cells.
IgE binding Fc
Receptors
The reaginic activity of
IgE depends on its ability
to bind to a receptor
specific for the Fcregion of
the € heavy chain. There
are 2 types of IgE receptor:
high affinity (Fc€RI) and
low affinity (Fc€RII or
CD23).
IgE binding Fc
Receptors
High affinity receptor Low affinity receptor
(Fc€RI) (Fc€RII or CD23)
•Mainly found on mast •Found on NK cells,