Hypersensitivity Flashcards
Heightened state of immune
responsiveness
Hypersensitivity
Cell bound antibody reacts with antigen to
release physiologically active substances
Hypersensitivity type 1
Are those in which free antibody reacts with
antigen associated with cell surface
Hypersensitivity type II
Antibody reacts with soluble antigen to form
complexes that precipitate in the tissues.
Hypersensitivity type III
• Antibody reacts with soluble antigen to form
Complement plays a major role in producing
tissue damage.
Hypersensitivity type 3
Sensitized T cells rather than antibody are
responsible for the symptoms that develop.
Hypersensitivity type 4
Immune mediators of type 1 to 4
Type 1 = ige
Type 2 = igg
Type 3 = igg origm
Type 4 = t cells
Which hypersensitivityhas complement involvement
Type 2 and 3
Mechanism of type 1 hypersensitivity
RELEASE OF
MEDIATORS
FROM MAST
CELLS AND
BASOPHILS
Hypersensitivity type 2 mechanism
CYTOLYSIS DUE
TO ANTIBODY
AND
COMPLEMENT
Hypersentivity type 3 mechanism
DEPOSITS OF Ag-
Ab COMLEXES
Hypersensitivity’s type 4 mechanism
RELEASE OF
CYTOKINES
Example oftype 1 hypersensitivity
ANAPHYLAXIS,
HAY FEVER,
FOOD
ALLERGIES
Example of type 2 hypersensitivity
TRANSFUSION
REACTIONS,
HDN
Type 3 hypersensitivity
SERUM
SICKNESS, SLE
Type 4 hypersensitivity
CONTACT
DERMATITIS,
TUBERCULIN
TEST
Antigen contact, typically low dose via mucous
membrane (respiratory, GI) → IgE production
Sensitization
Pre-formed IgE (allergens-specific) triggers
mast cell activation → mediator release
Elicitation
Can occur within seconds-minute of exposure
Severity ranges from irritating to fatal
Reactions
In type 1, Total IgE and specific antibodies are measured
by a
modification of enzymes immunoassay
(ELISA).
Increased IgE levels are indicative of
atopic
condition.
Type 1 teatment
Antihistamine, anchromolyn sodium
Leukotriene
Bronchodilators such as irsprotrenol derviatives
Thopylline
Hyposensitvity
Suppressor t cell
Igg blocing antibodies
nhibits mast cells
degranulation, probably by inhibiting Ca++
influx.
Chromolyn sodium i
elevates
cAMP-phosphodiesterase and inhibits
intracellular Ca++ release is also used to relieve
bronchopulmonary symptoms.
Thophylline
• that specifically inhibits IgE
antibodies may play a role.
Suppressor T cells
also known as cytotoxic hypersensitivity and
may affect a variety of organs and tissues
Type 2 hypersensitivity
The
antigens are normally endogenous, although
exogenous chemicals (haptens) which can attach
to cell membranes can also lead to
type II
hypersensitivity.
Can lead to type 2 hypertension
• Drug-induced hemolytic anemia,
granulocytopenia and thrombocytopenia
Diagnostic test of type 2
detection of circulating
antibody against tissues involved and the
presence of antibody and complement in the
lesion (biopsy) by immunofluorescence.
It is also known as immune complex
hypersensitivity.
Type 3 hypersensitivity
The reaction may be general
(serum sickness) or may involve individual
organs including skin (systemic lupus
erythematosus, arthus reaction), kidney (lupus
nephritis), lung (aspergillosis), blood vessels
(polyarteritis), joints (rheumatoid arthritis) or
other organs.
Type 3
Ho long is the reaction for type 3, what siit mediated by and what type of antigenis used
• The reaction may take 3-10 hours after exposure
to the antigen.
• It is mediated by soluble immune complexes.
They are mostly of IgG class, although IgM may
also be involved.
• They antigen may be exogenous or endogenous in
nature. The antigen is soluble and not attached
to the organ involved.
Diagnosis of type e
• Diagnosis involves examination of tissue biopsies
for deposits of Ig and complement by
immunofluorescence.
• Polyethylene glycol mediated turbidity
(nephelometry), binding of C1q and Raji
cell test are utilized to detect immune
complexes.
• The immunoflurorescent staining in type III
hypersensitivity is granular. Presence of immune
complexes in serum and depletion in complement
level are also diagnostic.
Treatment of type 3
Anti inflammation
It is also known as cell mediated or delayed type
hypersensitivity.
Type 4 hypersensitivity
The classical example of this hypersensitivity is
tuberculin (montoux) reaction which peaks
48hours after the injection of antigen (PPD or old
tuberculin). The lesion is characterized by
induration and erythema.
Type 4 hypersensitivity
is involved in the
pathogenesis of many autoimmune and infectious
diseases and granulomas due to infections and
foreign antigens.
Type IV hypersensitivity
Another delayed hypersensitivity is
contact
dermatitis (poison ivy, chemicals, heavy metals)
in which the lesions are more popular.
Mechanism for type 4
include T lymphocytes and
monocytes and/or macrophages. Cytotoxic T cells
(Tc) cause direct damage whereas helper T (TH1)
cells secrete cytokines which activate cytotoxic T
cells and recruit and activate monocytes and
macrophages, which cause the bulk of the
damage.
Major lymphokines involved in delayed
hypersensitivity reaction include
monocyte
chemotactic factor, interleukin-2, interferon,
TNF.
Diagnostic test in type 4 hypersensitivity
Diagnostic test in vivo include delayed cutaneous
reaction (montoux test) and patch test (for
contact dermatitis).
• In vitro tests for delayed hypersensitivity include
mitogenic response, lympho-cytotoxicity and IL-2
production.
Treatment fortype 4 hypersensitivity
Corticosteroids and other immunosuppressive
agents are used in treatment.
Mechanism of type 4
Mechanism:
• The mechanism includes T lymphocytes and
monocytes and/or macrophages.
• Cytotoxic T cells (Tc) cause direct damage
whereas helper T (TH1) cells secrete cytokines
which activate cytotoxic T cells, recruit and
activate monocytes and macrophages, which
cause the bulk of the damage
• The delayed hypersensitivity lesions mainly
contain monocytes and a few T cells.
