This presentation explores all the types of hypersensitivity reactions.

1. Hypersensitivity Reactions

2. Introduction
• Immune responses that normally are protective are also capable of
causing tissue injury.
• Injurious immune reactions are grouped under hypersensitivity, and
the resulting diseases are called hypersensitivity diseases.

3. Sensitized individual antigenic stimuli exaggerated
immune response
Tissue damage/disease/death

4. Coombs And Gell(1963) Classified Hypersensitivity Into Four Types
Based On The Different Mechanisms Of Pathogenesis
• TYPE I (ANAPHYLAXIS, IgE OR REAGIN DEPENDANT)
• TYPE II(ANTIBODY MEDIATED)
• TYPE III(IMMUNE COMPLEX)
• TYPE IV(DELAYED OR CELL MEDAITED)

5. Classification of hypersenstivity reactions
• TRADITIONALLY, Depending on the time required for a
sensitized host to develop cliinical reactions:
• IMMEDIATE (B cell mediated or humoral)
on administration of antigen, reaction occurs immediately
within seconds or minutes
Type I,II,III
• DELAYED ( cell mediated)
reaction is slower and develops within 24-48 hours
effect is prolonged.
Type IV

6. IMMEDIATE HYPERSENSITIVITY DELAYED HYPERSENSITIVITY
Appears and recedes rapidly Appears slowly, lasts longer
Induced by antigens or haptens by any
route
antigens or haptens intradermally or by
skin contact
Circulating antibodies present and
responsible for reaction ; antibody
mediated reaction
Circulating antibodies may be absent and
not responsible for reaction ; cell
mediated reaction

7. Causes of Hypersensitivity
Reactions
Autoimmunity
self-tolerance fails,
resulting in reactions
against the body’s own
cells and tissues
Reactions against microbes
the reaction appears to be
excessive or the microbial
antigen is unusually
persistent
Reactions against
environmental antigens.
genetically predisposed to
make unusual immune
responses to a variety of
noninfectious, harmless
antigens

8. Immediate (Type I) Hypersensitivity

9. Immediate (Type I)
Hypersensitivity
• occurs rapidly after the
interaction of antigen with
IgE antibody that is bound
to the surface of mast cells
in a sensitized host.
• The reaction is initiated by
entry of an antigen, which
is called an allergen
because it triggers allergy.

10. TYPE I (ANAPHYLAXIS, IgE OR
REAGIN DEPENDANT)
Two forms of reaction can occur-
• The acute, potentially fatal, systemic form called
Anaphylaxis
• The chronic or recurrent, nonfatal, typically localised
form called Atopy.

12. 1. Activation of
TH2 cells and
production of
IgE antibody.
2. Sensitization
of mast cells by
IgE antibody.
3. Activation of
mast cells and
release of
mediators
Sequence of Events in Immediate Hypersensitivity Reactions
Vasoactive amines released from granule stores
Newly synthesized lipid mediators
Cytokines

15. Mast cells release various classes of mediators
that are responsible for the immediate and late-
phase reactions.
ECF: eosinophil chemotactic factor;
NCF: neutrophil chemotactic factor
PAF: platelet-activating factor.

16. Summary of the Action of Mast Cell Mediators in Immediate (Type I)
Hypersensitivity

17. IgE-mediated diseases in humans
•Systemic (anaphylactic shock) potentially fatal due to airway
obstruction and a sudden fall in blood pressure
•Hay fever (allergic rhinitis)- mucosal edema, mucus secretion,
coughing, sneezing, difficult in breathing
•Allergic conjunctivitis
•Skin reactions- Urticaria (wheal and flare) -mediated by histamine
•Food allergies- enhanced peristalsis, increased fluid secretion from
intestinal cells, vomiting, and diarrhea
•Asthma

19. Antibody-Mediated Diseases (Type II
Hypersensitivity)

20. • Antibody-mediated (type II) hypersensitivity disorders are caused by
antibodies directed against target antigens on the surface of cells or
other tissue components.
• The antigens may be normal molecules intrinsic to cell membranes or
in the extracellular matrix, or they may be adsorbed exogenous
antigens (e.g., a drug metabolite).

21. Opsonization of cells by antibodies
and complement components, and
ingestion of opsonized cells by
phagocytes.
Inflammation induced by antibody
binding to Fc receptors of
leukocytes and by complement
breakdown products.

22. Antireceptor antibodies disturb the normal function of receptors.
For eg, antibodies against the thyroid-stimulating hormone (TSH) receptor
activate thyroid cells in Graves disease, and acetylcholine (ACh) receptor
antibodies impair neuromuscular transmission in myasthenia gravis

24. Immune Complex Diseases (Type III
Hypersensitivity)

25. • Antigen–antibody (immune) complexes that are formed in the
circulation may deposit in blood vessels, leading to complement
activation and acute inflammation.
• The antigens in these complexes may be exogenous antigens, such as
microbial proteins, or endogenous antigens, such as nucleoproteins.

26. • When these complexes are produced in large amounts, persist, and
are deposited in tissues, they are pathogenic.
• Pathogenic immune complexes may form in the circulation and
subsequently deposit in blood vessels, or the complexes may form at
sites where antigen has been planted (in situ immune complexes).
• Immune complex–mediated injury is systemic when complexes are
formed in the circulation and are deposited in several organs, or it
may be localized to particular organs (e.g., kidneys, joints, or skin) if
the complexes are formed and deposited in a specific site

27. The pathogenesis of systemic immune complex
disease can be divided into three phases:
(1) formation of antigen– antibody complexes in
the circulation
(2) deposition of the immune complexes in various
tissues
(3) an inflammatory reaction in various sites
throughout the body

28. Local Immune Complex Disease
• A model of local immune complex diseases is the Arthus reaction, in which
an area of tissue necrosis appears as a result of acute immune complex
vasculitis.
• The reaction is produced experimentally by injecting an antigen into the
skin of a previously immunized animal
• Because of the initial antibody excess, immune complexes are formed as
the antigen diffuses into the vascular wall; these are precipitated at the site
of injection and trigger the same inflammatory reaction and histologic
appearance as in systemic immune complex disease.
• Arthus lesions evolve over a few hours and reach a peak 4 to 10 hours after
injection, when the injection site develops visible edema with severe
hemorrhage, occasionally followed by ulceration.

30. T Cell–Mediated (Type IV) Hypersensitivity

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