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Hypersensitivity Reactions

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123 views5 pages

Hypersensitivity Reactions

Uploaded by

Abinayadevi S
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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HYPERSENSITIVITY REACTIONS

• Hypersensitivity refers to undesirable reactions or responses produced by the normal immune


system. These responses may be destructive, anxiety generating and occasionally lethal.
• Hypersensitivity reactions are immune responses that are exaggerated or inappropriate against an
antigen or allergen and mediated by either immunoglobulins or T-Lymphocytes.

Classification of Hypersensitivity Reactions


• Gell and Coomb described four types of hypersensitivity reactions (Types I, II, III and IV).
• The first three types are antibody-mediated and the fourth type is mediated mainly by T-cell and
macro-phases i.e. cell-mediated

A. Hypersensitivity Type I:
• Also referred as anaphylactic or immediate hypersensitivity.
• Commonly called Allergy
• This is commonest among all types which is mainly induced by certain type of antigens i.e.
allergens.
• Occurs in two forms:
✓ Acute, potentially fatal, systemic form, called Anaphylaxis
✓ Chronic or recurrent, nonfatal, localized form, called Atopy
• Anaphylaxis means “opposite of protection” and is mediated by IgE antibodies through
interaction with an allergen.
• The primary cellular component in this hypersensitivity is the mast cell or Basophils. The reaction
is amplified by Neutrophils and Eosinophil.
Mode of Action (Mechanism of Anaphylaxis):

• The overall mechanism of anaphylaxis can be summarized in following steps/phases:


1. Production of IgE antibody
2. Sensitization (First dose of antigen)
3. Shocking dose (second dose) of antigen
4. Degranulation of mast cell
5. Anaphylactic reaction
• During the activity, the class of antibody (IgE) binds with high affinity to FC (Fragment
crystalized) receptors on the surface of tissue mast cells and blood basophils.
• Such Mast cells and basophils bounded by IgE are said to be sensitized.
• Later, when the individual sensitized cell is exposed to the same allergen again, then it cross-links
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the membrane bound IgE on sensitized mast cells and basophils causing degranulation of these
cells.
• Degranulation causes release of pharmacological active mediators which act on surrounding tissue
causing vasodilation and smooth muscle contraction which may be either systemic or localized.
This effect is also termed as Allergy.

B. Hypersensitivity Type II:


• Also referred as Cytotoxic-Mediated Response or Cytotoxic reactions.
• Type II hypersensitivity reactions are those in which tissue or cell damage is the direct result of
the actions of antibody and complement.
• Here antibodies are produced against the body’s own antigens (auto-antibodies).
• It is primarily mediated by IgG and IgM.
• In this hypersensitivity reaction, antibody produced (IgG or IgM) bound to cell surface antigen and
destroy the cell. If the cell is microorganism, killing of cell is beneficial to host.
• These auto-antibodies when bound to antigens, trigger the T Cells and macrophages to kill the target
cell (hence Cytotoxic).
• These types of reactions are best seen by blood transfusion reactions, in which host antibodies react
with foreign antigens on the incompatible transfused blood cells and mediate destruction of these
cells.
• The killing of cell can occurs by one of the three mechanisms. They are-

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✓ Complement mediated cell lysis
✓ Antibody dependent cell mediated cytotoxicity (ADCC)
✓ Opsonization

Mode of action:

• This type of reaction is resulted by blood-transfusion reactions in which host antibodies react with
foreign antigens present on the incompatible transfused blood cells and mediate destruction of these
cells.
• Antibody can mediate cell destruction by activating the complement system to create pores in the
membrane of the foreign cell by forming membrane attack complex (MAC). This can also be
mediated by antibody dependent cell-mediated cytotoxicity (ADCC).
• A faulty cross-matching leads to haemolysis of the donor’s erythrocytes in the blood vessels of the
recipient due to the alloantigen of the donor’s erythrocytes.
• Donor’s erythrocytes react with the antibodies in the serum of the recipient and in combination with
activated complement, the erythrocytes undergo haemolysis

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C. Hypersensitivity Type III:

• Type III hypersensitivities are immune-complex reactions that were first characterized by Nicolas
Maurice Arthus in 1903.
• These reactions involve the interaction of IgG or IgM immunoglobulins with antigen to form immune
complexes.
• Reaction occurs when soluble antigens bind with IgG in a ratio (antibody excess with a low
concentration of antigen) that results in the accumulation of small antigen-antibody aggregates called
immune complexes.
• This immune complex gradually facilitates removal of antigen by phagocytic activity of body.
• Large amount of immune complexes lead to tissue-damaging Type III hypersensitivity. For this
reason Type III is called immune complex hypersensitivity.

Mode of action:

• These reactions develop when immune complexes activate the complement system’s array of immune
effector molecules. Complement components (C3a, C4a, C5a) split and produce anaphyla toxins
which cause localized mast cell degranulation and increase local vascular permeability.
• When formed bulky antigen-antibody complexes aggregate and combine with the activated
complement, they chemotactically attract the polymorphonuclear leucocytes. These cells release
lysosomal enzymes in large quantities to cause tissue damage.

D. Hypersensitivity Type IV:

• Type IV hypersensitivity is the only type of delayed hypersensitivity.


• It is mainly controlled by T-cells, macrophages and dendritic cells.
• It is not the instant response but it is manifested after the second exposure to an allergen. So there is
delayed appearance of allergic symptoms.

Mode of action:

• Delayed hypersensitivity is maintained by T- lymphocytes.


• T-cells (lymphocytes) have two main types—the CD4+ cells and CD8+ cells. Type IV
hypersensitivity requires CD4+ type.

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• The special group of CD4+ cells take part in type IV hypersensitivity and are called T-D cells
(delayed).
• Again T-helper cell (TH cell) includes T-D cells which constitutes the bulk of CD4+ T-cells.
• TH cells are again distinguished into TH-1 and TH-2 type, of which TH.2 cells are mainly responsible for
activation of B-cell to produce immunoglobulins and TH-1 cells are involved in causing the
inflammatory responses including delayed hypersensitivity reactions.

Comparison of Different Types of hypersensitivity

Type-I Type-II Type-III Type-IV


Characteristics
(anaphylactic) (cytotoxic) (immune complex) (delayed type)

Antibody IgE IgG, IgM IgG, IgM None

Antigen Exogenous Cell surface Soluble Tissues and organs


Type of immune
Humoral Humoral Humoral Cellular
Response

Response time 15-30 minutes Minutes-hours 3-8 hours 48-72 hours


Appearance Weal and flare Lysis and Erythema and Erythema
Necrosis edema, necrosis
Histology Basophils and Antibody and Complement and Monocytes and
Eosinophil Complement Neutrophils lymphocytes

Transferred with Antibody Antibody Antibody T-cells

Examples Allergic asthma, Erythroblastosis SLE, farmer's lung Tuberculin test,


hay fever fetalis, disease poison ivy,
Goodpasture's granuloma
Nephritis

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