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Hypersesnsitivity PDF / PPT

PHARMACEUTICAL
BIOTECHNOLOGY

Hypersesnsitivity

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INTRODUCTION

• Hypersensitivity reaction denotes an immune response resulting in

exaggerated or inappropriate reactions harmful to host.

• Hypersensitivity is an immune response mobilizes a battery of

effector molecules that act to removes antigen by various

mechanisms.

• Generally, these effectors molecules induce a localized inflammatory

response that eliminate antigen without extensively damaging the

host’s tissue.

 

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• Under certain circumstances, however, the inflammatory

response(Hypersensitivity) can have deleterious effects,

resulting in significant tissue injury, serious disease, or even

death.

• It is a harmful immune response in which tissue damage is

induced by exaggerated or inappropriate immune responses

in a sensitized individual on re-exposure to the same antigen.

• Both the humoral and cell-mediated arms of the immune

response may participate in hypersensitivity reactions.

 

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• Depending on the time taken for the reactions, and the

mechanisms that cause the tissue damage,

hypersensitivity has been broadly classified into

immediate type and delayed type. •

• In the former, the response is seen within minutes or

hours after exposure to the antigen and in the latter, the

process takes days together to manifest as symptoms.

 

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• Gell and Coomb described four types of hyper-
sensitivity 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

 

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1. Type I Hypersensitivity:

• Type I hypersensitive reactions are the com-

monest type among all types which is mainly

induced by certain type of antigens i.e. allergens.

Actually anaphylaxis means “opposite of protec-

tion” and is mediated by IgE antibodies through

interaction with an allergen

 

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(i) Mode of Action:

• During the activity, this class of antibody (IgE) binds with

high affinity to FC (Fragment crystalized) receptors on the

surface of constant domains of tissue mast cells and blood

basophils. Such IgE-coated mast cells and basophils are said

to be sensitized. When the individual is exposed to the same

allergen again, then it cross-links the membrane bound IgE

on sensitized mast cells and basophils and degranulation of

those cells result

 

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(ii) Biological effects:

1. Normally anaphylactic responses are of a mild type producing symptoms— like hay-

fever, running nose, skin eruptions called as ‘nives’ or breathing difficulties.

2. The pharmacologically active mediators released from the granules exert biological

effects on the surrounding tissues.

3. In some cases, the responses may be severe, develop within a few minutes (2-30

mins) and may even cause death before any medical help is called anaphylactic

shock.

4. The principal effects of vasodilation and smooth muscle contraction may be either

systematic or localized.

 

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(iii) Components of type-I reactions

1. Different allergens

2. Reaginic antibody (IgE)

3. Mast cells and basophils

4. IgE—binding FC receptors.

5. High—affinity and low-affinity receptors.

 

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2. Type II Hypersensitivity:

Type II hypersensitive reactions are those in which tissue or cell

damage is the direct result of the actions of antibody and

complement.

(i) 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.

 

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• 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 react with the antibodies in

the serum of the recipient and in combination with activated

complement, the erythrocytes undergo haemolysis

 

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(ii) Biological effect:

1. Haemolytic disease of the newborn develops when

maternal IgG antibodies specific for foetal blood-

group antigens cross the placenta and destroy foetal

red blood cells. Severe haemolytic disease of the new

born is called erythroblastosis foetalis, when an

Rh+ foetus expresses an Rh antigen on its blood cells

that the Rh– mother does not express it

 

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2. Certain antibiotics (e.g. penicillin, cephalo-

sporin and streptomycin) can absorb non-

specifically to proteins on RBC membranes,

forming a complex similar to a hapten-carrier

complex and gradually induces anaemia called

drug-induced haemolytic anaemia.

 

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3. Type III Hypersensitivity:

When an antigen enters within the body then the

antibody reacts with antigen and generates immune

complex. 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

 

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(i) Mode of action:

1. These reactions develop when immune complexes activate the complement

system’s array of immune effector molecules. Complement components

(C3a, C4a, C5a) split and produce anaphylatoxins which cause localized

mast cell degranulation and increase local vascular permeability.

2. 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.

 

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(ii) Biological effect:

1. The recipient of a foreign antiserum develops antibodies, specific for the foreign

serum proteins from circulating immune complexes and within days or weeks after

exposure to foreign serum antigens, an individual starts to develop serum sickness

including fever, weakness, vasculitis (rashes) with edema, erythema,

lymphadenopathy, arthritis and glomerulonephritis.

2. Due to deposition of IgG antigen complexes in the blood vessels cause local damage

and deposit in blood vessels of kidney glomeruli called Arthus Reaction.

3. Inhalation of bacteria and fungal spores gives rise to a disease called farmer’s lung

forming immune complexes in the epithelial layers of the respiratory tract.

 

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4. Type IV Hypersensitivity:

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. The

appearance of allergic symptoms come in delay.

 

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(i) 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. 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

 

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(ii) Biological effect:

1. A microbial agent that elicits a delayed hypersensitivity is tuberculin

which is a purified protein derivative (PPD) of tubercle bacilli

(Mycobacterium tuberculosis). Mycobacterium leprae, the microbial

agents also stimulate delayed hypersensitivity.

2. The tuberculin skin test (Mantoux test) is used to determine if a

person has T-cell mediated reactivity towards tubercle bacilli (also known as Koch’s bacilli).

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