1. Type I Hypersensitivity: Type I hypersensitive reactions are the com­monest type among all types which is mainly induced by certain type of antigens i.e. allergens. Actually anaphylaxis means “opposite of protec­tion” and is mediated by IgE antibodies through interaction with an allergen

1. SJM College of Pharmacy,
Chitradurga
Prepare By,
Adarsh Patil
Ass Professor(Pharmacognosy)
SJM College of Pharmacy
1
PHARMACEUTICAL
BIOTECHNOLOGY

2. 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.

3. • 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.

4. • 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.

5. • 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

7. 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

8. (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

10. (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.

11. (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.

12. 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.

13. • 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

15. (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

17. 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.

18. 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 hype-
rsensitivity. For this reason Type III is called immune
complex hypersensitivity

19. (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.

20. (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.

21. 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.

22. (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

24. (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).