Hypersensitivity

types of hypersensitivity

1. Hypersensitivity:
 Is defined as the violent reaction of the immune system leading
to severe symptoms and even death in a sensitized animal when
it is reexposed to the same antigen for the second time
 Portier and richet first to recognize and describe
hypersensitivities
 Immune system becomes a destructive process in hypersensitivy
 Only about 10% of humans suffer from hypersensitivity
 In clinical terms hypersensitivity are called allergens
Factors causing hypersensitivity:
 Factors causing allergy are called allergens
 They may be extrinsic factors(into the body from outside) and
intrinsic factors(remains within the body)
 Drugs like pencillin,aspirineetc
 Air borne particles like pollen grains ,spores,
 Food stuffs like shell fish
 Infectious organisms like bacteria, viruses fungi and parasite
 Blood transfusion
Types of hypersensitivity;
 Based on the time taken for the reaction:
Immediate hypersensitivity:
 Immune reaction manifest in a short duration of time within
minutes
 Drugs like pencillin,hay fever
 Antibody mediated hypersensitivity
 Passively transported form one host to another host by the
transfer of serum
Delayed hypersensitivity:
 Immune reaction manifest slowly from 24 hours to 72 hours
 Tuberculin reaction
 Reaction between antigens and T cells
 It is a cell mediated immunity (T cell involved)
 Cannot be transferred from one host to another host
Classification based on the different mechanism of
pathogenesis:

2.  Coombs and gell proposed 5 types of hypersensitivity
 Type I – anaphylactic hypersensitivity
 Type II – antibody dependent cytotoxic hypersensitivity
 Type III – immune complex mediated hypersensitivity
 Type IV – cell mediated hypersensitivity
 Type V – stimulatory hypersensitivity
Type I hypersensitivity:
 Anaphylaxis is defined as an allergic reaction of an organism to
a foreign substance to which it has previously become sensitized
result in the release of histamine,serotonin and other vasoactive
substances
 Anaphylaxis coined by richet
 Immediate type of hypersensitivity
Mechanism of anaphylaxis;
 IgE antibody involved in this type of hypersensitivity
 When a person receives the allergen for the first time
 The allergen gets attached to the B cells
 The allergens stimulate the B cell to change into plasma cells
 The plasma cells make Ig E antibodies(regains-IgE antibodies
are made by the people who are allegic)
 Regains(IgE) attached to the surface receptors of mast cells with
the help of their Fc segment
 Now the person is said to be immunized or sensitized for that
antigen(priming dose or sensitizing dose)
 Person exposed to the same antigen for the second time (shock
dose)
 Allergen cross links the IgE antibodies attached to the mast cells
 Triggers the mast cells
 Mast cell releases granules (histamine,serotonin,heparin)so
called degranulation
 They bring about their action quickly and immediately
 Brings about the anaphylactic reaction such as burning and
itching sensation ,vasodilation,capillarypermeability,smooth
muscle contraction,vasoconstriction ,bronchocontrictions and
platelet adhesion and aggregation

3. 
Prevention and treatment:
 Avoiding contact with allegens
 Desensitization
 Hyposenstivity
 Stabilizing mast cells by using isoprenaline and sodium
chromoglycate
 Inhibitors of histamine receptors by antihistamines
 Blocking the release of histamines by adrenergic drugs


Type II hypersensitivity
 Also called antibody dependent cytotoxic hypersensitivity
 Due to the interaction of antibodies and cell associated antigens
 When antibodies attach to the antigens located on the surface of
cells the cells become cytotoxic
Types of cytotoxic hypersensitivity;
1.isoimmune reaction:
 The reaction brought about by the antigen and antibody of two
individuals belonging to the same species are called
isoimmunereactios

4. Transfusion reaction
 The agglutination or lysis of recipient blood due to mismatched
blood group is called transfusion reaction
 It occurs in ABO blood groups as well as Rh blood group
Erythroblastosisfoetalis:
 Haemolytic disease caused by the reaction of Rh antigen and Rh
antibody
 It occurs in the Rh+ baby developing in an Rh – mother
 The Rh antibody involved in this reaction belongs of Ig G type
Transplant rejection reaction:
 A transplant can produce antibodies to transplantation antigens
these antibodies are cytotoxic to graft tissue
2.autoimmunereactios:
 The reaction brought about by the interaction of an antigen and
antibody of the same individual is called autoimmune reaction
 Ex; autoimmune haemolyticanaemia
 Antibodies produced against its own RBC antigens
 Autoimmune thrombocytopaenicpurpura
 Autoimmune thyroiditis
 Autoimmune glomerulonephritis
 Mechanism of type II hypersensitivity:
 IgG and IgM antibodies bound to the cellular antigens on the
surface of cells
 Leading to complement activation and cell lysis
 IgG can also activate ADCC (antibody dependent cell
cytotoxicity),macrophages, and neutrophils
Type III hypersensitivity:
 Also called as immune complex mediated hypersensitivity
 Produced by the antigen-antibody complex or immune complex
 These antigens and antibodies combine together to form an
insoluble precipitate called antigen antibody complex
 Anigens involved are soluble antigens
 Antibodies involved are IgG or Ig M
Mechanism of action;
 The antibodies bind with the antigen to form immune complexes

5.  These complexes attached in and around minute capillaries
 These complexes bind to the complement
 Activates the classical pathway
 C3 and C5 complement produces active factors called
anaphylotoxin and chemotoxin
 Anaphylotoxin triggers mast cells………….release of
amines…………tissue damage
 Chemotoxin attracts the polymorphs and mast
cells…….promote phagocytosis by the release of hydrolytic
enzymes ..,…leads to tissue damage
Examples:
Arthus reaction:
 Observed by arthus on rabbit by a repeated injection of horse
serum
 It is local immune complex reaction (specific area) o the ksin
 The antibodies produced are of Ig G type
Serum sickness;
 Immune complex disease caused by the enormous amount of
foreign serum
 Systemic form (affecting all organs) of type III hypersensitivity
 The antibodies involved are Ig G TYPE
TYPE IV hypersensitivity:
 Caused by the interaction between antigens and sensitized T
cells reaction leads to inflammation reaction and causes tissue
damage
 Antibodies are not involved in this type
 T cells are involved so called cell mediated hypersensitivity
 Delayed type hypersensitivity
 It cannot be transferred from one animal to another by the
transfer of antibodies
 Is caused by infectious pathogens like bacteria,viruses, fungi
and parasites

Examples:
 Tuberculin reaction, contact dermatitis, small pox, leprosy,
measles,

6.  Mechanism of type IV hypersensitivity:
 When T cell primed to an antigen ,come in contact with the
same antigen for the second time, the cells release soluble
proteins called lymphokines(cytokines)
 The lymphokines activates macrophages to kill intracellular
bacteria like tubercle bacilli etc.
Tuberculin reaction;
 When small dose of tuberculin is injected intradermally……..if
sensitized, the reaction will occur..if not sensitized there will be
no reaction
 Reaction produced by T cell so called cell mediated
hypersensitivity and occur only after 48-72 hours so called
delayed hypersensitivity
Contact dermatitis:
 Inflammation of the skin due to the contact with a substance to
which the person is allergic
 Dinitrochlorobenzene is a potent skin senstizer ,it evokes
contact dermatitis in 95% of people
Type V hypersensitivity:
 Is caused by the interaction of antibodies with cell surface
antigen leading to stimulation of cells
 In type II also the interaction between antibodies and cell
surface antigens causes destruction of cells but here stimulation
of cells occur
 Ex; graves disease
 Also called thyrotoxicosis
 Disease condition owing to the over activity of thyroid gland
 It is caused by an antibody called long acting thyroid stimulator
it is an IgG type
 It acts on the cell surface antigen which is basically a receptor
for thyroid stimulating hormone produced by the pituitary gland
 Causes the release of thyroxine in higher dose from the thyroid
cells