Hypersensitivity Reactions

basics

Dr.T.V.Rao MD

1 Dr.T.V.Rao MD

Hypersentivity Reactions

Allergies Greek = altered reactivity

1906 – von Pirquet coined term: hypersensitivity

Hypersensitivity reactions – ‘over reaction’ of the

immune system to harmless environmental

antigens

2 Dr.T.V.Rao MD

Definition

• Definition :

Hypersensitivity

refers to the

injurious

consequences in

the sensitized host

,Following contact

with specific

Antigen

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How we classify Hypersensitivity

• Hypersensitivity refers to undesirable

(damaging, discomfort-producing and

sometimes fatal) reactions produced by the

normal immune system.

• Hypersensitivity reactions require a pre-

sensitized (immune) state of the host.

• Hypersensitivity reactions can be divided into

four types: type I, type II, type III and type IV,

based on the mechanisms involved and time

taken for the reaction.

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Hypersensitivity

Immunity protects against

Infections, Toxins.

Many other functions.

But Immunity can be Injurious,

When exaggerated causes

Tissue Damage,

Disease and Death

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Immune response is

altered • In hypersensitivity

Antigen is not

Important But what

happens as a

result of Immune

reaction

• Allergy a Synonym

for Hypersensitivity.

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What happens in Hypersensitivity

• Initial contact sensitizes the

Immune system. The antigen acts

as priming dose

• Causes the priming of B/T

Lymphocytes,

• Subsequent dose a shocking

dose. 7 Dr.T.V.Rao MD

Classification of Hypersensitivity

Coombs and Gell • Classified into 4 types on Mechanism and

Pathogenicity

• Type I

Generalized – Anaphylactic shock.

Localized - Hay fever, Asthma

Type II Cytotoxic ( Antigen + Antibody )

Type III Immune complex

Type IV Cell Mediated.

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Hypersensitivity reactions

Type Mechanism Antigen Onset

I IgE-Ag triggers

Mast cell mediators Allergen minutes

II IgG or IgM binds to

cell surface; ADCC

or complement

Cell surface

molecule Few

hours

III

Immune complexes,

inflammation Soluble or

particulate Few

hours

IV Cytokines (T cells,

Macrophages, CTL) Chemicals,

intracellular 1-3

days 9 Dr.T.V.Rao MD

Classification of Hypersensitivity

• Immediate and Delayed.

Immediate type

Also called as Immediate

Hypersensitivity

Popularly called as B cell Mediated

Hypersensitivity

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Examples of Immediate

Hypersensitivity

• Anaphylaxis

• Atopy,

• Antibody mediated cell

damage.

• Arthus Phenomenon

• Serum sickness

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Hypersensitivity-1

• Inappropriate immune responses

• Type I are immediate type, in which

antigen binds to IgE on mast cells,

histamine released.

– Histamine: smooth muscle contraction,

vasodilatation.

– Results in asthma, diarrhea, shock depending

on where antigen enters body. Ex. Bee sting

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Type II Hypersentivity

• Type II are cytotoxic reactions like the Rh factor problem and bad blood transfusions.

– Rh is one of many blood groups, like ABO

– An Rh+ fetus in an Rh- mother means she gets immunized by baby’s blood cells, makes Antibodies.

– Second pregnancy, fetal RBCs are attacked.

– Solution: give Rho-gam during 1st pregnancy.

• .

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Type III and IV

• Type III are immune complex

disorders, where too many agn-

aby clumps cause inflammation

• Type IV are delayed type, T cell

produces various cytokines which

affect macrophages.

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Type IV

• Type IV are delayed type, T cell

produces various cytokines which

affect macrophages.

–The bar fight scenario: come, stay, get

angry.

–Angry macrophages cause much tissue

damage.

–Ex. Poison ivy; urushiol-coated cells

killed. 15 Dr.T.V.Rao MD

Delayed Hypersensitivity

T Cell Mediated

• Tuberculin

type.

• Contact

dermatitis.

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Type I Hypersensitivity

Dr.T.V.Rao MD 17

Examples of Immediate

Hypersensitivity

• Anaphylaxis

• Atopy,

• Antibody mediated cell damage.

• Arthus Phenomenon

• Serum sickness

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Type I hypersensitivity

• Anaphylaxis = Ana means without

Phylaxis protection ( Rich )

Sensitizing dose more effective when given parentally

Antigen can hapten also may take 2-3 weeks to produce sufficient IgE

Shocking dose is effective if given IV

The nature of antigen should correspond to antibodies

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Type I

• Anaphylactic Ig E ( Reagin )

• Antibodies are fixed on Tissue cells

• Eg Mast cells and Basophils

• Antigen + Antibody combination causes

release of Pharmacologically active

substances

• Occurs in Acute and Chronic or recurrent

form (Non Fatal and localized Atopy)

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Anaphylaxis

• Classical Immediate Hypersensitivity

• Experiments in dogs with Sea anemones

• Guinea pigs

• By any route with Antigens and Haptens

• 2-3 weeks later with sensitizing or

shocking dose I V

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The type I – anaphylaxis involves

• The target organs are several vital organs

and tissues,

• On the target tissue, causes

oedema,decreased coagabulity of Blood

• Leads to fall of Blood pressure

• Leucopenia and thrombocytopenia

• Guinea pigs are highly sensitive

• Human are intermediate in reactivity

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Experiment in Guinea pig

• A guinea pig is

injected with small

dose of antigen eg

Egg albumin no

reaction observed.

• The same animal

injected with egg

albumin after 2 weeks

by IV route

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2nd dose produces Anaphylaxis

• The 2nd produced anaphylactic shock

• Manifested with

Restlessness

Chewing and rubbing nose

Wheeze

Developed convulsions

Animal died

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Same is experienced in

Humans

• With bee

sting

• Penicillin

administration

• Happens in

sensitized

individuals 25 Dr.T.V.Rao MD

Local reactions happen

• Asthma

• Hay fever

• The reactions depend on the level of IgE

• The biologically active molecules are

present in in the mast cells and Basophilic

granules synthesize to active production

after triggering with antigenic stimulations.

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Nature of IgE

• Present in low

fractions compared

with other

Immunoglobulin's

• IgE is heat sensitive

inactivated at 560c in

2 – 4 hours heat

causes damage to Fc

particle

• IgA deficiency produces

excessive IgE

Dr.T.V.Rao MD 27

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The biological mediator on effect stage 1. Histamine:

Dilate blood vessel Increase vascular permeability

2. Leukotriene's:

Bronchial smooth muscles contract Asthmas

3. Prostaglandin:

High concentration of PGE Inhibit the secretion of histamine

low concentration of PGE promote the release of histamine

4. Platelet activating factor (PAF) :

Agglutinate and activate platelets to release histamine

5. Eosinophil chemotactic factor（ECF-A）:

6. Bradykynin :

Vasodilator function 29 Dr.T.V.Rao MD

Important chemical and substances

produced to cause reaction

• Histamine: Dilates and increases

permeability of blood vessels (swelling

and redness), increases mucus

secretion (runny nose), smooth muscle

contraction (bronchi).

• Prostaglandins: Contraction of smooth

muscle of respiratory system and

increased mucus secretion.

• Leukotriene's: Bronchial spasms.

– Anaphylactic shock: Massive drop 30 Dr.T.V.Rao MD

4. Skin allergy:

4. Common disease of type I hypersensitivity

1. Systemic anaphylaxis: a very dangerous syndrome

1) Anaphylactic drug allergy ：penicillin

2) Anaphylactic serum allergy ：

2. Respiratory allergic diseases :

1) Allergic asthma：acute response, chronic response

2) Allergic rhinitis

3. Gastrointestinal allergic diseases :

The lack of SIgA protein hydrolase Undigested protein Allergen

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Atopy

• When the antigen and antibody IgE react

produce certain pharmacologically active

substances

Can cause

Conjunctivitis,

Rhinitis

G E involvement

Dermal involvement Urticaria

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Dr.T.V.Rao MD 33

p. 374

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Primary Mediators of

Anaphylaxis • Histamine an vasoactive in human Anaphylaxis

• Histidine on Decarboxylation to Histamine

• Stimulates the sensory nerves

• Causes burning and itching

• Causes vasodilatation and hyperemia

• Smooth muscle stimulation

• Affects the Intestines, Uterus, Especially

bronchioles

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Effects of type I reactions

Systemic anaphylaxis

Respiration becomes difficult

Blood pressure drops

Smooth muscles of bladder and GI tract

contract

Bronchoconstriction

Countered by epinephrine

relaxes smooth muscles

decreases vascular permeability

improves cardiac output

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Mechanism of Anaphylaxis

• Ig E cell fixed on Mast cells and

Basophiles.

• Antigen + Antibody

• Bridges the gap

• Leads to deregulation

• Releases Biologically active substances

from granules of the cells.

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Histamine release occurs within

minutes

Binds to receptors on target cells

smooth muscles contract

eosinophil's attracted

mucus secretion

platelet activation

blood vessel dilation

Blocked by various compounds: antihistamines,

Epinephrine, corticosteroids 38 Dr.T.V.Rao MD

Secondary mediators of

Anaphylaxis

• Prostaglandins Leukotriene's

• Thromboxane's,

Lead to manifestation with

1Transient constriction of

Bronchioles

2 Dilatation of capillaries,

3 Platelet activation factor, 39 Dr.T.V.Rao MD

Serotonin

• Produces on Decarboxylation of

Tryptophan

• Found in Intestines, Mucosa, Brain tissue,

Platelets

• Causes smooth muscle contraction

• Increases capillary permeability

• Vasoconstriction

• Human ?

40 Dr.T.V.Rao MD

Other factors

• Heparin Not

in human

• Enzymatic

mediators

proteases

and

hydrolases

Dr.T.V.Rao MD 41

Effects of Histamine

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Many of us suffer

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Secondary factors in

anaphylaxis

• Prostaglandins and Leukotriene's releases

from disrupted cell membranes

• Mast cells and other leukotriene's

• Slow reacting substances

• Prostaglandins affects secretion by

mucosal glands

• Platelet activating factor – aggregates

platelets ad release vasoactive amines

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Other Mediators

• By complement

activation

• Bradykynin

• Anphylactoid

reactions can be

caused due to IV

Peptone, Trypsin

by IV routes

Dr.T.V.Rao MD 45

Clinical effects • Causes smooth muscle contraction.

• Increased vascular permeability

• Many organs Target organ – shock organ

• Causes

Edema Fall of BP, Coagulation of Blood, Leucopenia, thrombocytopenia

Guinea pigs most susceptible

Humans Intermediate

Bee stings, Penicillin,

Causes the constriction of smooth muscles( Bronchioles )

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Clinical effects in Humans

• Itching of scalp, Tongue

• Flushing of skin, Bronchial spasm

• Hypotension

• Loss of consciousness and Death

• Previously with serum

• Now with Antibiotics.

• Adrenaline is life saving 0.5 ml 1:1000 dils

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Clinical effects

Cutaneous Anaphylaxis • Intradermal Injection

in sensitized host

• Wheal and flare

reaction

• Useful in skin testing

( But dangerous )

• Passive cutaneous

anaphylaxis.

Dr.T.V.Rao MD 48

Skin tests

Skin test via intra

dermal injection of

allergens: if an

individual is allergic

to the substance

injected, local mast

cells de granulate

producing a “wheel

and flare” response

within minutes

49 Dr.T.V.Rao MD

Secondary Mediators of

Anaphylaxis

• Slow reacting

substances

• Prostaglandins,

• Platelet

activating factors

Cytokines

• IL3, IL4, IL5

Dr.T.V.Rao MD 50

Atopy

• Agent Inhaled – Pollens /Dust

• Ingested – Egg , Milk

• Contact with skin – Conjunctiva

• Ig E is over produced

• Bottle fed infants

• Estimation of Ig E by RAST

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5. Therapy of type I hypersensitivity

1. Allergen avoidance : Atopy patch test

2. Desensitivity therapy / Hyposensitization :

1) Allogenic serum desensitivity therapy:

2) Specific allergen desensitivity therapy

Repeated injection small amounts of allergen, Temporality

IgG+allergen Neutralizing antibody, Blocking antibody

3. Drug therapy：

1) Stabilization of triggering cells

sodium cromoglycate stabilize the membrane, inhibit mast cell degranulation

2) Mediator antagonism

Chlor-Trimeton Antihistamine

Acetylsalicylic acid Bradykinin antagonism

3) Improve the responsibility of target organs

4. New immunotherapy ：

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Hypersensitivity type II

Reactions

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Type II Hypersensitivity

• Type II hypersensitivity or cytotoxic

hypersensitivity is caused by

antibody-mediated reactions. When

the immune system reacts to antigens

it produces various Immunoglobulin's

or antibodies, usually long-lasting

immunoglobulin G (IgG) antibodies.

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Type II (Cytotoxic) Reactions

– Involve activation of complement by IgG or IgM binding to an antigenic cell.

– Antigenic cell is lysed.

– Transfusion reactions:

• ABO Blood group system: Type O is universal donor. Incompatible donor cells are lysed as they enter bloodstream.

• Rh Blood Group System: 85% of population is Rh positive. Those who are Rh negative can be sensitized to destroy Rh positive blood cells.

– Hemolytic disease of newborn: Fetal cells are destroyed by maternal anti-Rh antibodies that cross the placenta.

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What Happens in type II

• Ig G and Ig M combines with antigenic determinants on the cells.

• Leads to cytotoxic and catalytic effects

Eg - Anti erythrocyte antibodies in autoimmune anemia's and hemolytic disease of the new born.

Other free antigens or hapten may be absorbed on the cell surface

Subsequent reactions will lead to cell damage

Drugs too behave in the same way

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Type II Hypersensitivity

• LATS Antibodies

stimulate

determinants on

Thyroid – Leads to

excessive

secretion of

Thyroid hormones

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Haptens too can produce type

II Hypersensitivity • . The antigens are

normally endogenous,

although exogenous

chemicals (haptens)

which can attach to

cell membranes can

also lead to type II

hypersensitivity.

58 Dr.T.V.Rao MD

Type II Hypersensitivity

• The binding of these antibodies to

the surface of host cells then

leads to:

• opsonization of the host cells

whereby phagocytes stick to host

cells by way of IgG, C3b, or C4b

and discharge their lysosomes

59 Dr.T.V.Rao MD

Type II Hypersensitivity (Contd)

• Anti erythrocyte antibodies

• Autoimmune Anemia's Hemolytic

anemia's.

• Antigen + Antibody =Cell damage

• Even Hap tens act in the place of Antigen

• Disrupts the normal function

• Graves disease , Myasthenia gravis.

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Opsonization During Type-II

Hypersensitivity, Step-1

The Fab of IgG reacts with epitopes on the host cell membrane. Phagocytes bind to the Fc portion

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Opsonization During Type-II Hypersensitivity,

Step-2

Phagocytes binding to the Fc portion of the IgG and discharge their lysosomes causing cell

lysis.

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Examples of Type II Hypersensitivity.

• Pemphigus: IgG antibodies that react with the intracellular substance found between epidermal cells.

• Autoimmune haemolytic anaemia (AHA): This disease is generally inspired by a drug such as penicillin that becomes attached to the surface of red blood cells (RBC) and acts as hapten for the production of antibody which then binds the RBC surface leading to lysis of RBCs.

• .

63 Dr.T.V.Rao MD

Good pasture's syndrome

• Good pasture's

syndrome: Generally

manifested as a

glomerulonephritis,

IgG antibodies that

react against

glomerular basement

membrane surfaces

can lead to kidney

destruction

64 Dr.T.V.Rao MD

Type II Hypersensitivity

• Salmonella , and Mycobacterium can produce Hemolytic crisis

• Diagnostic tests include detection of circulating antibody against the tissues involved and the presence of antibody and complement in the lesion (biopsy) by immunofluorescence

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Type III Hypersensitivity

Reactions

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Introduction • Immune

complexes(Ag and Ab)

deposit in tissues

such as blood vessels

and glomeruli.

• activate

complement, and

cause tissue injury

or dysfunctional

responses.

67 Dr.T.V.Rao MD

Arthus reaction • Injecting repeatedly sc Normal horse serum

• Later injections leads edema, indurations

hemorrhagic necrosis

manifest as localize from of generalized hypersensitivity

Damage is caused due to Antigen and antibody complexes, leads to activation of complement

Release of inflammatory molecules

Vascular permeability, infiltration of neutrophils.

Causes tissue necrosis

Eg Inhalation of Actinomyctes from mouldy hay grain causes Farmer’s lung

68 Dr.T.V.Rao MD

Type III Hypersensitivity

• Example of a Type III hypersensitivity is

serum sickness, a condition that may

develop when a patient is injected with a

large amount of e.g. antitoxin that was

produced in an animal. After about 10

days, anti-antitoxin antibodies react with

the antitoxin forming immune complexes

that deposit in tissues.

69 Dr.T.V.Rao MD

Type III hypersensitivity

• Type III hypersensitivity is also known as

immune complex hypersensitivity. The reaction

may be general (e.g., serum sickness) or may

involve individual organs including skin (e.g.,

systemic lupus erythematous, Arthurs reaction),

kidneys (e.g., lupus nephritis), lungs (e.g.,

Aspergillosis), blood vessels (e.g., polyarteritis),

joints (e.g., rheumatoid arthritis) or other organs.

This reaction may be the pathogenic mechanism

of diseases caused by many microorganism

70 Dr.T.V.Rao MD

Type III Hypersensitivity

• Antigen and Antibody complexes

• Accumulate around the small blood vessels cause damage to cell

• Arthus Reaction

Occurs as a local manifestation

Antigen + Antibody complexes

Releases Inflammatory molecules,

Infiltration with Neutrophils

Reduces blood supply

Other example – Inhaled antigens produce Farmers lung

71 Dr.T.V.Rao MD

Neutrophil

C1 C2

C4

C3b & C5b

C5-C9

C3

C3a & C5a

Type III Hypersensitivity mechanism

72 Dr.T.V.Rao MD

2- Serum Sickness * A systemic immune complex phenomenon

* Injection of large doses of foreign serum

* Antigen is slowly cleared from circulation

* Immune complexes are deposited in various sites

fever

urticaria

* 10 days after injection Arthralgia

lymphadenopathy

splenomegaly

glomerulonephritis

antidiphtheritic serum

e.g. treatment with penicillin

sulphonamides

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Mechanism of damage in type-III

hypersensitivity

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Deposition of immune complexes

in blood vessel walls

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Disorders of the Immune System: Immune Complex Disease

Glomerular basement membrane of kidney

Large complex

Endothelial cell

Small complex 76 Dr.T.V.Rao MD

Type III Hypersensitivity (Cont )

• Serum Sickness –

Systematic form of Type III

Diphtheria Antiserum produces antibodies

Produces

Fever,

Lymphadenopathy

Splenomegaly

Arthritis

Glomerulonephritis

Endocarditis and Vasculitis

Mechanism – Foreign serum and antibodies Deposit in Endothelial Lining on Blood vessels.

Many times self limited.

77 Dr.T.V.Rao MD

78 Dr.T.V.Rao MD

Serum Sickness

• May last for 7-10 days.

• Bacterial Viral and Parasitic infection produce serum sickness.

• Important Diseases

Post Streptococcal Glomerulonephritis

Hepatitis B Infections

Auto immune conditions.

Disseminate malignancies.

79 Dr.T.V.Rao MD

Diagnosis and Treatment

• The presence of immune complexes in

serum and depletion in the level of

complement are also diagnostic.

Polyethylene glycol-mediated turbidity

(Nephelometry), binding of C1q and Raji

cell test are utilized to detect immune

complexes. Treatment includes anti-

inflammatory agents.

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Type IV Hypersensitivity

81 Dr.T.V.Rao MD

Type IV Hypersensitivity

• Type IV hypersensitivity is often

called delayed type hypersensitivity

as the reaction takes two to three

days to develop. Unlike the other

types, it is not antibody mediated but

rather is a type of cell-mediated

response

82 Dr.T.V.Rao MD

Type IV Reaction

Delayed Hypersensitivity • Also called as Cell Mediated

Immunity,

• Stimulates – Sensitizes CD4/CD8.

• Secretion of Lymhokines

Fluid/Phagocytes accumulate.

Not Induced by antibodies

T Cell Th1 Th2 Tc Take

active part

83 Dr.T.V.Rao MD

Delayed hypersensitivity.

• The reaction elicited by antigen occurs

relatively slowly (hence the name "delayed

hypersensitivity").

• The hypersensitivity is mediated via T-

cells and macrophages.

• The hypersensitivity illustrates both

antigen-specific (T-cell) and antigen non-

specific (macrophage) characteristics

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Dr.T.V.Rao MD 85

Type IV hypersensitivity is T cell

mediated

• The type IV hypersensitivity differs from the other three types of reactions in that it is not caused by antibodies, but by immunocompetent cells (lymphocytes). These lymphocytes are immunologically specific with receptors for the antigens, which can be different tissues (tissue antigens) or small molecular substances which, when fixed to the cell membrane, can function as antigens.

86 Dr.T.V.Rao MD

Type IV Reactions

• Type IV reactions, which are also called

delayed hypersensitivity reactions, as a

rule occur 12 - 48 hours after exposure to

the antigen. Type IV reactions lead to

inflammatory tissue damage and

infiltration of cells, which are principally

mononuclear (lymphocytes and

macrophages).

87 Dr.T.V.Rao MD

Type IV reactions

• The inflammatory reaction leads to

irreversible damage with deterioration of

the tissue. The classical examples of type

IV hypersensitivity are the positive

tuberculin reaction, contact dermatitis

(e.g. caused by nickel or chrome) and

rejection of tissues transplanted from other

individual

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Mechanisms of damage in delayed

hypersensitivity

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Several diseases based on

Delayed Hypersensitivity

• Type IV hypersensitivity is involved in the

pathogenesis of many autoimmune and

infectious diseases (tuberculosis, leprosy,

blastomycosis, Histoplasmosis,

toxoplasmosis, leishmaniasis, etc.)

granulomas due to infections and foreign

bodies

90 Dr.T.V.Rao MD

Tuberculin Type ( IV )

• Tuberculin reaction.

• Tuberculin Injection

• Sensitized to Tuberculin protein.

• Indurations develop at the site < 48 hours.

• Unsensitized

No response

Bacteria,

Fungi,

Viruses,

Parasites

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Tuberculin Test

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Measurement of Induration

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Immune Complex Mediated

Hypersensitivity

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Other agents stimulating Type IV

Hypersensitivity

• Topical application of Penicillin in

creams

• Lange ham cells in epidermis absorb

the drug or chemical T Cells are

stimulated

• Lymph nodes acts as store houses

• Repeated applications leads to

Eczema like conditions 95 Dr.T.V.Rao MD

96 Dr.T.V.Rao MD

3. Common disease of type IV hypersensitivity

1) Infectious delayed type hypersensitivity

OT( Old Tuberculin ) test

2) Contact dermatitis :

Paint, drug red rash, papula, water blister, dermatitis

3) Acute rejection of allogenic transplantation and

immune response in local tumor mass

Same disease (SLE), multiple immune injury ,hypersensitivity involved

Same drug (penicillin), several types of hypersensitivity

97 Dr.T.V.Rao MD

*a contact-sensitizing agent is usually a small molecule that

penetrates the skin then binds to self-proteins, making the

protein “look” foreign

Can be caused by poison ivy and mango sap Contact Dermatitis

DTH as a result of a contact-sensitizing agent*

98 Dr.T.V.Rao MD

Contact dermatitis

• Contact dermatitis

or Irritant dermatitis

is a term for a skin

reaction resulting

from exposure to

allergens (allergic

contact dermatitis) or

irritants (irritant

contact dermatitis).

99 Dr.T.V.Rao MD

Contact Dermatitis ( IV )

• Delayed hypersensitivity – Skin contact.

• Cell Mediated response.

• Nickel, Chromium, Dyes , Penicillin's

• Antigens absorbed,

• Langerhams cells capture – Migrate to

draining lymph nodes,

• Present the processed Antigens with MHC

molecules to Immune cells.

100 Dr.T.V.Rao MD

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