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Hyper sensitivity reaction type I and type II
1. HYPERSENSITIVITY
REACTION(TYPE I and TYPE II)
BY: JEGANATHAN C
DEPARTMENT OF BIOMEDICAL SCIENCE
E.Mail : jeganathanbms@gmail.com
Cell.no: 9626307988
2. INTRODUCTION
⢠Hypersensitivity (also called hypersensitivity
reaction or intolerance) is a set of undesirable
reactions produced by the normal immune
system, including allergies and autoimmunity.
⢠Inflammatory response can have deleterious
effects ,resulting in significant tissue damage
or even death. this appropriate immune
response is termed hypersensitivity or allergy.
5. IgE mediated hypersensitivity
⢠Type 1 reaction also called as immediate
hypersensitivity reaction
⢠It is induced by certain types of antigen ,referred
to as allergens
⢠The allergen induces a humoral antibody
response
⢠IgE binds with high affinity to Fc receptors on the
surface of tissue mast and basophils
⢠Such IgE- coated mast cells and basophils are
sensitized
6. ContinuousâŚâŚâŚ
⢠A later exposure to the same allergen cross-
links the membrane- bound IgE on sensitized
mast cells and basophils, causing
degranulation of these cells
⢠The pharmacologically active mediators
released from the granules act on the
surrounding tissues
7.
8. COMMON ALLERGEN ASSOCIATED
WITH TYPE 1 REACTION
⢠Proteins-foreign serum , vaccines
⢠Plant pollens-rye grass ,ragweed, timothy
grass,birch trees
⢠Drugs- penicillin, sulfonamides, local
anesthetics,salicylates
⢠Foods-nuts, seafood,eggs,peas,beans,milk
⢠Insect products-bee venom, wasp venom,ant
venom,cockroach calyx,dust mites
⢠Mold spores , animal hair and dander
9. MECHANISM OF ACTION
⢠Receptor cross linkage
⢠Intracellular events leading to mast-cell
degranulation
14. NON IgE ANTIBODY-RELATED INITIATORS
OF TYPE I HYPERSENSITIVITY
Complement Activation Products:
C3a, C4a, C5a
"Anaphylotoxins"
Various Drugs: ACTH, Codeine,
Morphine, Penicillin
16. Mediators of Type I Hypersensitivity:
Stored in Mast Cell Granules
Histamine, Heparin and Serotonin
Increased vascular
permeability;
Smooth Muscle Contraction
Chemotactic Factors for
Eosinophils and Neutrophils Attract Eosinophils & Neutrophils
Proteases Degrade Basement membranes of blood vessels;
Activate bronchial mucous secretions;
Activate Complement
17. Secondary Mediators of Type I Hypersensitivity:
Synthesized and Released After Mast Cell Activation
Platelet Activating Factor Platelet Aggregation&
Degranulation;
Smooth muscle contraction
Prostaglandins Vasodilation; Smooth muscle contraction
Leukotrienes (SRS-A)* Increased vascular permeability;
Pulmonary smooth muscle contraction
(*SRS-A : Slow Reacting Substance of Anaphylaxis)
Bradykinin Increased vascular permeability;
Smooth muscle contraction
Cytokines: Systemic Anaphylaxis;
(IL1 & TNF-a; Others*) Altered Cell adhesion
* See Slide 42
18. Detection of type I hypersensitivity
⢠Radioimmunosorbent test (RIST)- Quantify
Nano gram amounts of total serum IgE
⢠Radioallergosorbent test (RAST)-Quantify
Nano gram amounts of serum IgE specific for a
particular allergen
19. To Treat Type I Immediate Hypersensitivity Based on
the Underlying Mechanisms
⢠Block Effects of Primary Mediators on Target
Cells (e.g. respiratory smooth muscles or vascular
endothelium) : Antihistamines; Cortisone
⢠Block Calcium Ion Influx: Cromolyn
⢠Block the Effects of Calcium Ion Influx
a. Keep cyclic AMP (cAMP) from Falling
Theophylline
⢠Increase production of cAMP:
Adrenaline(epinephrine)
20.
21. ANTIBODY â MEDIATED CYTOTOXIC
HYPERSENSITIVITY
⢠Type II hypersensitivity reaction involve
antibody- mediated destruction of cells
⢠This type is best exemplified by blood â
transfusion reactions, in which host antibodies
react with foreign antigens on the
incompatible transfused blood cells and
mediate destruction of these cells
22. Type II Hypersensitivity
⢠Results when Ig or IgM bind to cell surface
Agâs
â Activating Complement
â Binding Fc receptors on Tc cells promoting ADCC
⢠Both processes result in lysis of the Ab-coated
cell
23. ⢠Clinical examples of Type II responses include:
â Certain autoimmune diseases where Abâs produced
vs membrane Agâs
⢠Graveâs Disease â Abâs produced vs thyroid hormone
receptor
⢠Myasthenia Gravis â Abâs produced vs acetylcholine
receptors
⢠Autoimmune hemolytic anemia â Abâs produced vs RBC
membrane Agâs
â Hemolytic Disease of the Newborn
â Hyperacute graft rejection
⢠Blood Transfusion
⢠Graft rejection
24. Type II Hypersensitivity:
Produced by mismatched blood
types
Destroys foreign RBC by
complement-mediated lysis
triggered by IgG
Produces fever, intravascular
clots, lower back pain, Hgb in
urine
Free Hgb produced has 2 fates:
passes to the kidneys â
hemoglobinuria
Breaks down to bilirubin. Can
be toxic
25. Type II Hypersensitivity:
Hemolytic Disease of the
Newborn
⢠Occurs via maternal IgG Abâs crossing the placenta
⢠In severe cases causes erythroblastosis fetalis
â Most commonly develops in Rh- mother with Rh+ fetus
â Exposure to Rh+ fetal RBCâs stimulates prod of
memory/plasma
â Activation of memory cells in subsequent pregnancy IgG
Abâs which can cross the placenta
â mild-severe hemolytic anemia ensues along with bilirubin
which affects the brain/CNS
26. ⢠Treatment centers on anti-Rh antibodies (Rhogam)
⢠Mothers can be tested for anti-Rh antibodies to
check for a rise in titer
⢠Isolated fetal RBCâs can be checked for anti-Rh IgG w/
Coombs test
28. Drug-induced hemolytic anemia
⢠Drugs such as aspirin and antibiotics can bind
to the surfaces of RBCâs
⢠These interactions act similar to hapten-
carrier conj.
⢠Such complexes can trigger Ab-mediated cell
lysis by complement activation