This document discusses the different types of hypersensitivity reactions classified by Gel and Coombs. Type I reactions are mediated by IgE and mast cells, causing immediate allergic responses. Type II reactions involve antibody-mediated cytotoxicity against cell surfaces. Type III reactions occur when immune complexes deposit in tissues, activating the complement system. Type IV reactions are delayed-type hypersensitivity responses driven by Th1 cells and long-lasting macrophage activation, resulting in chronic inflammation and granuloma formation. The document provides examples and mechanisms for each hypersensitivity type.
Hypersensitivity - medical information ( a detailed study )martinshaji
Hypersensitivity (also called hypersensitivity reaction or intolerance) refers to undesirable reactions produced by the normal immune system, including allergies and autoimmunity.
There is no cure for hypersensitivity vasculitis itself. The main goal of treatment will be to relieve your symptoms.
this chart is all about hypersensitivity , i made this for my academic purpose .
please comment
thank u
The symptoms resulting from allergic responses are known as anaphylaxis.
Mediated by IgE attached to Mast cells.
Includes: Hay fever, asthma, eczema, bee stings, food allergies.
Hypersensitivity/ Allergy ppt by DR.C.P.PRINCEDR.PRINCE C P
Hypersensitivity refers to undesirable reactions produced by the normal immune system, including allergies .
These reactions may be damaging, uncomfortable, or occasionally fatal.
ALLERGEN: non-parasite antigens that can stimulate a hypersensitivity response
Occurs in two stages : sensitization phase and shocking phase
Classified into Immediate and Delayed hypersensitivity based on time required to develop the symptoms
Type I hypersensitivity is also known as immediate or anaphylactic hypersensitivity.
The reaction may involve skin(urticaria and eczema), eyes(conjunctivitis), nasopharynx (rhinorrhea, rhinitis), bronchopulmonary tissues(asthma) and gastrointestinal tract (gastroenteritis).
Hypersensitivity - medical information ( a detailed study )martinshaji
Hypersensitivity (also called hypersensitivity reaction or intolerance) refers to undesirable reactions produced by the normal immune system, including allergies and autoimmunity.
There is no cure for hypersensitivity vasculitis itself. The main goal of treatment will be to relieve your symptoms.
this chart is all about hypersensitivity , i made this for my academic purpose .
please comment
thank u
The symptoms resulting from allergic responses are known as anaphylaxis.
Mediated by IgE attached to Mast cells.
Includes: Hay fever, asthma, eczema, bee stings, food allergies.
Hypersensitivity/ Allergy ppt by DR.C.P.PRINCEDR.PRINCE C P
Hypersensitivity refers to undesirable reactions produced by the normal immune system, including allergies .
These reactions may be damaging, uncomfortable, or occasionally fatal.
ALLERGEN: non-parasite antigens that can stimulate a hypersensitivity response
Occurs in two stages : sensitization phase and shocking phase
Classified into Immediate and Delayed hypersensitivity based on time required to develop the symptoms
Type I hypersensitivity is also known as immediate or anaphylactic hypersensitivity.
The reaction may involve skin(urticaria and eczema), eyes(conjunctivitis), nasopharynx (rhinorrhea, rhinitis), bronchopulmonary tissues(asthma) and gastrointestinal tract (gastroenteritis).
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
The presentation includes an overview of hypersensitivity and type 1 hypersensitivity with certain pictures elaborating the mechanism. The presentation also talks about asthma very briefly as an example of type 1 hypersensitivity.
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
The presentation includes an overview of hypersensitivity and type 1 hypersensitivity with certain pictures elaborating the mechanism. The presentation also talks about asthma very briefly as an example of type 1 hypersensitivity.
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4. Gel and Coombs 1963 classification of hypersensitivities.
5. TYPE I Hypersensitivity
Classic allergy
Mediated by IgE attached to Mast cells.
The symptoms resulting from allergic responses
are known as anaphylaxis.
• Includes: Hay fever, asthma, eczema, bee stings, food
allergies.
6. Allergens
Allergens are nonparasite antigens that can
stimulate a type I hypersensitivity response.
Allergens bind to IgE and trigger
degranulation of chemical mediators.
10. Allergen is easily aerosolized and inhaled.
Der P1 breaks down components of tight junctions
which helps it to cross mucosa.
Der P1 Allergen
11. Atopy
Atopy is the term for the genetic trait to have a
predisposition for localized anaphylaxis.
Atopic individuals have higher levels of IgE and
eosinophils.
12. Genetic Predisposition
Type I hypersensitivity
Candidate polymorphic genes include:
– IL-4 Receptor.
– IL-4 cytokine (promoter region).
– FceRI. High affinity IgE receptor.
– Class II MHC
(present peptides promoting Th2 response).
– Inflammation genes.
13. Mechanisms of allergic response
Sensitization
Repeated exposure to allergens initiates
immune response that generates IgE
isotype.
Th2 cells required to provide the IL-4
required to get isotype switching to IgE.
14. Mechanisms of allergic response
Sensitization
Th2/B cell interaction
IL-4
IL-4R
CD40
Drive B cell
Activation and IgE
isotype switch.
Busse and Lemanske NEJM Feb 2001. 344:350
15. Mechanisms of allergic response
Sensitization
The IgE can attach to Mast cells by Fc
receptor, which increases the life span of
the IgE.
Half-life of IgE in serum is days whereas
attached to FceR it is increased to months.
16. Mechanisms of allergic response
Fc e receptors (FceR)
FceR1
high affinity IgE receptor found on
– mast cells/basophils/activated eosinophils.
Allergen binding to IgE attached to FceR1
triggers release of granules from cell.
18. Mechanisms of allergic response
Effector Stage of Hypersensitivity
Secondary exposure to allergen
Mast cells are primed with IgE on surface.
Allergen binds IgE and cross-links to activate
signal with tyrosine phosphorylation, Ca++
influx, degranulation and release of mediators.
19. FceRI Triggers Release of Mediators
Early mediators
cause immediate symptoms
e.g. histamine (preformed in granules)
leukotriene C4 and prostaglandin D2
are quickly made 2' mediators
20. Mediators of Type I Hypersensitivity
Immediate effects
Histamine
– Constriction of smooth muscles.
Bronchiole constriction = wheezing.
Constriction of intestine = cramps-diarrhea.
– Vasodilation with increased fluid into tissues
causing increased swelling or fluid in mucosa.
– Activates enzymes for tissue breakdown.
Leukotrienes
Prostaglandins
21. Immediate vs Late Effects
(early mediators)
Early/Late
Effect on lung
airflow
OR
Wheezing
22. Mediators of Type I Hypersensitivity
Primary Mediators
Pre-formed mediators in granules
Histamine
Cytokines TNF-a, IL-1, IL-6.
Chemoattractants for Neutrophils and
Eosinophils.
Enzymes
– tryptase, chymase, cathepsin.
– Changes in connective tissue matrix, tissue
breakdown.
23. Type I Hypersensitivity
Secondary mediators
Mediators formed after activation
Leukotrienes
Prostaglandins
Th2 cytokines- IL-4, IL-5, IL-13, GM-CSF
24. Continuation of sensitization cycle
Mast cells control the immediate response.
Eosinophils and neutrophils drive late or
chronic response.
More IgE production further driven by
activated Mast cells, basophils, eosinophils.
25. Continuation of sensitization cycle
Eosinophils
Eosinophils play key role in late phase
reaction.
Eosinophils make
– enzymes,
– cytokines (IL-3, IL-5, GM-CSF),
– Lipid mediators (LTC4, LTD4, PAF)
Eosinophils can provide CD40L and IL-4
for B cell activation.
26. Localized anaphylaxis
Target organ responds to direct contact with allergen.
Digestive tract contact results in vomiting,
cramping, diarrhea.
Skin sensitivity usually reddened inflamed
area resulting in itching.
Airway sensitivity results in sneezing and
rhinitis OR wheezing and asthma.
28. Treatment for Type I
Pharmacotherapy
Drugs.
– Non-steroidal anti-inflammatories
– Antihistamines block histamine receptors.
– Steroids
– Theophylline OR epinephrine -prolongs or
increases cAMP levels in mast cells which
inhibits degranulation.
29. Treatment for Type I
Immunotherapy
– Desensitization (hyposensitization)
also known as allergy shots.
– Repeated injections of allergen to reduce the
IgE on Mast cells and produce IgG.
30. Treatment for Type I
Effect of allergy shots
Allergen Specific Antibodies
Change in amount of
each isotype from more
IgE to more IgG.
31. TYPE II Hypersensitivity
Antibody mediated cytotoxicity
Blood Transfusion reactions
Innocuous antigens on red blood cells.
EXAMPLE: ABO blood group antigens
A and B
carbohydrate
antigens
32. Antibody against rbc antigen binds and
mediates killing of rbcs via C’or ADCC
causes systemic inflammation.
ABO Blood Groups
Quex: Why do we have antibodies to these
innocuous antigens even before we get blood transfusion?
33. Drug reactions
Drug binds to rbc surface and antibody
against drug binds and causes lysis of rbcs.
Immune system sees antibody bound to
"foreign antigen" on cell. ADCC
TYPE II
Antibody mediated cytotoxicity
34. Rh factor incompatibility
IgG abs to Rh an innocuous rbc antigen
– Rh+ baby born to Rh- mother first time fine.
2nd time can have abs to Rh from 1st
pregnancy.
– Ab crosses placenta and baby kills its own rbcs.
– Treat mother with ab to Rh antigen right after
birth and mother never makes its own immune
response.
TYPE II
Hemolytic disease of newborn
36. TYPE III
Antigen antibody immune complexes.
IgG mediated
Immune Complex Disease
Large amount of antigen and antibodies
form complexes in blood.
If not eliminated can deposit in capillaries
or joints and trigger inflammation.
37. TYPE III
Immune Complexes
PMNs and macrophages bind to immune complexes via
FcR and phagocytize the complexes.
BUT
If unable to phagocytize the immune complexes can
cause inflammation via C’ activation ---> C3a C4a, C5a
and "frustrated phagocytes".
38. TYPE III
Immune Complex Disease
"Frustrated Phagocytes"
If neutrophils and macrophages are unable to
phagocytize the immune complexes these cells
will degranulate in the area of immune complex
deposition and trigger inflammation.
Unable to eat -------try to digest outside cell.
39. TYPE III
Immune Complex Disease
Localized disease
Deposited in joints causing local inflammation =
arthritis.
Deposited in kidneys = glomerulonephritis.
40. TYPE III
Immune Complex Disease
Serum sickness from large amounts of antigen
such as injection of foreign serum.
Serum sickness is usually transient immune complex disease
with removal of antigen source.
41. Serum Sickness
Systemic immune complex disease
Days after Antigen Injection
Large amounts of antigen
such as injection of
foreign serum.
42. Delayed type hypersensitivity
Th1 cells and macrophages
DTH response is from:
– Th1 cells release cytokines to activate macrophages
causing inflammation and tissue damage.
– Continued macrophage activation can cause chronic
inflammation resulting in tissue lesions, scarring, and
granuloma formation.
Delayed is relative because DTH response arise 24-72
hours after exposure rather than within minutes.
43. Stages of Type IV DTH
Sensitization stage
Memory Th1 cells against DTH antigens
are generated by dendritic cells during the
sensitization stage.
These Th1 cells can activate macrophages
and trigger inflammatory response.
44. Stages of Type IV DTH
Effector stage
Secondary contact yields what we call DTH.
Th1 memory cells are activated and produce
cytokines.
– IFN-g, TNF-a, and TNF-b which cause tissue
destruction, inflammation.
– IL-2 that activates T cells and CTLs.
– Chemokines- for macrophage recruitment.
– IL-3, GM-CSF for increased monocyte/macrophage
45. Stages of Type IV DTH
Effector stage
Secondary exposure to antigen
Inflamed area becomes red and fluid filled can
form lesion.
– From tissue damage there is activation of clotting
cascades and tissue repair.
Continued exposure to antigen can cause chronic
inflammation and result in granuloma formation.
46. Type IV DTH
Contact dermatitis
The response to poison oak is a classic Type IV.
– Small molecules act as haptens and complex with skin
proteins to be taken up by APCs and presented to Th1
cells to get sensitization.
– During secondary exposure Th1 memory cells become
activated to cause DTH.
48. Delayed type hypersensitivity
(DTH)
DTH is a type of immune
response classified by
Th1 and macrophage
activation that results in
tissue damage.
DTH can be the result of
Chronic infection or
Exposure to some antigens.