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New page: <big><center>'''BACK TO Hypersensitivity'''</center></big> ---- * Also known as IgE-mediated or anaphylactic hypersensitivity. * Ranges from mild cases, s...
<big><center>[[Hypersensitivity - WikiBlood|'''BACK TO Hypersensitivity''']]</center></big>
----
* Also known as IgE-mediated or anaphylactic hypersensitivity.
* Ranges from mild cases, such as hayfever, to life-threatening reactions, such as bee-stings.
* Antigens that induce a type I reaction are known as allergens.
* Affects face, eyes, nose and feet
* IgE has a high affinity to IgE receptors on mast cells and basophils, and so binds these receptors.
* The individual mechanisms of cell degranulation may only have a marginal effect, but the combination can be highly effective in removing parasite infection
* Eosinophils can also target IgE bound to helminths.
** May either be attracted to the site of inflammation or produced de novo in response to cytokines.
** Binding triggers their degranulation.
*** Potent biological molecules are released.
**** Eosinophil peroxidase.
**** Eosinophil basic protein.
* This system can be invoked with inappropriate and innocuous antigens.
** E.g. pollen.
** Under these circumstances we get hay fever.
'''Common allergens:'''
* Proteins : Foreign serum
* Plant pollens : Rye grass, ragweed, timothy grass, birch trees
* Drugs : Penicillin, sulphonamides, local anaesthetics, salicylates
* Foods : Nuts, seafood, eggs, milk
* Insect products : Bee venom, wasp venom, dust mites faeces, flea saliva
[[Image:Sensitisation phase1.jpg|right|thumb|150px|IMAGE 1: Sensitisation phase1.jpg
-Brian Catchpole RVC 2008]]
[[Image:Immediate-type hypersensitivity.jpg|right|thumb|150px|IMAGE 2: Immesdiate-type hypersensitivity-Brian Catchpole/M Maidment RVC 2008]]
'''1. Initial antigen exposure sensitises immune system (Image 1):'''
* Allergen exposure causes IgE production.
* IgE coat mast cells by binding to Fc receptors.
'''2. Subsequent exposure to the specific allergen (Image 2):'''
* mast cell degranulation.
* basophils with IgE receptors are recruited and also degranulate.
Mast cells secrete mediators which cause:
* The release of inflammatary cytokines
**Steroid mediators, e.g. prostaglandins and leukotriens
*Chemoattractants (attracts mainly neutrophils but also eosinophils, monocytes and basophils and plasma)
*Some mast cell cytokines (especially eosinophils) release factors which promote growth and maturation of leukocytes
*Vasoactive and inflammatory peptides (e.g. histamine and serotonin) which causes acute contraction of smooth muscle fibres
**Leading to bronchoconstriction and vasoconstriction
**Violent constriction can lead to the expulsion of parasites
*The release of mast cell proteases
**Promotes mucous production
**Inhibits parasite interactions with the epithelial surface
* Vasodilation (leads to redness)
* Oedema (from leaky blood vessels)
'''3. The late phase response:'''
* Mediated by eosinophils.
* Takes longer (several hours) as the eosinophils are mobilised from the bone marrow.
'''Examples of Type I hypersensitivity'''
* Atopy
* Flea allergic dermatitis
* Sweet itch
itivity - WikiBlood|'''BACK TO Hypersensitivity''']]</center></big>
----
* Also known as IgE-mediated or anaphylactic hypersensitivity.
* Ranges from mild cases, such as hayfever, to life-threatening reactions, such as bee-stings.
* Antigens that induce a type I reaction are known as allergens.
* Affects face, eyes, nose and feet
* IgE has a high affinity to IgE receptors on mast cells and basophils, and so binds these receptors.
* The individual mechanisms of cell degranulation may only have a marginal effect, but the combination can be highly effective in removing parasite infection
* Eosinophils can also target IgE bound to helminths.
** May either be attracted to the site of inflammation or produced de novo in response to cytokines.
** Binding triggers their degranulation.
*** Potent biological molecules are released.
**** Eosinophil peroxidase.
**** Eosinophil basic protein.
* This system can be invoked with inappropriate and innocuous antigens.
** E.g. pollen.
** Under these circumstances we get hay fever.
'''Common allergens:'''
* Proteins : Foreign serum
* Plant pollens : Rye grass, ragweed, timothy grass, birch trees
* Drugs : Penicillin, sulphonamides, local anaesthetics, salicylates
* Foods : Nuts, seafood, eggs, milk
* Insect products : Bee venom, wasp venom, dust mites faeces, flea saliva
[[Image:Sensitisation phase1.jpg|right|thumb|150px|IMAGE 1: Sensitisation phase1.jpg
-Brian Catchpole RVC 2008]]
[[Image:Immediate-type hypersensitivity.jpg|right|thumb|150px|IMAGE 2: Immesdiate-type hypersensitivity-Brian Catchpole/M Maidment RVC 2008]]
'''1. Initial antigen exposure sensitises immune system (Image 1):'''
* Allergen exposure causes IgE production.
* IgE coat mast cells by binding to Fc receptors.
'''2. Subsequent exposure to the specific allergen (Image 2):'''
* mast cell degranulation.
* basophils with IgE receptors are recruited and also degranulate.
Mast cells secrete mediators which cause:
* The release of inflammatary cytokines
**Steroid mediators, e.g. prostaglandins and leukotriens
*Chemoattractants (attracts mainly neutrophils but also eosinophils, monocytes and basophils and plasma)
*Some mast cell cytokines (especially eosinophils) release factors which promote growth and maturation of leukocytes
*Vasoactive and inflammatory peptides (e.g. histamine and serotonin) which causes acute contraction of smooth muscle fibres
**Leading to bronchoconstriction and vasoconstriction
**Violent constriction can lead to the expulsion of parasites
*The release of mast cell proteases
**Promotes mucous production
**Inhibits parasite interactions with the epithelial surface
* Vasodilation (leads to redness)
* Oedema (from leaky blood vessels)
'''3. The late phase response:'''
* Mediated by eosinophils.
* Takes longer (several hours) as the eosinophils are mobilised from the bone marrow.
'''Examples of Type I hypersensitivity'''
* Atopy
* Flea allergic dermatitis
* Sweet itch
itivity - WikiBlood|'''BACK TO Hypersensitivity''']]</center></big>