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Hypersensitivity
Allergy is a type of immunopathology and it can be defined as a disease following a response by the
immune system to an otherwise innocuous antigen (an antigen it shouldn’t respond to)
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In Europe 50% of the
population have an allergy to common environmental allergens
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It has the same basic structure as the
other Igs (2 heavy and 2 light chains), produced locally (really dangerous if produced around the whole
body), not systemically, produced on a first encounter with an innocuous substance (e
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pollen, dust,
dander, food)
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The allergen is taken up by the
dendritic cell by phagocytosis, its
processing skews for a Th2 response
meaning that Th2 cytokines IL4 and
IL13 get released
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The IgE
then binds via its heavy chain to FcR
receptors on the surface of mast cells
and basophils
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When you see the
allergen a second time you have a
massive response where you have
degranulation of the mast cells and the
release of all kinds of potent effectors
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These effectors can be various chemicals:
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Histamines (it can increase smooth muscle contraction and vascular permeability, infiltration of
liquid mucus),
Th2 cytokines IL-4 and IL13 release which promotes further release of IgE (cascade effect),
cytokine TNFa production (tissue inflammation)
Leukotrienes increase vascular permeability, cause smooth muscle contraction, stimulates
mucus secretion by goblet cells
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Under normal circumstances mast cells do have a positive effect and play an important role in immunity
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E
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in the gastrointestinal tract once you get release of these effectors you get fluid secretion peristalsis
so you get diarrhoea, respiratory system you get constriction and mucus secretion which results in
blocking airway passages, in blood vessels increases permeability and blood flow which can increase
blood pressure which is also a part of anaphylactic shock
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They serve a good purpose in healing and also express
FcR on their surface and have degranulation effects and release histamines and produce Th2 and extra
release of IgE
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They can directly kill parasites and microorganisms or can release effectors to do it indirectly
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in the context of anaphylactic shock and asthma you get this rearrangement of
your epithelium which adds to the inability to breathe
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TGF cytokine is important because it stimulates
epithelial proliferation (important when you get epithelial rearrangement where damage can occur)
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Primary antigen encounter
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This stimulates B cells to release
IgE which can bind to mast cells and basophils
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The T cell is a central mediator of which way you will respond to a pathogen
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In the case that you are not prone to allergy (nonatopic) then
this allergen won’t cause the release of Ig but will cause a mild Th1 response which will cause the
release of Th1 cytokines INFy which will stimulate B cells to release IgG not IgE
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Although you are responding to it you are
not producing a massive response
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2) Route of admission- if you inhale deeply you get them deep in your alveolar spaces from where
they can diffuse into the mucosa
3) Dose- you will get an allergen in a low dose you will initiate Th2 rather than Th1 response
In susceptible individuals these characteristics will initiate an allergic reaction
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Very hereditary
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Some polymorphisms in certain genes are involved in
having better or worse outcomes in response to allergens
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e
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FOXP3 is involved in T regulatory cell control
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In terms of environmental factors, if you grew up in the city and your body was constantly challenged by
smog/pollution/detergents/commonly occurring microorganisms/maternal IgE/what infections you’ve
had (reaction to similar antigens, concept of cross-priming) and you were atopic then you have a higher
chance of developing asthma
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Cell mediated: You get an allergen/medication that you
shouldn’t mount an immune response to
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g
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They are
recognized as an antigen and an immune response is
mounted
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Antibody-dependent cell-mediated cytotoxicity: IgM and IgG
bind to the antigen and are recognized by NK cells and
macrophages which then induce cytotoxicity
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g
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Type III
Related to the immune complexes
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The antibody and antigen form
aggregate complexes which deposit in small vessels (vascularized organs), that leads to organ failures,
skin lesions or strokes
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g lupus- antibodies that are reactive against normal nuclear proteins, the aggregates block the small
vessels in your kidneys so kidney failure occurs
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g
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Type IV
Antibody independent
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Type II and III can take from 2 hours to days to develop so delayed is not the best way to call
them but antibody independent is better
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Then you get
recognition through MHCI and cytotoxicity
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This causes the formation of multinucleated giant cells which cause
local inflammation (e
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TB example in L16, chronic transplantation rejection, multiple sclerosis)
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This is as a
result of inverse relation between parasitic infections and allergy atopy autoimmune disease
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In individuals which have this high IgE secretion as a result of worms you see
little allergy
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“lack of practice in dealing with real infections can reveal a propensity to perceive danger where it does
not exist”
Developed:
No close daily contact with pathogens, high hygiene levels, we don’t get sick because we are not
exposed to pathogens so much, sterility of environment
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This concept is beyond just allergy inverse
relation between parasitic infections and cleanliness to autism, diabetes, multiple sclerosis (pretty much
any autoimmune reaction)
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