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Type I hypersensitivity rxns mediated by

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IgE

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Type 2 mediated by

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IgG

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Type 3 mediated by
Type 4 mediated by

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IgG
Th1, Th2, CTLs

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Type 1 characteristics

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antigens are soluble leading to mast cell activation and leads to asthma, anaphalaxis and allergies

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Type 2 characteristics

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Tyoe 2 mediated by igG and cellular or matrix associated antigen leads to complement Fcr activation (phagocytes, NK cells an) this is the case of some drug allergies. IgG also responds to cell surface receptors in which it changes the cell surface signaling and leads to chronic urticaria .

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Type 3 mediated by igG target is soluble and activates

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activates complement and phagocytes leading to serum sickness and arthus reaction where the complement is accumulating and causes constriction

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Type 4 leads to

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Classic disease is dermititis as well as tuberculin reaction

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Graft rejection, hypersensitivity type 4 is mediated by

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CTL

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Systemic anaphylaxis allergens

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Drugs, Venoms, Food. they enter via IV or orally before getting blood stream

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Systemic anaphylaxis results in

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Laryngeal Edema, circulatory collapse, death

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Acute Uticaria allergens

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Animal hair, insect bites. They enter through skin.

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Acute Uticaria leads to

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Edema, local increase in blood flow

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Seasonal rhinoconjunctivitis allergen

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Pollen, trees, grasses, dust mites. They enter through contact with the eye and nasal mucosa

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Seasonal rhinoconjunctivitis results in

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Edema of conjuctiva and nasal mucosa. Sneezing

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Astha allergens and results

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Danders (cats), Pollen, dust mites lead to bronchial constriction increase mucous production and airway inflammation

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Food allergies cause

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vomiting, diarreha, pruritis (itching) urticaria (hives) rarely anaphylaxis

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Food allergies, Astha, Seasonal rhinoconjunctivitis Acute Uticaria allergens mediated by

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IgE so they're type 1 hypersensitivity rxns

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DERP 1 the most common allergen in the US acts by

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1)cleaving occluding in tight junctions and enters mucosa
2)Derp 1 is taken up by dendritic cells for antigen presentation and Th2 priming
3)Th2 cell induces Bcell switch to IgE production
4)IgE binds to Fc receptor on mast cells
5)Mast cell granule contents causing allergic run

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Once you’ve been sensitized to a particular antigen you make Ig antibodies and remain bound to the FceRI on mast cells but the signalling is not enough to cause mast cell unloading, so once we are exposed to the allergen again, they

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cross react with the antibodies on the recerptors and leads to IL 4 to produce more Ige.

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feats associated with the priming of th2

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they are proteins with carbohydrate chains which only induce Tcell responses via MHC class 2. So low dose of proteins it favors activation of Il4 leading to CD4 T Cells (TH2 t cells) These protein allergens can diffuse out of particles into the mucosa. These proteins are also very stable and can survive in dessicated particles

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: some people have predisposition to allergies mostly due to

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the inability to maintaina balance between th1 and th2. TH1 high levels suprres tH2 and viceveersa.

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What type of genes involved in asthma genetic susceptibility?

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Gene triggering the immune response or directing cd4
Genes regulating TH2 cell differentiation and effector afunction
Genes expressed in epithelial cells
Genes identified by positional cloning

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if individual has early exposure to organisms like Helminth infection, Hepatitis A or gut microbiota and lives in high hygienic environment

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The individual will develop allergies

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Eosinophils are very important in aggravating the allergic reactions and are promoted by

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mast cell release of IL3, IL5, GM-CSF

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what do eosinophils do?

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potentiate the rxns being carried by mast cells

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Mast cells granule release effect on GI

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Diarrhea, vomiting (increased peristalsis and fluid secretion)

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Mast cells granule release effect on eyes nasal passages and airways

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Wheezing, coughing phlegm, swelling in nasal passages

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Mast cells granule release blood vessels

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Increased blood flow and increased permeability (more effector cells in tissues)
Hypotension potentially leading to anaphylactic shock

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When injected with an allergent, the immediate response is

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collapse of respiratory injection fraction response, but during the late phase it recovers

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If allergen enter via IV,

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gentle release of histamine to increase permeablitity leading to anaphalatyc shock

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. If route of entry is subcutaneous and host responds by

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releasing histamine locally and inflammatory response.

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Inhalation of allergen increases

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mucous production.

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Ingestion of allergen results in

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contraction of smooth muscles and diarrhea in some cases.

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The acute response in allergic asthma leads to

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Th2-mediated chronic inflammation of the airways

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Acute response in asthama

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Mediators cause mucus secretion and smooth muscle contraction leading to airway obstruction
Recruitment of cells from circulation takes place

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Chronic response to asthma

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Casued by Th2 releaing cytokines and eosinophil products

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Tbet is a transcription factor only in

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in tH1 and faciliates Il2 production and amplificatio of th1 response. Tbet in animal was knock out, so th2 took over leading to chronic hypersensitivity

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Risk factors for the development of food allergy

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are immature mucosal immune system. Early introduction of solild fuctor, hereditary increase in mucosal permeability. IgA defficiency

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Allergies can be treated by targeting

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mediator action
chronic inflammatory rxns
Th2 response
IgE binding to mast cells

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Anti-histamines and B-blockers

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Inhibit effects of mediators and synthesis

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Corticosteroids

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antiinflammatory effects

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Desensitazion therapy by injection of specific antigens

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Induction of regulatory T cells to inhibit tH2 response

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Anti IgE antibodies

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so IgE doesnt bind to mast cells

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INF Gamma administration of cytokines is for

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Th1 to lower th2.

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Inhibtion of IL3 and CCR3

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block cytokine and chemokine receptors that mediate eosinophil recuitment and activation

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Serum sickness is a classic example of

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a transient immune complex mediated syndrome

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Inject with serum and plasma concentration increases and eventually gets cleared as the antigen complexes are formed. During this time fever, vasculitis, arhtithis, and nephritis take place when they accumulate and the antibody against foreing proteins increase and all the symptoms of complex go away. However if antibodies don’t increase

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then it leads to problems Know serum sickness (acute) and arhtors disease (chronic).

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Type 4 hypersensitivity rxns

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Delayed type
Contact
Gluten sensitive enteropathy (celiac disease)

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Delayed hypersensitivity antigen

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insect venom
mycobacterial proteins (tuberculin, lepromin)

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Delayed hypersensitivity results in

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Local skin swelling

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Contact hypersensitivity antigen

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Haptens (posion Ivy)
Nickel, chromate

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Contact hypersensitivity response

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Local epidermal rxn: Erythema, cellular infiltrate, vesicles, intraepidermal abscess

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Celiac disease antigen and response

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Gliadin. Villious atrophy leadig to malabsorption

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The stages of delayed type hypersensitivity

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1)antigen is injected into subcutanenous tissue and processed by local antigen presenting cells
2) A Th1 effector cell recognizes antigen and releases cytokines, which act on vascular endothelium
3) recruiment of phagocytes and plasma to site of antigen injection causes visible lesion

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elicitation of a DTH response to a contact sensitizing agent

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1)contact sensitizing agent enters the skin and binds self proteins which are taken up by Langerhans cells
2)Langerhan cells present the self peptide haptenated with the contact sensitizing agent to th1 cells, whic secrete IFN g
3) activated keratinocytes secrete cytokines such as IL1 and TNF a and chemokines such as CXCL8, CXCL11 and CXCL9
4) the products of keratinocytes and Th1 cells activate macrophages to secrete mediators of inflammation

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Recognition of gluten in celiac disease

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1) peptides naturally produced from gluten do not bind mhc class 2
2)An enzyme, tissue transglutaminase modifies the peptides so they now can bind to the MCH 2
3)the bound peptide activates gluten specific cd4 T cells
4) Activated T cells can kill mucosal epithlial cells by binding Fas. They also secrete IFN g which activates the epithelial cell.