Immuno 16 Flashcards
What is Type I Hypersensitivity?
IgE-dependent triggering of mast cells
What is Type II Hypersensitivity?
IgG antibody that is reactive with cell-surface or matrix antigens
What is Type III Hypersensitivity?
Involves production of antigen-antibody complexes
What is Type IV Hypersensitivity?
T cell-mediated hypersensitivity
What cells can induce class switching from IgM to IgE for Type I Hypersensitivity?
TH2 cells
What are allergens?
antigens that selectively stimulate TH2 cells that drive an IgE response
What are common properties of allergens?
Small proteins
Soluble
Carried on desiccated particles
In order to be a Type I Hypersensitivity, initial response must be what Ig response?
IgE
How do TH2 cells stimulate class switching to IgE?
Effector TH2 cells deliver signals to favor class switching in B lymphocytes to IgE. Once the TCR of TH2 becomes ligated, TH2 CELLS: produce IL4,5,13 upregulated surface expression of CD40L and CD23 (low affinity receptor for IgE) The combination of these signals induces class switching to IgE
Type I Hypersensitivity reactions are generally initiated by what cell?
Mast cells (with eosinophils and basophils involved)
What three cell types have IgE receptor FcgammaR1
Mast cells, eosinophils and basophils
How does IgE work in mast cells, eosinophils and basophils?
The IgE receptor becomes cross-linked by the antigen, which triggers the cell to degranulate, causing an inflammatory reaction
What are the two tests of testing an individual’s sensitivity to a particular allergen?
1st: injection of allergen to see a characteristic inflammatory reaction known as wheal and flare (appx 30 min duration)
2nd: 6-8 hrs post injxn, late phase rxn occurs at injxn site with widespread swelling, mediated by leukotrienes, chemokines and cytokines produced by mast cells following IgE-mediated activation
What is systemic anaphylaxis?
Wide-spread activation of mast cells degranulation causing both increase in vascular permeability and widespread constriction of smooth muscle. Caused by allergens in the blood.
What is anaphylaxis vs prophylaxis?
Anti-protection vs protection by the immune response. Basically fatal vs helpful
How can potential allergens be introduced directly to the blood?
Insect bite, drug injections, food or drugs that are rapidly absorbed
What is the most common cause of anaphylaxis?
IgE-mediated allergy to penicillin or other drugs (100 fatalities/yr)
What is an anaphalactoid reaction?
Resembles anaphylaxis but no interaction between allergen and IgE.
What is allergic rhinitis?
Hay fever, mild allergic response with violent bursts of sneezing and runny nose in response to inhaled allergens
What is allergic asthma?
More serious that hay fever (allergic rhinitis), causing chronic breathing difficulties. Characterized by increased fluid into respiratory tract. Overall effect is trapping of air in lungs.
Is chronic asthma a type IV hypersensitivity reaction?
YES
What is urticaria?
Hives, caused by release of histamine by mast cells
What is angioedema?
Inflammation caused by mast cell activation in deep subcu tissue. Swelling is more diffuse than urticaria.
What are three strategies used to reduce the effects of allergic disease?
- Modification - of behavior and environment
- Pharmacological - drugs that reduce impace of contact with allergen (antihistamines, corticosteroids, cromolyn sulfate, epinephrine)
- Immunological - prevent production of IgE, shifting towards IgG response
What are the effects of corticosteroids in allergic treatment?
Suppresses leukocyte function, used to treat chronic inflammation of asthma, eczema or rhinitis
What are the effects of cromolyn sulfate in allergic responses?
Prophylactic inhalant, preventing degranulation of mast cells and granulocytes
What is the mechanism of epinephrine in allergic treatment?
Stimulates reformation of tight junctions between endothelial cells, reducing the permeability of blood vessels, diminshing tissue swelling and raising BP. also relaxes, bronchial smooth muscle and stimulates the heart
Why do people rarely develop allergic disease to parasite infections?
While a vast amount of IgE is produced in response, only a part of that is parasite-specific. The non-specific IgE outcompetes the parasite-specific for binding on mast cells,basophils and eosinophils. Prevents the parasite from triggering an IgE effector mechanism. Allows the parasite to evade immune response
What is a side effect of living in an area that has high rates of parasitic infection?
Having low allergic reactions rates
What is Type II Hypersensitivity?
Reactions caused by antibodies specific for altered components of human cells, mediated by IgG.
What are examples of Type II hypersensitivity?
Penicillin, quinidine and methyldopa allergic reactions
How does penicillin cause Type II hypersensitivity?
Penicillin causes new epitopes to be formed on cell surfaces that stimulate production of IgM and IgG antibody specific for the new epitope. Pencillin-modified RBCs must be coated with complement, facilitating phagocytosis by macrophages. Macrophages present the newly formed epitopes to CD4 T cells to produce Effector TH2 cells. These cells supply help to antigen-specific B cells. IgG Abs bind to altered RBCs a stimulate destruction by complement cascade or macrophages. End result is RBCs destroyed.
What is Type III hypersensitivity?
Reactions caused by immune complexes (Ab-antigen) formed from IgG and soluble antigens
How is treatment of large immune complexes different from small ones?
Large immune complexes are more efficiently taken up by macrophages, while small ones remain soluble and deposited along blood vessel walls.
How does the accumulation of immune compexes lead to Type III hypersensitivity?
When sufficient immune comlexes accumulate, circulating leukocytes recognize the immune complexes thru the Fc and complement receptors, activating their inflammatory responses.
What is serum sickness?
A type III hypersensitivity that is the result of IV administration of drugs used to treat a variety of illnesses. Caused by an accumulation of immune complexes. Characterized by chills, fever, rash, arthritis, vasculitis and sometimes glomerulonerphritsi
What are two jobs that are often associated with type III hypersensitivity due to constant inhalation of antigens?
Farmers and Bird-Breeders
What is Type IV Hypersensitivity?
Allergic reaction mediated by antigen-specific effector T cells.
What is the other name for Type IV hypersensitivity?
Delayed-Type because they usually occur 1-3 days after contact with the antigen
What are the most common causes of Type IV Hypersensitivity/
mycobacterial proteins, insect venoms, poison ivy, and small metal ions, and tuberculin
What is the difference between poison ivy expose the first vs. subsequent times?
The first time results in the formation of immunological memory and effector T cells, due to the intracellular and extracellular mechanisms of the toxin.
The following times result in the typical visible response of rash and inflammation.
