Question

 

Jayne was an eighteen year old freshman in college. On her second day at the college, she and her new roommate went to a “meet and greet” get together in their dorm. There were a lot of snacks and drinks there. After eating a cookie Jayne started developing nausea, itchy skin with large welts, a tingling sensation and tightness in her throat, dizziness and difficulty breathing, and a feeling of doom. She tried to speak to her roommate but her voice was very hoarse. She became unconscious and was rushed to the ER. When the medical personnel examined her she was hypotensive, with tachycardia; her skin was clammy. When the nurse looked in her purse she saw and Epipen injector. On questioning the RA from the residence hall, the ER staff found out that the cookies had peanuts in them. On administering epinephrine, Jayne quickly regained consciousness, her blood pressure rebounded to normal, and the heart rate slowed down. She was discharged the next day.

Prompts:

1) What is your diagnosis about Jayne’s condition?

2) What is an “antigen-presenting cell” and what role does this type of cell play in an immune response?

3) Explain the interaction that occurs between a T-helper lymphocyte and a B cell when the B cell is being induced to produce peanut-specific IgE. In your explanation, explain the role that the peanut allergen plays in this interaction.

4) In immediate hypersensitivity, the initial exposure to an allergen usually does not produce any symptoms. The symptoms, such as those involved in anaphylaxis, usually appear in the second exposure. What events are occurring during this initial exposure that sensitizes a person to an allergen? In your description include the role of B cells, T cells, IgE, mast cells, basophils and the allergen.

5) Describe how IgE binds and reacts with basophils and mast cells.

Answer 1

1.The diagnosis of Patient J is Peanut allergy or Peanut reaction.

Peanut allergy is the predominant food allergy in the United States. Peanut and Tree nuts account for nearly 80% of fatal or nearly fatal anaphylactic reactions. Pudding, cookies, baked goods, pies, hot chocolated, african, asian and mexican dishes, chili sauce, hot sauce, pesto, gravy, mole suace, salad dressing, egg rolls, pan cakes, speciality pizzas, glazes, marinades, pet food are all the sources of peanuts.

The source of allergy may be by i. direct contact like eating peanuts or peanut containing foods (cookies in this case) ii. Cross contact or accidentally eating food which is exposed to peanuts during processing or handling of a food product.

2. Antigen Present cells bind antigens (peanut allergens in this case) and present them to helper T cells. Peanut antigen binds to Antigen present cells and antigen is bound to Major Histocompatibility Complex (MHC Class II) when presented to T helper cells. Helper T cells have receptors that bind to antigens presented by Antigen Presenting Cells and the type of immune response triggered is dependent on the type of Helper T cell which is bind to the antigen. In peanut allergy Type 2 helper T cells (Th2) send chemical signals, Interleukins 4, 5, and 13 to stimulate growth of B cells to make IgE

3. Helper T cells have receptors that bind to antigens presented by Antigen Presenting Cells and the type of immune response triggered is dependent on the type of Helper T cell which is bind to the antigen. In peanut allergy Type 2 helper T cells (Th2) send chemical signals, Interleukins 4, 5, and 13 to stimulate growth of B cells to make IgE.

B cells upon stimulation with Th2, mature (mature fully active B cells are called plasma cells and are capable of producing more amounts of antibodies) and produce Ig E antibodies.

4. In immediate hypersensitivity, sensitization occurs where the initial exposure to peanut allergen stimulates the immune system to produce allergen specific IgE antibodies.

Phase I sensitization events: Exposure to peanut antigen results in binding of peanut antigen to Antigen Presenting Cell (APC) and antigen is bound to MHC Class II when presented to Th2. Th2 releases chemical signals such as Interleuking 4, 5 and 13 to B cells resulting in maturation and production of IgE antibodies. The peanut specific IgE will bind to mast cell receptors.

Phase II: When there is subsequent exposure to allergen, there is massive production of allergen specific IgE which leads to clinical symptoms of anaphylaxis. The events that take place are:

Mast cells have high affinity for Receptors of IgE. The antibodies bind to mast cells and basophils resulting in degranulation and release of mediators such as histamine leukotrienes, prostaglandings, cytokines which are responsible for allergic symptoms like itching, hives, swelling, nausea, vomiting, cramps, diarrhoea, airway obstruction, hypotension, arrythmia, anaphylaxis.

5. Basophils and Mast cells have FcER1 whihc shows high affinity for IgE. The IgE bind to Fc of IgE irrespective of specificity or binding occurs by reversible covalent interaction (ionic or hydrophobic). When IgE is bound to the FcER1, antigen binding leads to cross linking and degranulation of basophil or mast cells.

Epinephrine (which is used in this case as treatment) increases cAMP, relaxes the bronchiole smooth muscles and decreases mast cell degranulation.