1. Which antibodies and cells are involved in this allergic reaction, how do they cause it, and how does it lead to anaphylaxis? Why didn't this happen on the first stings?

Question

Case Study

A 60-year-old woman was fit and well until late in the summer she was out tending to her lovely tulip garden when she was stung on the back of her right hand by a pesky wasp. This was nothing new, unfortunately as she had been stung a couple times in the last two weeks. With in minutes after this sting Charlotte fell to the ground and looked as though she was becoming pale/grayish and was gasping for air. After five minutes it was getting worse, but likely a neighbor doctor rushed over and administered an epinephrine shot, which provided support until the ambulance could arrive.

Answer 1

Hi there! My goal is to break this down in an easy way so you can fully understand why this allergic reaction happened, how it led to anaphylaxis, and why it didn’t happen the first time. Let’s dive in!

Quick Answer:

The antibody IgE and mast cells are the main players. The first wasp stings created IgE antibodies. On later stings, those antibodies triggered mast cells to release histamine and other chemicals, causing a severe allergic reaction (anaphylaxis).

Example:

Think of your immune system like a club bouncer. The first time the wasp stings you, the bouncer takes note of the troublemaker but lets them in. The second time they show up, the bouncer recognizes them and overreacts, calling security and causing chaos inside the club. That’s how your body reacts after it’s “trained” by those first stings!

Explanation:

When the woman was stung the first couple of times, her immune system was exposed to the venom for the first time. It produced IgE antibodies to recognize that venom in the future. Those IgE antibodies attached to mast cells in the body.

On the later sting, the venom bound to the IgE antibodies on the mast cells. This caused the mast cells to release histamine and other chemicals. The result: swelling, airway constriction, and other symptoms that can lead to anaphylaxis.

It didn’t happen the first time because the body hadn’t built up these IgE antibodies yet.

Fun Fact:

Once made, IgE antibodies can stick to mast cells for months or even years. This is why someone can suddenly have a big reaction later, even if earlier stings or exposures didn’t cause much trouble.

Hope this helps clear it up! Best of luck with your studies.

Answer 2

There are five subclasses of antibodies: IgA, IgD, IgE, IgG, and IgM.

IgA is present on mucosal surfaces and contributes to immunity there. It's the most produced antibody, but it's nor present in high amounts in the blood stream.

IgD has an unclear role in immunity, there is still lots of ongoing research to determine its function.

IgE binds to mast cells and basophils and mediates immediate hypersensitivity to allergens by causing them to release lots of inflammatory molecules, like histamine, that can lead to anaphylaxis.

IgG is the most abundant in the bloodstream. It has a lot of different functions in protecting the body from various immune insults, including bacterial toxins and viruses. Generally, its presence indicates a lasting immunity to the antigen.

IgM is the antibody produced first in response to any sort of antigen.

An allergic reaction needs to have an exposure first, in order to make the IgE antibody to the respective antigen. Once the body has already recognized it and created a IgE antibody for the antigen, then the allergic reaction can occur in the subsequent exposures.