Why Does Cheese Make Me Sneeze? | Sydney Rudko

Recently while at a birthday party I overheard some people talking about a friend of theirs who is allergic to apples. Listening to their conversation, it occurred to me that the vast majority of people probably don’t know how they develop allergies.

There are a variety of different kinds of allergies, but in this article I’ll focus on the most common kind, which are mediated by the antibody IgE.  These are the kind of allergies we associate with sneezing, coughing, itchy eyes, and asphyxiation. This article is very basic, and is intended for an audience with little to no immunology experience, for those with an advanced understanding of the immune system I’ve included links to a few great papers and reviews that go into more detail.

Antibodies: the Basics

There are a lot of components to your immune system; one of the most recognizable components is the antibody. Antibodies are part of the reason you don’t get the same flu virus twice. They are lock and key structures that coat (the technical term is opsonize) bits of bacteria or virus and direct other components of the immune system to destroy them. A special immune cell in your body called a B cell makes antibodies. B cells have numerous roles, but I like to think of them like the Borg in Star Trek, they kill stuff.  Antibodies come in a variety of flavors, but the most important for understanding allergies is IgE (Ig stands for immunoglobulin, a fancy word for antibody), but there are also IgA, IgD, IgG, and IgM. These antibodies can attach to each other into different shapes. Some shapes are better for different functions. For instance, pregnant mothers produce more IgA as its shape enables the antibody (and thus protection from a pathogen) to be transferred to the infant in breast milk.

Figure 1. B cells begin by making IgM. This diagram shows the gene cluster which corresponds to antibody production. The green region is a gene that is unchanged and present in all the antibody types. When all genes encoding for the immunoglobulin types are present, only the IgM gene will be used to produce antibody. The cell will not produce IgD,G,A, or E.

The recognition and annihilation of a pathogen by our immune system is an extremely complex process, but generally a specialized subset of immune cells recognize a pathogen, replicate themselves to build an army against the pathogen, tell all their friends about this pathogen to get the entire immune system in on the fight, and then some of these cells produce antibodies which bind to and help out in the fight. The question is, what kind of antibody does the body produce, and how does it do this? The answer lies in a process called class switching. This is the process by which an immune cell decides what kind of antibody it wants to produce.

Class Switching

Figure 2. When the B cell receives a signal to produce another type of immunoglobulin, such as IgA, specialized enzymes cleave and remove the immunoglobulin genes which precede that gene. For instance, IgM, D and G are removed when the cell wants to produce IgA. The genes which are removed are degraded and discarded and the helix is then repaired. These excised genes cannot be reintroduced into the chromosome.

When a B cell starts making antibodies it starts out making IgM, but it doesn’t have to make IgM forever (Figure 1).As the B cell circulates around the body it receives signals from other immune cells, the signaling is complex, but basically the B cell is told to change its antibody type and it responds. If the cell receives a signal to make IgA, the DNA encoding for IgM,D and G is cut out of the DNA strand and degraded; never to return (Figure 2). Only then can the cell begin making IgA (Figure 3).  It is important to note that once a cell is making IgA, it will not make IgM, D or G again.

As I mentioned above, the IgE antibody primarily causes allergies. I’ll pause for a moment here as some of you have an “AHA!” moment, but if you don’t have the “AHA!” moment, don’t worry! Your time will come shortly. Look back at Figure 1. IgE is at the back of that chain of antibody types. So when a B-cell is told to make it, there is no going back. The B-cell is stuck making IgE.

Figure 3. Without the discarded IgM, D and G segments our gene cluster looks significantly different. Now only IgA is the antibody produced. If the cell then receives a signal to produce IgE, the IgA gene will be excised in a similar fashion to how the IgM, D and G genes were removed in Figure 2, and then only IgE would be produced.

This means every time you encounter a particular allergen your body will produce IgE and an allergic response. (For more detailed information, see For Inquiring Minds) When the allergen is encountered this stimulates the IgE antibodies to find specialized cells called mast cells. These cells then undergo degranulation. This is a fancy word that can be summed up with a really basic image, baking soda mixed with vinegar.  The cells foam up. The foaming of these cells is what ultimately leads to the symptoms of an allergy, swelling, rash, irritation and even asphyxiation.

Why Do We Have Allergies?

There are a number of theories as to why we have allergies, and many hypotheses regarding the increase in allergies in the past 2-3 decades. It is believed the IgE antibody may have an important role in mediating killing of parasites.

For Inquiring Minds

As I described in the introduction, a lot of what I have described above has been generalized to a very basic level. Some of you may be curious about people who have become tolerant to an allergen (who no longer experience allergy symptoms). Others may be curious to learn about the antibody gene cluster in more detail, or perhaps some of you are lactose intolerant and are curious as to what that means. Maybe some of you are immunology majors and are cursing me. For these individuals I’ve included some papers and reviews to read if you’re interested in learning more details, and to show that I at least did a little research on this topic.

Class Switching: Mechanism and Regulation of Class Switch Recombination 

The hygiene hypothesis: Allergy, Parasites, and the Hygiene Hypothesis 

Allergen tolerance: Therapies for allergic inflammation: refining strategies to induce tolerance 

Grass Pollen Immunotherapy Induces an Allergen-Specific IgA2 Antibody Response Associated with Mucosal TGF-β Expression

Non IgE mediatied allergies: Non IgE Mediated Food Allergy 

More information can also be found in the Immunobiology textbook by Charles A Janeway, Jr, Paul Travers, Mark Walport, and Mark J Shlomchik. This book is available from NCBI for free!

Sydney is a 4th year Honours Immunology and Infection student with a passion for science and writing. Follow her on twitter @SPResistant

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