Why Do We Get Allergies?

YouTube subscriber Chase P. asks: Do a video on why humans have allergies.


It’s that time of year when tissue companies nationwide rejoice at the excessive mucus caused by allergies. If you’re one of the unlucky, you might ask yourself why we get them anyway? Why would our immune systems react to seemingly harmless things like pollens, dust mites, and the dander from cats and dogs?

There are two proposed theories here; the most widely accepted involves an evolutionary mechanism for expelling parasitic worms, a frequent problem for our ancestors before the advent of modern medicine and potentially living in a more hygienic environment. A relatively newly suggested competing theory is that the reaction is due to how the immune system responds to a type of cell, known as a mast cell, when it releases its chemicals of inflammation.

Before we can understand the two theories, it’s important to know how the immune system works in general when it encounters a potential allergen. There are two ways it can deal with a foreign pathogen- either kill it (type 1 reaction) or attempt to expel it from the body (type 2 reaction). Should you have a large pathogen, like say a parasitic worm, the body would generally illicit the type 2, expulsion tactic. A smaller microbe, like a bacteria or virus, will generally trigger the type 1 response.

What exactly is happening when the immune system gets stimulated? (In an attempt to avoid writing a book on the topic, I will only touch on the parts pertaining to allergies themselves and not the immune system as a whole.)

All the cells of your immune system revolve around a class of cells called white blood cells. One type of white blood cell is a B cell. B cells have antibodies on their surface; known as Immunoglobulins (Ig), they are Y shaped proteins. When an allergen contacts your skin, eye, nasal passage, mouth, airway, or in your digestive tract, it will attach to the antibody on the B cell. The B cell will then become activated.

Once activated, they will begin to multiply. Some turn into memory B cells that will recognize the same molecule later in life and be able to more quickly mount a defense. Some turn into plasma B cells (effector cells). These make more identical antibodies that attach to the molecule its predecessor just recognized. They’re so good at it that one effector cell can produce about 2000 identical antibodies per second! Those antibodies will then attach to the invader and mark it for recognition by other white blood cells that will destroy the suspicious molecule. They do this by attaching themselves in a process called opsonization. Different allergens will end up producing different antibodies.

In 1967, two research groups from Colorado and Sweden identified a new type of Ig, known as IgE. This little antibody proved to be the main force starting a cascade of events that leads to those sinister allergy symptoms. More recently, scientist have been able to genetically engineer mice to stop making IgE. Those mice don’t get allergies. Science!

In any event, once produced, IgE begins circulating around and attaches to the receptors (Fc type I and II) on the previously mentioned mast cell. These cells are responsible for most of the processes involved in the symptoms you feel when suffering from allergies. When stimulated, they begin secreting a barrage of chemicals, called degranulation.

One example is the release of histamine. Histamine is important for several of our allergic reaction symptoms- things like the constriction of your bronchioles, the dilation of your arteries, the perception of itching, and the production of hives. It’s also responsible for many of the processes involved with inflammation.

So to sum up on the how, or at least as it’s generally understood (there is some controversy here as we’ll get into in a moment) an allergen enters the body, attaches to B cells; IgE is created and stimulates mast cell degranulation; inflammation ensues and all the symptoms you feel begin causing their web of woe. The immune system stays activated until it senses no more allergen to attack, and you’re now you’re back to normal!

With the “how” covered, this bring us back to the question of why we get allergies to things that are seemingly harmless? No one has definitively answered the question, but everyone seems to agree that IgE is the main antibody responsible for all the immune system reactions and the inflammation it brings. So, what in natural selection made IgE an important trait required for our ancestor’s survival given today some consider it mostly useless, and more than a little annoying for those with allergies?

Until recently, the leading theory revolved around parasitic worms. In 1964, scientist Bridget Ogilvie showed that IgE was found to be in abundance in rats infected with worms. Our ancestors also had a problem with worms. They didn’t have access to modern medicine and hygienic environments that have reduced the infection rate down to the current 20% worldwide (with most that are infected residing in underdeveloped countries). Throughout much of history, everything from roundworms, such as hook-worms, to flatworms, like tapeworms and liver flukes, were relatively common. IgE and the symptoms it creates, like sneezing coughing and diarrhea, all serve to expel those nasty little freeloaders. As Dr. David Dunne from the university of Cambridge states, “You’ve got about an hour to react very dramatically in order to reduce the chance of these parasites surviving… Allergy is just an unfortunate side-effect of defense against parasitic worms.” So IgE’s ability to kick things into high gear to quickly react to such an invader would seemingly be very handy here.

What do parasitic worms have to do with allergies? The idea here is that the reason we get…

Getting dengue first may make Zika infection much worse

dengue antibody and dengue virus
FRIEND OR FOE A dengue antibody (blue, shown bound to a dengue virus protein, red, in this molecular model) can ease Zika’s entry into cells, a new study finds.

Being immune to a virus is a good thing, until it’s not. That’s the lesson from a study that sought to understand the severity of the Zika outbreak in Brazil. Experiments in cells and mice suggest that a previous exposure to dengue or West Nile can make a Zika virus infection worse.

“Antibodies you generate from the first infection … can facilitate entry of the Zika virus into susceptible cells, exacerbating the disease outcome,” says virologist Jean K. Lim. Lim and colleagues report the results online March 30 in Science.

The study is the first to demonstrate this effect in mice, as well as the first to implicate West Nile virus, notes Sharon Isern, a molecular virologist at Florida Gulf Coast University in Fort Myers.

Zika is similar to other members of its viral family, the flaviviruses. It shares about 60 percent of its genetic information with dengue virus and West Nile virus. Dengue outbreaks are common in South and Central America, and dengue as well as West Nile are endemic to the United States.

Exposure to a virus spurs the body to create antibodies, which prevent illness when a subsequent infection with the virus occurs. But a peculiar phenomenon called antibody-dependent enhancement has been described in dengue patients (SN: 6/25/16, p. 22). The dengue virus has four different versions. When a person with immunity to one dengue type becomes sick with another type, the illness is worse the second time. The antibodies from the previous dengue exposure actually help the subsequent dengue virus infect cells, rather than blocking them.

Outcomes of Zika infections for mice depended on whether certain viral antibodies were present in their systems….

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Ebola virus
TEAM PLAYERS Researchers are designing antibody pairs that can help detect the Ebola virus (shown) sooner.

WASHINGTON — Diagnosing Ebola earlier is becoming almost as easy as taking a home pregnancy test.

Scientists are developing antibodies for a test that can sniff out the deadly virus more quickly and efficiently than current tests, researchers reported February 6 at the American Society for Microbiology Biothreats meeting.

Detecting Ebola’s genetic material in patients’ blood samples now takes a full day and requires access to a specialized laboratory. Simpler and speedier tests are available. They use antibodies — specialized proteins that latch onto and flag virus particles — and work somewhat like a pregnancy test. Within…