Your Amazing Immune System

Your Amazing Immune System

By COVID-19 SMA 

 

In our “new normal” world, we hear about antibodies, vaccines, and immunity almost every day, and if you’ve never studied immunology, all of this can be very confusing. Immune systems are complicated, and everyone is different, but anyone can understand the basic mechanisms our bodies use to keep us safe from infections. 

 

Our immune system, or the way the body protects itself from viruses such as COVID-19, is amazingly well put together. The more you get to know about it, the more you will understand what a truly fascinating system it is. It is made up of myriad players that work together in close coordination to protect our bodies from foreign invaders. 

 

So how does the immune system protect us from microbes like the coronavirus? 

 

Since this answer literally affects everyone’s life and the future, we thought we’d spend some time talking about it. 

 

Everybody’s immune system is different 

 

All living things are subject to attack from disease-causing agents. Even bacteria, so small that more than a million could fit on the head of a pin, have systems to defend against infection by viruses. But how each of us does that is different because in our DNA (our genes) lie unique and complicated chemical codes that exist in every cell of our bodies (including immune cells) and controls what makes you, you—and me, me. 

 

The genes that control your immune system are among the most complicated of all, and just like with genes for eye color, not everybody’s immune system genes are the same (Prevention, 2020). And this has actually been very important for us to survive. Imagine, for a second, that we all had exactly the same immune system. One particularly bad infection could wipe us all out if our immune systems were identical. So, before we go any further, it’s extremely important to understand that we all have very different immune systems, and this, on the whole, keeps us safer as a species. But it is also important to consider the other side. As individuals in the middle of a pandemic, that also means some of us are better at fighting off disease than others. 

 

Our immune system has two main parts: 

 

The innate immune system 

The innate immune system is inherited and is active from the moment you are born and thought to remain until the day you die. This is your rapid response system that just knows what to do. It patrols your body and is the first to respond when it finds an invader. Think of this as the ambulance crew that comes when you call 911—they triage and stabilize the scene. 

 

These first lines of defense include outer barriers like the skin and mucous membranes that keep invaders out, and when pathogens breach these outer barriers (like when a virus is inhaled into the lungs), powerful allies inside the body called phagocytes recognize these invaders and go into action immediately. A phagocyte surrounds a pathogen, takes it in, and attempts to neutralize it. (Johns Hopkins Medicine, (2018) 

 

The acquired immune system 

While healthy phagocytes are critical to good health, they are unable to address all types of infectious threats by themselves and usually not complicated ones like SARS-CoV2. 

 

So, in contrast to innate immunity, acquired immunity allows for a very targeted response against a specific pathogen. Think of this like that ambulance you called to take you to a heart hospital for a heart attack so you can get the specialized care that you need. 

 

Our immune system remembers the invaders and goes to battle 

 

For the sake of simplicity, we are only going to talk about the parts of the acquired immune system that remember and protect us from reinfection. This part of our immune system has two main branches of military: B cells and T cells. Both of these types of cells learn to recognize infectious microbes (invaders) and destroy them. And both of these cells live on past the battle, ready to fight again…. sometimes for the rest of your life. This protects us from reinfection because if that invader ever comes back, your B cells and T cells are there and ready to go to battle again to destroy them. But just as the Marines and the Air Force go into battle with different tools and strategies, B cells and T cells use different methods to combat infections. 

  • T cells travel around your body, patrolling your cells to make sure they’re not infected with invaders (diseases) they have seen before (these are the long-term memory immune cells). If they find infected cells (say lung cells infected with SARS-CoV2), the T cells will initiate a self-destruct program in those human cells. While this sounds ominous, it is actually very good. Viruses specifically can’t make copies outside of living cells, so when the infected cells are killed, that usually stops the virus from spreading. The T cell immune response is difficult to measure and is usually only evaluated in specialized research settings. Because this is such a new virus, there is a lot that is unknown about our T cell immune response to SARS-CoV2. 
  • B cells have only one humongous job that is essential to our immune system. They can mature and change into plasma cells that produce a very special protein called an antibody. However, B cells alone are not particularly good at making antibodies and rely on T cells to provide a signal that they should begin the process of maturation.

 

So, what is an antibody? 

Antibodies are small proteins that recognize the shapes on the surfaces of microbes (Steven Woloshin, 2020). When they come across the shape they match, they connect to the surface of that microbe, like a jigsaw puzzle. Once the antibody is attached to its target, it won’t become unattached. The antibody jigsaw connection serves two purposes: it blocks the microbe from infecting your cells (another piece can’t fit in the puzzle), and it acts as a signal to your immune system to go to battle and destroy whatever they are hanging on to. This antibody complex doesn’t kill the invaders, so the T cells are called in to help. The T cell then calls in phagocytes to help finish off the invaders and then help clean up the mess. One big happy family is going to battle for you! 

 

The antibodies stay in the body, some for a short period, some forever. So, if the invaders come again, they’re available; they’re ready to go back to battle to help destroy them as soon as they show up. This complicated war against invaders helps keep the body free of many toxic/harmful bacteria and viruses. 

 

How do antibodies find their targets to begin with? 

We’ve been talking about the immune system recognizing invaders that it’s fought before, but how does the immune system deal with a microbe it’s never encountered before like SARS-CoV-2? This is the crazy cool part… even before there is an infection, the B cells in your body make millions of different antibodies, totally randomly. All these antibodies are made without knowing what microbes they are going to match. Think of B cells as a locksmith making millions of keys, without knowing what locks they are going to open. These B cells patrol your body, ready for action when it comes. Then, when an invader comes along, all the B cells test their antibodies to see if their key is a match to the microbe. Once a match is found, your body starts making lots of copies of that antibody, and soon a whole puzzle is made which helps fight the infection. This is how our bodies develop what we call an “antibody response” to an infection. 

 

If we have antibodies, does this mean we will always be protected? 

 

This novel coronavirus is new to the human population—we have never been exposed to it before—so there are many unknowns about how we respond to it. What we do know is related to that discussion we had earlier that everyone’s genes are different. Across any population, there is a high degree of individual variability in the genes that dictate our immune response to a pathogen in the amount, type, and quality of antibodies that we make (Johns Hopkins Medicine, 2018). 

 

Some people make many rock-star quality antibodies that are exceptionally good at recognizing the relevant invader and binding to it. If this happens, the virus is rapidly bound by antibodies and eliminated before it can even cause an infection. 

 

Other people make so-so antibodies, and they’re just not as effective at recognizing and binding the pathogen—like a puzzle piece in the wrong spot. In this situation, the antibodies only provide partial protection: they slow the virus down, but the virus can still cause some degree of infection. These individuals usually exhibit some symptoms and shed the virus for a longer period. 

 

Then there are also some people who are just not great at the whole antibody thing all together….and they either produce little or very poor-quality antibodies. In this case, although these people produce antibodies, the immunity is not highly effective so they can experience a prolonged infection with more severe symptoms. This is one of the big unknowns with this new coronavirus: What percentage of the population falls into this category? 

 

Fortunately, sometimes individuals with a very vigorous T cell immune response will be protected from a pathogen even though they produce low amounts of antibody. Again, because T cells are more complicated to measure, we’re still learning what this will mean. 

 

So, if our acquired immunity isn’t working as well, can’t we rely on our innate immunity to go to battle? 

 

This is one of the big unknowns with COVID-19. In general, scientists think the innate immune response remains fairly intact throughout life, even as we age. The problem is if we have an extremely poor acquired immune response, our innate immune response must work twice as hard to try to make up for it. This is known as immune dysregulation and may be one of the reasons we observe more severe infections in older patients (Johns Hopkins Medicine, 2018).

 

Is this related to why some coexisting conditions worsen the effects of an infection? 

 

The immune system is wildly complex and is made of lymph nodes, the spleen, bone marrow, and other organs. We know that, in general, chronic diseases tend to weaken our immune systems because different parts of our body aren’t working as well as others, making the whole system less efficient. The system needs a proper functioning environment to be able to do its job well. Therefore, people with underlying chronic diseases often have some loss of innate and acquired immunity and therefore are at greater risk for developing a more severe infection. 

 

Why is it important to understand more about COVID-19 immune response? 

 

Antibodies can tell us who has been exposed to a pathogen and potentially what protection they might have against a reinfection. As we discussed above, there are so many unknowns with this new coronavirus. Scientists need to know more about how we, as individuals and as a population, are responding to the virus, particularly whether immunity to the virus is regulated by antibodies, T cells, or both. Armed with this information, they will be better able to design safe and effective vaccines and to predict outcomes for individuals who become infected. 

 

Now, you are a beginner immunologist, congratulations! 

 

www.facebook.com/covid19sma 

 

Works Cited

Johns Hopkins Medicine. (2018, June 25). The Immune System. Retrieved from Johns Hopkins Medicine: https://www.hopkinsmedicine.org/health/conditions-and-diseases/the-immune-system

Prevention, C. f. (2020, June 16). How COVID-19 Spreads. Retrieved from CDC: https://www.cdc.gov/coronavirus/2019-ncov/index.html

Steven Woloshin, M. N. (2020). False Negative Tests for SARS-CoV-2 Infection — Challenges and Implications. New England Journal of Medicine, DOI: 10.1056/NEJMp2015897.

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