Five life lessons from your immune system



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Are you exhausted? Your immune cells might be too.
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Joanna Groom, Walter and Eliza Hall Institute

This article is part of our occasional long read series Zoom Out, where authors explore key ideas in science and technology in the broader context of society and humanity.


Scientists love analogies. We use them continually to communicate our scientific approaches and discoveries.

As an immunologist, it strikes me that many of our recurring analogies for a healthy, functioning immune system promote excellent behaviour traits. In this regard, we should all aim to be a little more like the cells of our immune system and emulate these characteristics in our lives and workplaces.

Here are five life lessons from your immune system.




Read more:
The bugs we carry and how our immune system fights them


1. Build diverse and collaborative teams

Our adaptive immune system works in a very specific way to detect and eradicate infections and cancer. To function, it relies on effective team work.

At the centre of this immune system team sits dendritic cells. These are the sentinels and leaders of the immune system – akin to coaches, CEOs and directors.

They have usually travelled widely and have a lot of “life experience”. For a dendritic cell, this means they have detected a pathogen in the organs of the body. Perhaps they’ve come into contact with influenza virus in the lung, or encountered dengue fever virus in the skin following a mosquito bite.

Dendritic cells form a surveillance network – shown here as reddish stained cells in skin.
Ed Uthman (Houston, TX, USA) via Wikimedia Commons, CC BY

After such an experience, dendritic cells make their way to their local lymph nodes – organs structured to facilitate immune cell collaboration and teamwork.

Here, like the best leaders, dendritic cells share their life experiences and provide vision and direction for their team (multiple other cell types). This gets the immune cell team activated and working together towards a shared goal – the eradication of the pathogen in question.

The most important aspect of the dendritic cell strategy is knowing the strength of combined diverse expertise. It is essential that immune team members come from diverse backgrounds to get the best results.

To do this, dendritic cells secrete small molecules known as chemokines. Chemokines facilitate good conversations between different types of immune cells, helping dendritic cells discuss their plans with the team. In immunology, we call this “recruitment”.

This 3D image of a lymph node shows the cells that produce chemokines in red and blue.
Joanna Groom/WEHI, Author provided

Much like our workplaces, diversity is key here. It’s fair to say, if dendritic cells only recruited more dendritic cells, our immune system would completely fail its job. Dendritic cells instead hire T cells (among others) and share the critical knowledge and strategy to steer effective action of immune cells.

T cells can then pass these plans down the line – either preparing themselves to act directly on the pathogen, or working alongside other cell types, such as B cells that make protective antibodies.

In this way, dendritic cells establish a rich and diverse team that works together to clear infections or cancer.

2. Learn through positive and negative feedback

Immune cells are excellent students.

During development, T cells mature in a way that depends on both positive and negative feedback. This occurs in the thymus, an organ found in the front of your chest and whose function was first discovered by Australian scientist Jacques Miller (awarded the 2018 Japan Prize for his discoveries).




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As they mature, T cells are exposed to a process of trial and error, and take on board criticism and advice in equal measure, to ensure they are “trained” to respond appropriately to what they “see” (for example, molecules from your own body, or from a foreign pathogen) when they leave the thymus.

Importantly, this process is balanced, and T cells must receive both positive and negative feedback to mature appropriately – too much of either on its own is not enough.

In the diverse team of the immune system, cells can be both the student and the teacher. This occurs during immune responses with intense cross-talk between dendritic cells, T cells and B cells.

In this supportive environment, multiple rounds of feedback allow B cells to gain a tighter grip on infections, tailoring antibodies specifically towards each pathogen.

The result of this feedback is so powerful, it can divert cells away from acting against your own body, instead converting them into active participants of the immune system team.

Developing avenues that promote constructive feedback offers potential to correct autoimmune disorders.

The colours in this magnified slice through a lymph node show different cell types interacting as part of an immune response.
Joanna Groom/WEHI, Author provided



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3. A unique response for each situation

Our immune system knows that context is important – it doesn’t rely on a “one-size–fits-all” approach to resolve all infections.

This allows the cells of our immune system to perfectly respond to different types of pathogens: such as viruses, fungi, bacteria and helminths (worms).

In these different scenarios, even though the team members contributing to the response are the same (or similar), our immune system displays emotional intelligence and utilises different tools and strategies depending on the different situations, or pathogens, it encounters.

Importantly, our immune system needs to carefully control attack responses to get rid of danger. Being too heavy handed leaves us with collateral tissue damage, such as is seen allergy and asthma. Conversely, weak responses lead to immunodeficiencies, chronic infection or cancer.

A major research aim for people working in immunology is to learn how to harness balanced and tailored immune responses for therapeutic benefit.




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4. Focus on work/life balance

When we are overworked and poorly rested, we don’t function at our peak. The same is true for our immune cells.

An overworked immune cell is commonly referred to as being “chronically exhausted”. In this state, T cells are no longer effective at attacking tumour or virus-infected cells. They are lethargic and inefficient, much like us when we overdo it.

For T cells, this switch to exhaustion helps ensure a balanced response and avoids collateral damage. However, viruses and cancers exploit this weakness in immune responses by deliberately promoting exhaustion.

The rapidly advancing field of immunotherapy has tackled this limitation in our immune system head-on to create new cancer therapeutics. These therapies release cells of their exhaustion, refresh them, so they become effective once more.

This therapeutic avenue (called “immune checkpoint inhibition”) is like a self-care day spa for your T cells. It revives them, renewing their determination and efficiency.

This has revolutionised the way cancer is treated, leading to the award of the 2018 Nobel prize in Medicine to two of its pioneers, James P. Allison and Tasuku Honjo.




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5. Learn from life experiences

The cornerstone of our adaptive immune system is the ability to remember our past infections. In doing so, it can respond faster and in a more targeted manner when we encounter the same pathogen multiple times.

Quite literally, if it doesn’t kill you, it makes your immune system stronger.

Vaccines exploit this modus operandi, providing immune cells with the memories without the risk of infection.

Work still remains to identify the pathways that optimise formation of memory cells that drive this response. Researchers aim to discover which memories are the most efficient, and how to make them target particularly recalcitrant infections, such as malaria, HIV-AIDS and seasonal influenza.

While life might not have the shortcuts provided by vaccines, certainly taking time to reflect and learn after challenges can allow us to find better, faster solutions to future problems.




Read more:
Explainer: how viruses can fool the immune system


The Conversation


Joanna Groom, Laboratory Head, Walter and Eliza Hall Institute

This article is republished from The Conversation under a Creative Commons license. Read the original article.

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A strong immune system helps ward off colds and flus, but it’s not the only factor



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Winter bugs are impossible to escape.
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Hui-Fern Koay, University of Melbourne and Jesseka Chadderton, University of Melbourne

It’s peak flu season. You’re cold, rugged up and squashed on public transport or in the lift at work. You hear a hacking cough, or feel the droplets of a sneeze land on your neck. Will this turn into your third cold this year?

No matter how much we try to minimise our exposure to respiratory viruses, it’s far more difficult in winter when we spend so much time in close proximity to other people.

On top of this, viruses tend to be more stable in colder and drier conditions, which means they stick around longer.




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The common cold is caused by more than 200 different viruses, the most common of which are rhinoviruses (rhino meaning nose). Rhinovirus infections tend to be mild; you might get a sore throat and a head cold lasting just a few days.

Influenza, or the flu, is generally caused by type A or B influenza viruses. The flu is far more aggressive and often includes a fever, fatigue and body aches, in addition to all the classic cold symptoms.

The flu tends to be more severe than the common cold.
healthdirect

When it comes to getting sick, there’s always an element of bad luck involved. And some people, particularly those with young children or public transport commuters, are likely to come into contact with more viruses.

But you may have noticed that illness often strikes when you’re stressed at work, not sleeping properly, or you’ve been out partying a little too much. The health of our immune system plays an important role in determining how we can defend against invading cold and flu viruses.

How the immune system fights viruses

Your skin and saliva are key barriers to infection and form part of your immune system, along with cells in every tissue of your body, including your blood and your brain.

Some of these cells migrate around to fight infection at specific sites, such as a wound graze. Other cells reside in one tissue and regulate your body’s natural state of health by monitoring and helping with the healing process.

The cells that make up your immune system need energy too, and when you’re low on juice, they’ll be on low-battery mode. This is when our natural immune defences are weakened and normally innocuous bugs can begin to cause strife.

Our immune system requires a lot of energy to defend our bodies. Feeling tired and achy, overheating, and glands swelling are all signs that our immune system is busy fighting something.




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Explainer: how does the immune system work?


Boosting our natural defence system

Our immune system has evolved to naturally detect and eliminate viral infections. And we can actively strengthen our immunity and natural defences by looking after ourselves. This means:

  • getting adequate sleep. Sleep deprivation increases the hormone cortisol, which suppresses immune function when its levels are elevated

  • exercising, which helps the lymphatic system, where our immune cells circulate, and lowers levels of stress hormones

  • eating well and drinking enough water. Your immune system needs energy and nutrients obtainable from food. And staying well hydrated helps the body to flush out toxins

Good food feeds your immune system.
Anna Pelzer
  • not smoking. Smoking, or even secondary smoke, damages our lungs and increases the vulnerability of our respiratory system to infection.



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Educating our immune system

Natural defences aren’t always enough to keep us safe and we need the help of flu vaccinations.

Vaccines are designed to educate an army of B and T cells which make up your adaptive immune system. This arm of your immune system learns by exposure and provides long-term immunity.

These T and B cells need a bit of time from the initial influenza exposure before they can be activated. This activation lag time is when you feel the brunt of the flu infection: lethargy, body aches, extreme fatigue and unable to get off the couch for a day or two.

To overcome this delay and protect people before they are exposed to potentially harmful flu strains, flu vaccination introduces fragments of the influenza virus into the body, which acts like prior exposure to the bug (without actual infection).

You can still get the flu if you’ve been vaccinated but you might not get as sick.
VGstockstudio/Shutterstock

Seasonal vaccines are designed to match currently circulating strains and target those strains before you’re infected.

You can still catch the influenza virus if you are vaccinated. But because of this pre-education, the symptoms will likely be milder. The immune system has been trained and the army of B and T cells can move into action quicker.

Already have a cold or the flu?

If you’ve been sniffling and sneezing your way through winter, be comforted by the fact that these bugs are strengthening your immune system. Our body remembers the particular strain of rhinovirus or influenza we get, so it can recognise and mount a stronger defence if we encounter it again.


The Conversation


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Explainer: what’s new about the 2018 flu vaccines, and who should get one?


Hui-Fern Koay, Research Fellow in Immunology, University of Melbourne and Jesseka Chadderton, PhD Candidate, University of Melbourne

This article was originally published on The Conversation. Read the original article.

The bugs we carry and how our immune system fights them



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The immune system has to establish which cells belong to us and which are foreign, no mean feat.
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Peter C. Doherty, The Peter Doherty Institute for Infection and Immunity

This article is part of a three-part package exploring immunity and infectious diseases around the world. Read the other articles here.


Human beings are large, complex, multicellular, multi-organ systems. We reproduce slowly and rely on a breadth of mechanisms that allow us to control the myriad of rapidly replicating, simple life forms that have evolved to live in or on us.

The system of defence is referred to collectively as immunity.

The word itself comes from the Latin immunis, describing the status of returned soldiers (Genio immunium) in the Roman state who were, for a time, exempt from paying taxes.

Our immunity protects us from many illnesses, including some forms of cancer. New cancer therapeutics, called immunotherapies, work by boosting our immune cells to fight cancer cells that have found ways to evade them.

The immune system is divided into two interactive spheres, the much older “innate” sphere, and the more recently evolved “adaptive” sphere. A primary challenge for the very specifically targeted cells that form the basis of adaptive immunity is to distinguish “self” (our own body cells and tissues) from “non-self” – the foreign invaders. When that goes wrong, we can develop autoimmune diseases such as multiple sclerosis or rheumatoid arthritis.




Read more:
Explainer: what are autoimmune diseases?


The organisms we carry around with us

The human body is host to many organisms over a lifetime. Some are dangerous to health (pathogens), some are benign, and some are necessary for proper functioning.

Most of the genetic material we carry around with us is “non-self”: principally harmless bacteria (called “commensals”) that live in the gastrointestinal tract.

Traditionally, studies focused on the “bad bugs” in our gut that cause diarrhoea and dysentery. But more recently, we’re learning there are also good guys. And there’s a general consensus we need to know more about the “microbiome”, the mass of bacteria in any “clinically normal” gut.

Gut bacteria provide essential vitamin B12 and when they die, release myriad proteins that will be broken down into amino acids, which the body needs. About 30% of our poo is comprised of dead bacteria.

Apart from our microbiome, normal human beings also have a substantial “virome”. Viruses differ from bacteria (which are cells in their own right) in that they are much simpler and can only replicate in living cells.

The greatest number of viruses we carry around are the “bacteriophages”, which infect the commensal bacteria in our gut. Not all “phages” are, however, benign. For example, the toxin that causes human diphtheria is encoded in the genome of a bacteriophage.

There’s also a spectrum of viruses that persistently infect our body tissues. The most familiar are herpes viruses, like those that cause cold sores (H. simplex) and shingles (H. zoster). Both viruses hide out in the nervous system and are normally under immune control. They re-emerge to cause problems as a consequence of tissue stress (such as a sunburnt lip) or as immunity declines with age (shingles). This is why a booster shingles vaccine is recommended for the elderly.




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Our innate and adaptive immune systems

The innate system ranges from processes as basic as phagocytosis (ingestion of bacteria), to molecules like the interferons produced by any virus-infected cell that can limit replication. Such innate systems are found right across the evolutionary spectrum and don’t target specific pathogens.

The much younger adaptive immune system is what we stimulate with vaccines. A property of small white blood cells called lymphocytes, it divides broadly into two lineages: the B cells and T cells. These bear the extraordinarily diverse and very specific immunoglobulin (Ig) and T cell receptor (TCR) recognition molecules that detect invading pathogens (bacteria, virus, fungi and so on).

The immunoglobulins bind to “non-self” (foreign) proteins called “antigens”, while the T cell receptors are specifically targeted to “self” transplantation molecules.

The assassins of the immune system are then switched on; the killer T cells that eliminate virus-infected (or cancer) cells. Also activated are the “helper” T cells that secrete various molecules to “help” both the B cells and killer T cells differentiate and do their work.




Read more:
Explainer: what is the immune system?


How does our immune system learn and remember?

All lymphocyte responses work by massive cell division in the lymph nodes (the “glands” in our neck that swell when we get a sore throat). This process is started by small numbers of “naive” B and T cells that haven’t encountered the invader before, and only stops when the foreign invader is eliminated.

The B cells differentiate into large protein-secreting cells called plasma cells, which produce the protective antibodies (immunoglobulins) that circulate for years in our blood.

Most of the T cells die off after they’ve done their job, but some survive so they can remember how to target specific invaders. They can be rapidly recalled to their “killer” or “helper” function.

Prior infection or the administration of non-living or “attenuated” (to cause a very mild infection) vaccines sets up the memory so protective antibodies are immediately available to bind (and neutralise) pathogens like the polio or measles virus. While immune T cells are rapidly recalled to “assassin” status and eliminate pathogen-infected cells.

As you may have gathered from this very brief and far too simplified account, the immune system is extraordinarily complex. And it’s also very finely balanced with, for example, cross reactive responses to bacterial proteins sometimes setting us up for autoimmune diseases.




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No, combination vaccines don’t overwhelm kids’ immune systems


Another example of autoimmunity is rheumatoid arthritis, which can be triggered by blood-borne chemicals from tobacco smoke that modify “self” transplantation molecules in the joints.

The ConversationAnd when we talk about the possible effects of the microbiome, or the “too clean” hypothesis, we’re discussing how exposure to bacteria and viruses can modify that immune balance in ways that directly affect our wellbeing. This is a very active area of research which, given the underlying complexity, presents scientists with big challenges as we seek to reach verifiable conclusions.

Peter C. Doherty, Laureate Professor, The Peter Doherty Institute for Infection and Immunity

This article was originally published on The Conversation. Read the original article.