One question many people are asking is whether the immunity you get from contracting COVID and recovering is enough to protect you in the future.
The answer is no, it’s not.
Remind me, how does our immune response work?
Immune responses are innate or acquired. Innate, or short-term immunity, occurs when immune cells that are the body’s first line of defence are activated against a pathogen like a virus or bacteria.
If the pathogen is able to cross the first line of defence, T-cells and B-cells are triggered into action. B-cells fight through secreted proteins called antibodies, specific to each pathogen. T-cells can be categorised into helper T-cells and killer T-cells. Helper T-cells “help” B-cells in making antibodies. Killer T-cells directly kill infected cells.
Once the battle is over, B-cells and T-cells develop “memory” and can recognise the invading pathogen next time. This is known as acquired or adaptive immunity, which triggers long-term protection.
What happens when you get reinfected? Memory B-cells don’t just produce identical antibodies, they also produce antibody variants. These diverse set of antibodies form an elaborate security ring to fight SARS-CoV-2 variants.
Natural immunity is not enough
Getting COVID and recovering (known as “natural infection”) doesn’t appear to generate protection as robust as that generated after vaccination.
And the immune response generated post-infection and vaccination, known as hybrid immunity, is more potent than either natural infection or vaccination alone.
People who have had COVID and recovered and then been vaccinated against COVID have more diverse and high-quality memory B-cell responses than people who’ve just been vaccinated.
Studies indicate mRNA vaccines generate a more potent immune response with previous infection, at least against some variants including Alpha and Beta.
And studies have shown that antibody levels were higher among those who’d recovered from COVID and were subsequently vaccinated than those who’d only had the infection.
Memory B-cells against the coronavirus have been reported to be five to ten times higher in people vaccinated post-infection than natural infection or vaccination alone.
Is one dose enough after COVID?
Some reports have suggested people who’ve had COVID need only one dose of the vaccine. Clinical trials of approved vaccines didn’t generate relevant data because people who’d already had COVID were excluded from phase 3 trials.
One study from June showed people with previous exposure to SARS-CoV-2 tended to mount powerful immune responses to a single mRNA shot. They didn’t gain much benefit from a second jab.
A single dose of an mRNA vaccine after infection achieves similar levels of antibodies against the spike protein’s receptor binding domain (which allows the virus to attach to our cells) compared to double doses of vaccination in people never exposed to SARS-CoV-2.
We need more studies to fully understand how long memory B-cell and T-cell responses will last in both groups.
Also, a single dose strategy has only been studied for mRNA-based vaccines. More data is required to understand whether one jab post-infection would be effective for all the vaccines.
At this stage, it’s still good to have both doses of a COVID vaccine after recovering from COVID.
Does Delta change things?
The development of new vaccines must keep pace with the evolution of the coronavirus.
At least one variant seems to have evolved enough to overtake others, Delta, which is about 60% more transmissible than the Alpha variant. Delta is moderately resistant to vaccines, meaning it can reduce how well the vaccines work, particularly in people who’ve only had one dose.
There’s no data available yet about how effective a single jab is for people who were previously infected with Delta and recovered.
The most important thing you can do to protect yourself from Delta is to get fully vaccinated.
According to a Public Health England report, one dose of Pfizer offered only about 33% protection against symptomatic disease with Delta, but two doses was 88% effective. Two doses was also 96% effective against hospitalisation from Delta. The AstraZeneca vaccine was 92% effective against hospitalisation from Delta after two doses.
A few vaccine manufacturers, including Pfizer, are now planning to use a potential third dose as a booster to combat the Delta variant.
Both vaccines are also safe and effective at generating immune responses in the elderly. But what about another vulnerable group — people with immunodeficiencies? Many people with immunodeficiencies are included in group 1b and will now be thinking about getting their vaccine.
Although we’re still gathering data to determine whether COVID vaccines will work as well in people with immunodeficiencies as they do in the general population, they’re likely to offer at least a reasonable degree of protection. And importantly, we know they’re safe.
What are immunodeficiencies?
Immunodeficiencies are conditions that weaken the body’s ability to fight infection. People’s immune system may be compromised for many reasons, and this can be transient or lifelong.
Primary immunodeficiencies occur when some or all of a person’s immune system is missing, defective or ineffective. These are rare and often genetic diseases that may be diagnosed early in life, but can occur at any age.
Secondary immunodeficiencies are acquired, and more common. They may occur as a result of other diseases (for example, via HIV infection), treatments and medications (such as chemotherapy or corticosteroids), or environmental exposure to toxins (for example, prolonged exposure to heavy metals or pesticides).
Sometimes the immune system in people with immunodeficiencies can react in exaggerated ways too, and cause autoimmune disease (such as rheumatoid arthritis or gut inflammation). So it sometimes makes more sense to describe the immune system as “dysregulated”, rather than “deficient”.
Immunodeficiencies, COVID-19 and vaccines
People with secondary immunodeficiencies are generally at higher risk of becoming infected with SARS-CoV-2 and of developing severe disease. Surprisingly, although people with primary immunodeficiency may be at greater risk of getting infections, including COVID, most are no more susceptible to developing severe COVID compared with the overall population.
This may be because the most severe COVID-19 symptoms are usually not due to gaps in immunity, but to an overactive immune response to SARS-CoV-2.
In fact, immune-suppressing steroids may be an effective treatment for severe COVID. Clinical trials looking into this are underway.
However, as vaccines work by mobilising our immune systems, for people who have a weaker immune system to begin with, vaccines may not be as effective. They may generate an incomplete or short-lived response, so people with immunodeficiencies may need additional boosters to maintain protective immunity.
It’s difficult to assess COVID vaccine efficacy in people with immunodeficiencies, because people with primary immunodeficiencies or cancer weren’t included in clinical trials.
A very small number of people with HIV have been included in trials of a few of the vaccines, but limited data is publicly available. So it’s too early to draw any firm conclusions on whether the vaccines will be as effective in people with HIV as for the general population.
We also don’t yet know how long immunity to COVID-19 or COVID vaccines lasts. This will be particularly important for immunodeficient people. Research is underway to determine whether they’ll need booster jabs more frequently to maintain immunity.
We do know the vaccines are safe for this group.
Neither the AstraZeneca nor the Pfizer vaccines can cause an infection, so they won’t present a problem for people with immunodeficiencies (or for elderly people, who may also have weakened immune responses).
Usually, we avoid giving “live attenuated” vaccines (vaccines that contain weakened elements of the virus) to anyone with immunodeficiency. Because of their weakened immune systems and increased susceptibility to infection, there’s a chance they could develop a full-blown infection. An example of this is the chickenpox vaccine. But no live attenuated COVID vaccines have been approved anywhere in the world.
Preliminary evidence from vaccine rollouts around the world has shown COVID vaccines are safe for immunocompromised people with cancer. Although, if you’re going through cancer treatment, you should discuss the timing of your vaccination with your specialist.
Vaccination is most definitely recommended for people with immunodeficiencies, and they’re included in priority groups for vaccine rollout in Australia. Group 1b includes people with underlying medical conditions which may place them at higher risk from COVID-19, including “immunocompromising conditions”.
If you have a diagnosed immunodeficiency or autoimmune disease, you can talk to your doctor or specialist for specific advice on the timing of your COVID vaccination and your condition. There’s generally no reason to change your normal medications or therapies before receiving the vaccine.
The Oxford vaccine trial at the centre of safety concerns this week highlights the idea that people’s immune systems respond to vaccines differently.
We don’t yet know whether reports of immune complications in one or two trial participants have been linked to the COVID-19 vaccine itself, or if they were given the placebo vaccine.
But it does highlight the importance of phase 3 clinical trials in many thousands of people, across continents. These not only tell us whether a vaccine is safe, but also whether it works for people of different ages or with particular health issues.
An effective vaccine should generate long-lasting protective immunity against SARS-CoV-2, the virus that causes COVID-19.
This can be by generating antibodies to neutralise the virus and likely also by helping the immune system memorise and quickly respond to infection.
We know, from developing vaccines against other viruses, that people’s immune response to a vaccine can vary. There’s every reason to believe this will also be the case for a COVID-19 vaccine.
1. Vaccine type and how it’s delivered
Many COVID-19 vaccine candidates contain parts of the SARS-CoV-2 spike protein to stimulate protective immunity. However, there are many different ways of delivering these proteins to the body, and some may be more effective than others at stimulating your immune system.
For example, the Oxford vaccine combines the spike protein with another virus to mimic the actions of SARS-CoV-2.
Meanwhile, the candidate developed by the University of Queensland contains the spike protein packaged with another compound (an adjuvant) to stimulate the immune system.
Some people have poor protective immune responses to COVID-19 vaccine candidates. These people may have existing immunity to the adenovirus used in some vaccines to deliver the SARS-CoV-2 spike protein.
In other words, their body mounts an immune response to the wrong part of the vaccine (the delivery mechanism) and not so much to the characteristic part of the virus (the spike protein).
3. Our genetics
Our genes play a large part in regulating our immune system.
Any new infectious disease poses unique challenges to people who are pregnant during an outbreak. The effects of Sars, Zika and influenza in pregnancy highlight the potential immediate and longer term detrimental health outcomes a virus can have for both mother and baby. These risks include premature delivery of the baby with Sars, birth defects with Zika and greater risk of severe influenza.
Should we be as worried about pregnancy and COVID-19? There are a number of things we need to think about. These fall into two broad areas related to the effects on the foetus and the effects on the pregnant person themselves.
In both cases we need to think about the immediate effects during the pregnancy as well as the longer term health effects for both parent and child. The early evidence we have shows that changes to the immune system during pregnancy could be somewhat protective against the disease.
Early data from pregnant women with COVID-19 indicates that the disease is linked to premature birth and changes to the placenta that might reflect altered blood flow. This suggests that virus-associated disruptions do occur between parent and foetus.
However, these studies were of women with severe cases of the disease. We know very little about the effect of mild disease or asymptomatic infection in pregnancy. Understanding this is critical, as studies have highlighted that asymptomatic and mildly infected pregnant women far outnumber those requiring hospitalisation for COVID-19.
This indicates that pregnant people are not more susceptible to severe COVID-19, which was one of the greatest concerns at the beginning of the pandemic and led to them being categorised as vulnerable.
The apparent protective effect of pregnancy against severe disease might simply reflect the different immune responses to severe COVID-19 seen in men and women, and the fact that more men than women die from the disease in general. However, we do not see the same response in pregnancy with other viruses, such as influenza, suggesting something else is at play with SARS-CoV-2.
So far, it seems that the foetus is very well protected from the passage of SARS-CoV-2 from mother to child (known as vertical transmission) and such passage, while possible, seems to be uncommon. This might be down to the natural features of the placenta, which produces molecules that stop the virus binding to placental cells. It could also be that the placental membranes limit infection by the virus.
Of course, it is very difficult to study the placenta prior to birth. Alternative measures, such as analysing cellular debris released from the placenta (known as extracellular vesicles) which can be found in a sample of the mother’s blood, are really needed to find out what features of the placenta might protect the foetus from infection and what effects the virus has on the placenta.
Any antibodies that a mother infected with SARS-CoV-2 makes will pass to the foetus across the placenta (known as passive immunity). This provides short-term protection from many infectious agents for the last months of pregnancy and for some months after the baby is born. These antibodies will also continue to be provided in breast milk if the baby is breast fed.
Early studies from China have shown that antibodies that protect against COVID-19 are present in newborns of women who had such antibodies. This confirms that passive immunity, where a baby essentially inherits antibodies from a parent, occurs with SARS-CoV-2. We now need some larger studies to investigate whether anti-SARS-CoV-2 antibodies are present in human milk to better understand the role of these antibodies in neutralising the virus and protecting the baby.
Molecules other than antibodies can also pass from parent to foetus. Pregnant women with severe COVID-19 have many of the hallmarks of an inflammatory response that we see in other people with similar symptoms. This includes elevated levels of molecules such as interleukin-6 (IL-6), which indicates that the immune response has been activated.
There are a number of studies showing that maternal immune activation can have detrimental effects on the developing foetus. Such activation is associated with increased risk of respiratory, cardiovascular, neurodevelopmental and other disorders in the offspring. Whether SARS-CoV-2 will have such long-term effects on the health of these children remains to be seen.
The role of the immune system
In a previous article, we discussed how the immune system changes during pregnancy, and it might be that unique features of this and other dynamic adaptations that occur with pregnancy provide protection from severe COVID-19.
Other examples of possible protective mechanisms include differences in the receptor molecules used by SARS-CoV-2 to invade human cells. Angiotensin-converting enzyme 2 (ACE2) is the best known of these viral entry receptors but CD147, CD26 and others also have this role.
All of these receptors undergo changes during pregnancy, which might contribute to resilience. These receptors also occur as soluble forms that can be measured in blood and breast milk and might act as decoy receptors, stopping the virus from binding to cells.
Elaborating on why both the pregnant person and their child seem to be relatively resilient to severe forms of COVID-19 might help us understand other disease processes and identify ways to combat the disease.
Work from the UK Obstetric Surveillance System has shown that, as with the wider population, Asian and Black pregnant women are more likely to be admitted to hospital with SARS-CoV-2 infection. Therefore, we really need to consider the effects of ethnicity and other risk factors in our studies of COVID-19 in pregnancy.
This is especially important as these studies will support efforts towards the use of any vaccine in pregnancy.
During the COVID-19 pandemic we’re constantly being reminded to practise good hygiene by frequently washing our hands and regularly cleaning the spaces where we live and work.
These practices aim to remove or kill the coronavirus that causes COVID-19, and thereby minimise our risk of infection.
But there have been some suggestions using hand sanitiser and practising other hygiene measures too often could weaken our immune system, by reducing our body’s exposure to germs and with it the chance to “train” our immune defences.
The good news is, there’s no evidence to suggest this will be the case.
For healthy immune function, it’s important we’re exposed to a diverse range of bugs in the environment, known as microbes. Most of these don’t make us sick.
The belief that a high level of cleaning and personal hygiene weakens our immune system is a common interpretation of what’s called the “hygiene hypothesis”.
The hygiene hypothesis is a theory that suggests a young child’s environment can be “too clean”, and they won’t be exposed to enough of these microbes to effectively stimulate their immune system as it develops.
The argument is that this results in increased allergies, asthma and certain autoimmune disorders. But scientists have refuted this hypothesis in recent years, as research has shown there are multiple other reasons for the increased incidence of these conditions.
Importantly, being too dirty doesn’t help our immune system either. It generally makes inflammation worse.
What is the immune system?
The immune system works to protect our bodies against things that threaten to make us sick — from harmful chemicals, to bacteria and viruses, to cancer cells.
It’s made up of two lines of defence. The first is the “innate” immune system, which responds rapidly to a range of pathogens to fight infection and prevent tissue damage.
Next is the “adaptive” immune system, made up of immune cells that develop a more targeted or specific response to fight off harsher germs such as viruses. Adaptive immune cells work by recognising small parts of the virus on the outside of the infected cell (for example, lung cells), and destroying them.
These cells then become what we call “memory cells”. The next time they encounter the same virus, they can eliminate it straight away.
This development of the immune system starts after birth and declines in old age.
Cleaning refers to the removal of microbes, dirt and impurities from surfaces. It doesn’t kill microbes, but by removing them, it lowers their numbers and therefore reduces the risk of spreading infection.
In contrast, disinfecting refers to using chemicals, known as disinfectants, to kill microbes on surfaces.
A combination of cleaning and disinfecting is the most effective way to get rid of microbes such as coronavirus.
We’ve been advised to clean our hands with soap and water for at least 20 seconds. If this is not possible, use hand sanitiser with at least 60% ethanol or 70% isopropanol.
Frequent hand-washing, especially if a sanitiser is used, can disrupt the natural skin biome, which can lead to increased skin infections. This can be managed with the use of moisturisers.
But the extra hygiene measures during COVID-19 won’t weaken our immune systems. On the contrary, they are vital in controlling the pandemic.
If you’re worried about your immune system, don’t stop washing your hands or keeping your house clean. Importantly, follow a healthy balanced diet, do regular exercise and look after your mental health.
Don’t shake hands, don’t high-five, and definitely don’t hug.
We’ve been bombarded with these messages during the pandemic as a way to slow the spread of COVID-19, meaning we may not have hugged our friends and family in months.
This might be really hard for a lot of us, particularly if we live alone. This is because positive physical touch can make us feel good. It boosts levels of hormones and neurotransmitters that promote mental well-being, is involved in bonding, and can help reduce stress.
So how can we cope with a lack of touch?
Touch helps us bond
In humans, the hormone oxytocin is released during hugging, touching, andorgasm. Oxytocin also acts as a neuropeptide, which are small molecules used in brain communication.
Touch also helps reduce anxiety. When premature babies are held by their mothers, both infants and mothers show a decrease in cortisol, a hormone involved in the stress response.
Touch promotes mental well-being
In adults with advanced cancer, massages or simple touch can reduce pain and improve mood. Massage therapy has been shown to increase levels of dopamine, a neurotransmitter (one of the body’s chemical messengers) involved in satisfaction, motivation, and pleasure. Dopamine is even released when we anticipate pleasurable activities such as eating and sex.
Due to social distancing measures during the COVID-19 pandemic, we should be vigilant about the possible effects of a lack of physical touch, on mental health.
It is not ethical to experimentally deprive people of touch. Several studies have explored the impacts of naturally occurring reduced physical touch.
For example, living in institutional care and receiving reduced positive touch from caregivers is associated with cognitiveanddevelopmental delays in children. These delays can persist for many years after adoption.
Less physical touch has also been linked with a higher likelihood of aggressive behaviour. One study observed preschool children in playgrounds with their parents and peers, in both the US and France, and found that parents from the US touched their children less than French parents. It also found the children from the US displayed more aggressive behaviour towards their parents and peers, compared to preschoolers in France.
Another study observed adolescents from the US and France interacting with their peers. The American kids showed more aggressive verbal and physical behaviour than French adolescents, who engaged in more physical touch, although there may also be other factors that contribute to different levels of aggression in young people from different cultures.
Maintain touch where we can
We can maintain touch with the people we live with even if we are not getting our usual level of physical contact elsewhere. Making time for a hug with family members can even help with promoting positive mood during conflict. Hugging is associated with smaller decreases in positive emotions and can lessen the impact of negative emotions in times of conflict.
In children, positive touch is correlated with more self-control, happiness, and pro-social skills, which are behaviours intended to benefit others. People who received more affection in childhood behave more pro-socially in adulthood and also have more secure attachments, meaning they display more positive views of themselves, others, and relationships.
This can feel like we have little control, but there are several evidence-based protective measures we can take in the interim to ensure we are as healthy as possible to fight off infection and prevent mental health problems that escalate with uncertainty and stress.
There is recent evidence that some younger people suffer strokes after contracting the virus, but the majority of people who end up hospitalised, in intensive care or dying from COVID-19 have an underlying medical condition. One study showed 89% of those hospitalised in the US had at least one.
These underlying medical conditions include high blood pressure, high blood sugar (especially type 2 diabetes), excessive weight and lung conditions. An analysis of data from the UK National Health Service shows that of the first 2,204 COVID-19 patients admitted to intensive care units, 72.7% were either overweight or obese.
All of these health issues have been associated with our lifestyle including poor diet, lack of exercise, smoking, excessive alcohol and high stress.
It’s obvious we have created a society where being active, eating healthily, drinking less and keeping our stress under control is difficult. Perhaps it’s time to push back. This may be important for major conditions like heart disease and diabetes as well as the added threat we face from emerging infectious diseases.
One study shows only 12% of Americans are in optimal metabolic health, which means their blood pressure, blood glucose, weight and cholesterol are within a healthy range. This rate is likely similar in many Western countries.
There is now a body of evidence linking our unhealthy lifestyle with viral, especially respiratory diseases. High blood sugar reduces and impairs immune function. Excessive body fat is known to disrupt immune regulation and lead to chronic inflammation. Insulin resistance and pre-diabetes can delay and weaken the immune response to respiratory viruses.
If we are going to restrict and change our lifestyles for 12 to 18 months while we wait for a vaccine, and if we want to protect ourselves better now and in the future, we could address these lifestyle factors. They not only affect our recovery from viruses and respiratory infections, but are also the biggest cost to the quality of life in most countries.
Optimising the health of the nation must be at the forefront. And this is long overdue. There has been a substantial under-investment by most developed countries in preventive medicine to reduce chronic diseases and improve both longevity and quality of life through healthy lifestyles.
Healthy organisms are naturally resistant to infections. This is true in plants, animals and people. Maintaining optimal health is our best defences against a pandemic until a vaccine is available.
We identify three modifiable risk factors:
Research shows better nourished people are less likely to develop both mental and physical problems. Certain nutrients, such as vitamins C and D and zinc have been identified as essential for improving immunity across the lifespan. A better diet is associated with a lower chance of developing mental health problems in both children and adults. Low levels of specific nutrients, such as vitamin D, have been recognised as risk factors for COVID-19. These nutrients are easy (and cheap) to replenish.
What does it mean to be better nourished? Eating real whole foods – fruits and vegetables, nuts, legumes, fish and healthy fats and reducing the intake of ultra-processed foods.
Being physically fit adds years to your life – and quality of life. High cardiorespiratory (lung and heart) fitness is also associated with less respiratory illness, and better survival from such illnesses.
How do you get fit? Set aside time and prioritise walking at a minimum, and more vigorous activity if possible, every day. Ideally, you would get outside and be with important others. The more the better, as long as you are not overdoing it for your individual fitness level.
Stress impairs our immunity. It disrupts the regulation of the cortisol response which can suppress immune function. Chronic stress can decrease the body’s lymphocytes (white blood cells that help fight off infection). The lower your lymphocyte count, the more at risk you are of catching a virus.
How do we lower stress? Meditation, yoga, mindfulness, cognitive-behaviour therapy, optimising sleep and eating well can all help in mitigating the negative impact of stress on our lives. Taking additional nutrients, such as the B vitamins, and the full breadth of minerals like magnesium, iron and zinc, during times of stress has a positive impact on overall stress levels.
Modifying lifestyle factors won’t eliminate COVID-19 but it can reduce the risk of death and help people to recover. And these factors can be in our control if we and our governments take the initiative.
Vitamin A maintains the structure of the cells in the skin, respiratory tract and gut. This forms a barrier and is your body’s first line of defence. If fighting infection was like a football game, vitamin A would be your forward line.
We also need vitamin A to help make antibodies which neutralise the pathogens that cause infection. This is like assigning more of your team to target an opposition player who has the ball, to prevent them scoring.
Vitamin A is found in oily fish, egg yolks, cheese, tofu, nuts, seeds, whole grains and legumes.
Further, vegetables contain beta-carotene, which your body can convert into vitamin A. Beta-carotene is found in leafy green vegetables and yellow and orange vegetables like pumpkin and carrots.
2. B vitamins
B vitamins, particularly B6, B9 and B12, contribute to your body’s first response once it has recognised a pathogen.
They do this by influencing the production and activity of “natural killer” cells. Natural killer cells work by causing infected cells to “implode”, a process called apoptosis.
At a football match, this role would be like security guards intercepting wayward spectators trying to run onto the field and disrupt play.
B6 is found in cereals, legumes, green leafy vegetables, fruit, nuts, fish, chicken and meat.
B9 (folate) is abundant in green leafy vegetables, legumes, nuts and seeds and is added to commercial bread-making flour.
B12 (cyanocobalamin) is found in animal products, including eggs, meat and dairy, and also in fortified soy milk (check the nutrition information panel).
3. Vitamins C and E
When your body is fighting an infection, it experiences what’s called oxidative stress. Oxidative stress leads to the production of free radicals which can pierce cell walls, causing the contents to leak into tissues and exacerbating inflammation.
Pregnant women, some people with chronic health conditions, and people with conditions that mean they can’t eat properly or are on very restrictive diets, may need specific supplements. Talk to your doctor, Accredited Practising Dietitian or pharmacist.
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.
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.
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.
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”.
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).
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.
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.
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.
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.
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.
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.
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.
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).
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.