Our immune systems are bombarded every day with bacteria, viruses and other foreign bodies, which may or may not cause us harm. We all learnt about the immune system in school, but how much do you really remember? In coronavirus times, I think it is important to understand how our bodies work at trying (and most of the time succeeding) at fighting disease.
The media is flooded with covid-19 research and statistics no matter which part of the world you’re from. Experts are everywhere providing many opinions based on numerous research studies and models, but who is breaking it down? I realised my posts have been no different, I’ve reported on the virus, track and trace methods, vaccines, ventilators and plasma therapy but not gone back to basics: What is our immune system, how does it work, and where is it going wrong? Our immune system is our best line of defence from potentially harmful pathogens (e.g. bacteria, viruses, parasites etc.) which we encounter every day. It consists of a vast network of cells, organs, proteins and tissues throughout the body which are constantly on the lookout for invaders.
The biggest player in the immune system is our white blood cells (WBC). Unlike red blood cells, white blood cells have a nucleus and carry information. WBCs patrol our bodies in our blood vessels, watching for pathogens and if they find one, WBCs will multiply and send out signals to other cell types to come and help. There are two main types of WBC: (1) Phagocytes and (2) Lymphocytes and each breaks down into further smaller groups.
What role do WBCs play in an immune response? Phagocytes surround and absorb a pathogen, breaking them down for removal (I always imagined they were eating the pathogen). The four subgroups of phagocytes are: neutrophils, monocytes, macrophages, and mast cells; each of these has a different role in the removal of pathogens from the body. Lymphocytes however help the body to remember what it has encountered before, enabling us to attack the same invader more effectively if we come into contact with it again. Lymphocytes begin in the bone marrow, but differentiate into two main groups: B and T lymphocytes (or cells). B cells produce antibodies (we’ll come back to these) to alert the T cells which “destroy” cells which have been invaded by a pathogen, and subsequently inform other WBCs that help is needed.
How can WBCs tell what is “self” and “non-self”? By now we’ve all seen the image of covid-19 with its surface spike-proteins. Our cells also have proteins on their surface, albeit not quite as spikey and vast as those on viruses. From an early stage, our body learns what our surface proteins are and can therefore deduce when it encounters a foreign one. Another term you will have heard is antigen (short for antibody generator), this is any substance which can spark an immune response. B cells spot an antigen and begin to secrete antibodies, special proteins which lock on to the corresponding antigen. Antibodies themselves do not “kill” the antigen, they only mark it for “death”/removal/destruction (pick your favourite); the “killing” is left for the hungry phagocytes. T cells are further broken down into two categories: Helper T cells which are the communicators, telling other cells what to do, and Killer T cells which attack and destroy cells which have been infected. Our bodies remember antibodies we have created so we can use them again if we encounter the same pathogen in the future.
What about when the immune system goes wrong? Most of the time our immune systems are great at differentiating between our healthy cells (self) and pathogens (non-self). However, our immune system can occasionally go rogue, producing little to no response or being overactive and recognising our “self” as foreign. Instances where the immune system is overactive are usually autoimmune diseases, damaging our own tissues and decreasing the individual’s ability to fight disease, leaving them vulnerable to infections. Such conditions include rheumatoid arthritis (where antibodies attack joints, causing inflammation and swelling), lupus (affects sites throughout the body, most commonly joints, lungs, blood cells, nerves and kidneys), type I diabetes (antibodies attack and destroy insulin producing cells in the pancreas) and MS (multiple sclerosis – where the immune system attacks nerve cells leading to a host of complications. It is a degenerative disease) to name just a few. Treatments usually focus on reducing the individual’s immune system activity, thus leaving them more vulnerable to infections.
In such instances, those individuals are more at risk of more severe symptoms from covid-19 for example, as their reduced immune response may not be able to fight the virus as effectively as an individual without a suppressed immune system. To help individuals whose immune systems may be weaker or suppressed, we usually look to immunity, which is usually achieved through vaccinations. In the case of covid-19, the need for a vaccination is more prominent than ever as it is spread so easily. However, other avenues such as plasma therapy (i.e. using the antibody containing part of a blood donation) are also being explored as potential ways for patients with more severe symptoms to get faster immunity to the disease. Immunity is a different post altogether and depends on how you acquired the antibodies and defence against a pathogen. For the time being we must wait for the research, but I hope this post has helped you understand how our immune systems help us fight disease, and why we must protect those whose immune systems aren’t working properly.