All our immune cells start off life as haematopoietic stem cells, found in the bone marrow. These stem cells can renew themselves throughout our lives and may become any of the immune cells listed below. This is a very flexible path, and the cells do not commit to become a particular type of immune cell until they reach specific checkpoints. The decision at each of these checkpoints is influenced by many things: location in the body, infection, and which cells may need replacing at the time.
Neutrophils are the most abundant white blood cell in your body and the first response to an injury such as a grazed knee or a cut finger. They are the body’s rapid response force which is able to quickly congregate at the site of an infection or cut and eat up invaders. If the pathogen has been coated in antibodies (a process called opsonisation) the neutrophil will find it even more delicious!
Neutrophils are also known as granulocytes because of the granules which can be seen inside them. These granules contain highly toxic reactive oxygen species to kill engulfed pathogens. When a neutrophil ‘de-granulates’ it releases these granules (like bombs) at the site of inflammation to help kill the pathogens.
Neutrophils are the most abundant cells in pus, giving it its yellow/white appearance.
Dendritic cells are found in every part of the body, including our skin, gut and immune organs (thymus, lymph nodes, bone marrow and spleen), where our immune cells develop. Dendritic cells collect parts of pathogens from around the body and take them to the lymph nodes, where many other immune system cells can be found. They present the pathogen parts to T cells, stimulating them to multiply and attack the pathogen. This is called antigen presentation. In the image shown, the dendritic cells are seen in red.
T cells come in different forms:
Helper T cells produce chemical messages called cytokines which boost antibody production by B cells and activate macrophages. Special Helper T cells in the spleen and lymph nodes help control the responses of B cells. Here they test and help those B cells trying to make their antibodies more efficient.
Killer T cells patrol the body checking our own cells for invaders such as viruses. Viruses are hidden within our cells and so cannot be directly detected by our immune system. Killer T cells look for indicators on the surface of our cells which show when they are infected by viruses and can then directly kill those cells.
Regulatory T cells suppress other T cells. By doing this they control the immune system and help make sure that it does not respond to self-antigens. Regulatory T cells are an important self-check which prevent excessive immune reactions and reduce autoimmune disease.
The main job of B cells is to make antibodies, Y shaped proteins, which bind to antigens on the surfaces of pathogens. Your body can make many different antibodies to recognise the different pathogens you might encounter, but each individual B cell will only make antibodies specific to one antigen.
On infection, B cells that recognise a pathogen will respond with a simple stock of antibodies and start to multiply, producing more and more antibodies. Later B cells in the germinal centres (special structures that can form in your lymph nodes and spleen) can modify their antibodies and compete to produce the ‘best’ antibodies. B cells use their antibody receptors to capture an antigen and present it to helper T cells. The B cells with the best antibodies are instructed to multiply and then are sent out to attack the pathogen.
After a pathogen has been overcome, a few B cells remain in the body as memory B cells, which are long-lived and slow to multiply under normal circumstances, but can expand very rapidly when the same antigen is encountered again, e.g. if the same infection returns.
Antibodies are Y- shaped proteins, each with a different ‘variable’ region, the top of the Y shape, where antigen-recognition and binding takes place. These differences mean that our immune system has the potential to produce 10 billion different antibodies. Recombination or shuffling of genes to create variations in the binding site of the antibodies is the first step in generating this huge repertoire. See if you can assemble your antibodies in time, play our antibody game here.
The ‘constant’ region determines the mechanism used to destroy antigens. Antibodies are classified according to their constant region structure and immune function.
Macrophages ‘eat’ anything, such as bacteria and pollen and even bits of our own damaged cells. At sites of infection and inflammation (where you see ‘weeping’ and pus) these cells mop-up the debris left over from battles fought between immune system cells and pathogens. Antibodies produced by B cells can cover pathogens, making the pathogen irresistible to a macrophage. Macrophages present parts of the pathogen they have gobbled up to T cells to activate them – in a similar way to dendritic cells.
Some immune cells reside in our tissues, but others travel around your body using two main routes: the circulatory system and the lymphatic system. Both of these networks are made up of many tiny vessels allowing the cells to reach every nook and cranny of your body. The spleen and lymph nodes are meet-up points within the networks where immune cells share information they have found, and instruct each other to help in the fight against an infection. Immune cells use signalling molecules, such as cytokines, to exchange information.
Your immune system has two strategies for destroying pathogens, innate and adaptive immunity. The cells of the innate immune system respond quickly within hours of infection and are a great line of first defence. Adaptive immunity is much slower (it can take up to a week to reach full force) but is far more specific.
The key players in innate immunity are always on guard and ready for action, they include macrophages, neutrophils and dendritic cells as well as the epithelial barriers – cells on our skin, in our gut and respiratory tract which act as physical barriers for pathogens.
B cells, antibodies, helper T and Killer T cells make up the adaptive immune response. They can mount a specific immune response to a particular invader. After an attack some T cells and B cells become memory cells and act as scouts looking for the same pathogen in the future. This process is called immunological memory and allows you to mount a quicker and more effective immune response the next time you are infected with the same pathogen. Vaccination makes use of this amazing memory response. By infecting the body with a small amount, or attenuated (killed) version, of a pathogen a vaccine causes your immune system to initiate an attack without you getting sick. If, in the future, you are infected by the same pathogen the immune system is primed and ready to attack.
T cells have antigen receptors; they recognise fragments of one speciﬁc antigen, so the T cells can identify a certain invader and decide how to deal with it. This is called antigen speciﬁcity. Dendritic cells help T cells recognise pathogens by engulﬁng the pathogen and presenting parts of it to the T cells – this is called antigen presentation. As T cells grow up they go through a sort of T cell “school” in the thymus. It is here that any T cell which binds to a self-antigen gets censored so that it doesn’t start fighting against you!
Our own cells, as well as pathogens, have unique identifiers which are recognised by immune cells and antibodies – these identifiers are called antigens. A single pathogen can have hundreds of antigens and this allows many immune cells or antibodies to identify and start a counter-attack on it.
Our immune system protects us from diseases. It changes throughout our lives, getting stronger and stronger from birth to becoming an adult.
As we age, our immune system has trouble defending against attack, so we are more likely to catch infections. This happens because the thymus shrinks and produces fewer and less diverse T cells; also fewer B cells are made, reducing the range of antibodies produced.
At the Babraham Institute we’re trying to work out why the immune system changes as we get older. Once we know, vaccines for older people may be adapted so they will be more effective. Check out the ‘Babraham Institute Research’ page to learn more about immunology research at the Babraham Institute
This image shows the effect of the ageing process on the mouse thymus. As the mouse ages the thymus shrinks, and changes in its structure occur which means that fewer T cells are produced. (image from Frontiers in Bioscience 16, 2461 – 2477, June 1, 2011)
If something goes wrong with your immune system you may suffer from immune-deficiencies or autoimmune disease. Some people are born with immunodeficiency; others become immune-deficient following infections or treatment for other diseases. Immunodeficiency occurs when your immune system becomes compromised or it is not present at all; this means that the body is very vulnerable to infections. Autoimmunity is when your immune cells mistakenly recognise your body’s cells as pathogens and attack. Rheumatoid arthritis is an example of an autoimmune disease – it occurs in the joints and causes pain and impaired movement.