In part 1 we discussed our physical barriers to infection and our innate immune system, which provides a rapid, general, response when triggered by certain typical signals of infection or tissue damage. The adaptive immune system is the next, more sophisticated, phase of our immune response.
Adaptive immune system
Unlike innate immunity, which is not specific for any particular infectious agent, the adaptive immune response creates a system that reacts only to a particular pathogen (a pathogen is any disease-causing organism) and creates an ‘immune memory’ enabling the immune system to swing into action very quickly if the pathogen is encountered again. This is where antibodies come into play and is the basis for how vaccination works.
The creation of adaptive immunity uses fragments of protein found on the pathogen in question (or which are produced by virus-infected host cells). These protein fragments are called antigens.
I need to introduce two more kinds of immune cells at this point. They are lymphocytes, which are divided into so-called B cells (which develop in the Bone marrow) and T cells (which develop in the Thymus gland). B cells are the antibody producers.
B cells make antibodies
Antibodies and immune memory
Each B cell made by the bone marrow carries a unique structure on its surface, which binds to a single antigen. The range of possible antigens that can be recognised by the immune system is absolutely enormous: there seems to be no end to its capability in this respect. This structure is actually an antibody and when it first encounters an antigen that matches its shape, the antibody and antigen stick together which triggers that B cell to start to multiply and the new cells so created (called plasma cells) secrete enormous numbers of copies of this unique antibody. These secreted antibodies circulate in the blood and wherever they encounter the specific antigen, they can bind to it, so labelling it for destruction by other immune cells. Some of the new B cells, will become “memory cells” and they will act like a blueprint that is stored in the immune system’s memory enabling rapid production of antibodies should we ever come across this antigen again. Because of the need for the B cell that produces the specific antibody to come across the antigen, be activated and multiply many times over in order to produce enough antibody to be effective against an infection, the first time the body is exposed to a new pathogen, the levels of antibodies take quite a time: at least a week, during which time, the infection may be sufficient to cause symptoms. Subsequent exposures trigger a much faster antibody response, such that symptoms are mild to none. One reason for the faster antibody response in later infections is that the B cells change the type of antibody they are making from so-called IgM (immunoglobulin M) antibodies to IgG (immunoglobulin G) antibodies, and, depending on the type of antigen other variations in antibodies exist (e.g., IgE is a form created against parasites and in allergies).
Antibodies may attack antigens through several mechanisms.
Neutralization: antibodies prevent interaction of the antigen or pathogen with cells and consequent cellular damage and invasion.
Opsonization: antibodies attached to the pathogen act like tags labelling it for destruction by other immune cells through phagocytosis.
Complement: antibodies coat foreign particles and activate the complement system (described in part 1).
The ability for antibodies to protect us from a second infection depends on a few things.
How well the antigen fits with the B-cell’s antibody: if it is not a good fit, the antibodies produced may not be especially effective against that pathogen.
Whether there is more than one antigen that has interacted with B cells (i.e., creating more than one type of antibody).
Which part of the pathogen the antigen comes from as this may affect how well the antibody can incapacitate the pathogen.
Individual variations between people, perhaps due to age, immune system balance, previous or current immune system exposures, genetics, underlying health conditions.
These factors are, of course, also very important when developing a vaccine. Making an effective vaccine requires that the antigen chosen to create the vaccine generates a strong antibody response and creates long-lasting memory cells.
T cells have wide-ranging functions
The adaptive immune system is not all about B cells. T cells are equally important. Their role is to carry out the localised actions of the adaptive immune system (hence they are sometimes called effector cells). Whereas antibodies can work at a distance from the B cells that secreted them, T cells execute their functions locally.
T cells can be subdivided into several other types all with different functions, for example:
Some kill bacteria and virus-infected cells, parasites and cancer cells
Some assist B cells to make antibodies (and with this help, the resulting antibodies tend to be more effective)
Some enhance the activity of macrophages to kill pathogens
Some act to regulate the immune response so that it does not become over-active.
Like B cells, T-cells need to be activated by antigen, but unlike B cells, they need this antigen to be presented to them in a special way by macrophages or other antigen-presenting cells. Once activated, T cells produce a range of cytokines specific to their particular type, which trigger the next steps in the process. The exact functions executed by the T cells will depend on the kind of infection or threat that is being countered by the immune system.
Although I have divided this article to talk separately about the innate and the adaptive immune systems, both systems work in close cooperation and, importantly, the adaptive immune system relies upon the innate immune system to alert it to potential targets and shape its response to them.
Nutritional considerations
Like the innate immune system, the adaptive immune system relies on a range of nutrients to work optimally.
Effective antigen presentation requires vitamins A, D, C, E, B6 and B12; zinc, iron, copper and selenium.
To make antibodies, we need vitamins A, D, C, E, B6, B12 and folate; zinc, copper, selenium and magnesium.
Our T-cell functions depend on vitamins A, D, C, E, B6, B12 and folate; zinc, iron, copper and selenium. The regulatory T cells which prevent the immune system becoming over-active need vitamins D, E and B6. The essential fatty acids found in fish oils and similar foods inhibit over-active T cells.
Fragments of proteins from food, may also act as antigens and cause the immune system to generate antibodies to them. This can cause food allergy or, in some cases, autoimmune disease.
As there is a huge population of immune cells in the tissues of the gut (as the gut is one way that pathogens can enter the body, so there are many sentinel cells there), gut health is crucial for immune health. Thus, probiotic foods that can influence the gut bacteria have been shown to benefit the immune system.
Want to know more?
In these two articles, I have given a very broad overview of how the immune system works. Naturally, things are much (much) more complicated and there are many nuances and details that are beyond the scope of this overview. Indeed, since I first studied immunology in the 1980s, more types of immune cells, more cytokines and many more complexities have been discovered. If you would like to increase the depth of your understanding, I really recommend this great video explaining the immune system (note that this was made before the coronavirus pandemic kicked off).
In my next posts, I’ll be looking at how the immune system can malfunction: giving rise to difficulties clearing infections, autoimmune conditions such as rheumatoid arthritis, thyroiditis, type 1 diabetes and many more, and how chronic inflammation is behind many chronic diseases, particularly those associated with weight gain.