An effective immune system is successful in protecting the body against disease and infection. However, if the immune system fails, it can mistake healthy cells and tissues for a threat and attack them wrongfully. In instances where the immune system targets a healthy body, it is called an autoimmune disease. The effects of autoimmune diseases vary widely but can be debilitating for those who suffer from them.
Currently, there are more than eighty autoimmune diseases know of. Some are well known, such as type 1 diabetes, rheumatoid arthritis and lupus, whilst others are rarer and less commonly discussed. Autoimmune diseases are common, with an estimated 3,225 cases per 100,000 people. A combination of genetic and environmental factors is thought to be responsible for the effects of autoimmune disorders.
What controls an autoimmune response?
Autoimmune responses are mediated by T and B lymphocytes, which release various factors thought to be responsible for the response. These factors can lead to tissue damage.
In the case of rheumatoid arthritis, the joints are affected. B and T cells are key in the symptoms of rheumatoid arthritis. B cells release specific proteins such as pro-inflammatory cytokines, which have a role in the immune response. B cells are also responsible for activating T cells, as they can express stimulatory molecules. T cells can go on to activate macrophages and fibroblasts and stimulate them to transform into cells capable of destroying healthy tissues.
Ulcerative colitis (UC) is a fairly common chronic inflammatory disease of the colon. As an immune response involves many different factors, sometimes it can be difficult to pinpoint exactly which ones are responsible for the immune response. For example, in UC, antibodies against epithelial cells and bacteria have been detected, but it is not yet clear whether or not these are related to the disease. There is, however, a noticeable increase in immune cells that release antibodies. Some of these antibodies are against currently unknown colonic antigens. An overproduction of antibodies may be important in the pathogenesis of UC.
How can infections trigger an autoimmune disease?
In some cases, infectious agents can trigger specific autoimmune diseases through various mechanisms. It is important that all environmental, epigenetic, and genetic factors are taken into consideration when assessing an autoimmune disease.
One method in which an infection can trigger an autoimmune disease is through molecular mimicry. In this, B and T cells are activated due to an infection. However, they cannot recognise self-molecules and inappropriately trigger a response. Another method is called epitope spreading. In this instance, the response is a result of the similarities between self-epitopes and a microorganism’s epitopes. A third mechanism is called bystander activation. This involves the activation of reactive T cells and swelling as a result of an infection. In this, cells are activated inappropriately and may be autoreactive.
In cases of chronic inflammation, there can be excessive apoptosis or necrosis. There can be complications associated with cell death, such as a failure to remove the dead cells effectively. In cases of clearance deficiency, there can be a link to a second step of cell death. For example, in SLE (Systemic lupus erythematosus) when there is a clearance deficiency, there can be changes to how well the immune system recognises self-cells and how well dead material is cleared. This causes a build-up of material, which can cause an inflammatory environment.