Immune Cells as Villains: Misdirected Immune Attack During Autoimmune Diseases


For the body to operate at equilibrium, the cells in the immune system must play a crucial role in protecting the body against infections or diseases. However, in some cases, the same cells expected to play the protective role become “villainous.” The T cells and antibodies start attacking the same cells and tissues they are expected to protect from infections and diseases. They create a state of autoimmunity, a misdirected attack on the body’s cells and tissues. When this occurs, experts claim that the person has an autoimmune disease. Various situations arise that result in the immune system becoming a villain instead of a hero. Firstly, a person can have weak immunity or primary immune deficiency from infancy. Secondly, one can acquire immune deficiency by developing a disease or infection that affects the immune system. Thirdly, allergic reactions can increase the activity of the immune system. Finally, the body’s immune system can turn against the healthy body in the event of an autoimmune disease. Although the immune system cells are expected to fight against infections and diseases, the protective cells can become villains when a person’s autoimmune system fails to function optimally. 

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Autoimmune Diseases

Autoimmune diseases happen when the body’s natural defense system (the immune system) begins to attack healthy tissues. However, situations occur in which particular adaptive immune responses are targeted toward self-antigens. Typically, the adaptive immune response appears to fight against and eliminate an antigen from the body. For instance, cytotoxic T cells destroy virus-infected cells while antibody and antigen’s immune complexes occur to clear soluble antigens. Nonetheless, in some cases, an adaptive immune response emerges to fight against self-antigens, making it hard for the immune effector mechanisms to eliminate antigens effectively, causing a sustained reaction (Mackay & Rose, 2014). The situation leads to chronic inflammatory injury to tissues caused by the immunity’s effector pathways. The tissue damage mechanism, in this case, is the same as the one that occurs in protective immunity. Individuals can develop defects in the immune system, making it incapable of playing its defensive role and even attacking the same systems it is expected to protect. 

Autoimmune disease is an abnormality that can even be fatal. Experts have used different theories to explain the reason for the occurrence of this abnormality. The human body perceives a danger from an infection, such as a virus or bacteria, causing the immune system to respond by attacking the disease. The process is referred to as an immune response. In some cases, healthy cells and tissues are affected by the immune response, leading to autoimmune disease (Kumar et al., 2019). Some scientists are convinced that the process results from rheumatoid arthritis, an autoimmune disease. The condition is known to attack joints and commonly occurs following strep throat. Other autoimmune conditions emerge as the body responds to cells, such as cancerous cells. Another potential condition is Orbai points to scleroderma, which thickens the skin and connective tissues (Latorre et al., 2018). In such conditions, the immune system gets to an inflammatory response after fighting cancerous cells. 

Environmental Factors

While some people could be born with genetic defects increasing the susceptibility to autoimmune disease, some environmental conditions may trigger autoimmune attacks on the body. Antigen-specific T cells’ activation initiates the adaptive immune response. According to Mackay and Rose (2014), the activation of autoimmunity occurs in the same manner as the antigen-specific T cells’ activation. Family studies show that people have an underlying genetic susceptibility to autoimmune disease and the body’s attack against itself, particularly in twins. Researchers compare monozygotic and dizygotic twins in terms of the proportion of susceptibility to certain conditions, such as autoimmune disease. Diseases that are highly prevalent in all twins reveal common genetic and environmental causes. The explanation is the typical environmental conditions in which all twins grow up. However, in situations where the prevalence rate is limited to monozygotic, genetic factors play a more significant role than environmental factors in the disease occurrence. 

Studies have shown the connection between environmental factors and the development of autoimmune conditions, such as rheumatoid arthritis, type I IDDM, multiple sclerosis, and SLE. In most cases, about 20% of monozygotic twins reveal disease concordance. The percentage differs from less than 5% shown in dizygotic twins (Janeway Jr et al., 2001). The results indicate the possibility of inheritability of the conditions from parents. Nonetheless, regardless of the genetic susceptibility of the autoimmune disease, common environmental factors have been implicated in developing the state in which the body turns against itself. Twin and family studies have revealed the importance of genetic and environmental factors in autoimmune diseases attacking healthy cells and tissues. Hence, to some extent, autoimmunity is evident in everyone but does not exist in a harmful manner. However, cases occur when autoimmunity develops to a pathogenic state involving the entire immune system: “antigens, antigen-presenting cells, T and B lymphocytes, messenger molecules, cytokines, chemokines and their receptors, and signaling and co-stimulatory molecules” (Brower, 2004). In such cases, some external influences could develop autoimmune diseases in already vulnerable individuals. 

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The most challenging aspect of the autoimmune disorder is identifying the early factors that trigger autoimmunity or immune dysregulation. Current evidence indicates that environmental agents (such as “solvents, crystalline silica, mercury, pesticides, pristine, and cigarette smoking”) are responsible for up to 70% of all autoimmune diseases (Vojdani, 2014; Khan & Wang, 2018, p. 22). The gut microbiome has also been implicated in the development of autoimmunity. Notably, dysbiosis of the gut, oral, and skin microbiome has been revealed to cause the conditions in vulnerable people (Dehner et al., 2019). The microbiome can change, leading to autoimmunity by altering microbial compositions. The situation can lead to inflammation and low immunity. Multiple immune diseases can even result from dysbiosis because it affects the gut microbiome’s ability to achieve nutrient absorption and mucosal immune system regulation (Khan & Wang, 2020). Such changes triggered by environmental factors can cause autoimmune disease. 

Differences in Prevalence

Another source of evidence to indicate the role of environmental factors in developing an autoimmune disease is the higher prevalence in some countries than others. The rate of autoimmune disease has been revealed to be higher in countries with developed economies, indicating the potential implications of environmental factors in developing the condition. The US National Institutes of Health (NIH) reveals an estimated 80 autoimmune diseases, affecting “14–22 million Americans, or 5%–8% of the population” (Brower, 2004, p. 758). Unfortunately, the rate of conditions in the country is increasing. Women are shown to have a higher rate of the infection than men (“a female to male ratio of 50:1 in Hashimoto’s syndrome (hypothyroiditis), 9:1 in lupus, primary biliary cirrhosis and antiphospholipid syndrome, 7:1 in Graves’ disease, 4:1 in RA and 2:1 in multiple sclerosis (MS) and myasthenia gravis” (Brower, 2004, p. 758). The higher rate of the condition in women shows that sex hormones could play a key role in developing and progressing this condition. Another condition trend is ethnic disparities, with “lupus being three times as common in African Americans and Latinos/Hispanics, whereas MS and type 1 diabetes are seen more frequently in Caucasians” (Brower, 2004, p. 758). The differences in prevalence reveal a genetic susceptibility worsened by environmental factors. 

The primary role of sex hormones in the development of autoimmune disease is quite evident. The hormones are important in modulating T-cell receptor signaling, activating “cytokine genes and lymphocyte homing” (Brower, 2004). An Albert Einstein College of Medicine-based study by Betty Diamond revealed that estrogen potentially predisposes women to SLE since they reduce B-cell tolerance and dampens apoptotic processes. Another research at the Baylor College of Dentistry revealed that low estrogen levels cause a reaction chain of inflammations (Brower, 2004). The study and others revealed the role of estrogen receptors in mediating various autoimmune diseases. Furthermore, researchers have established that autoimmune conditions such as lupus and RA have common susceptibility genes. However, their prevalence rates differ from one region to another, indicating a potential role of environmental factors. 

Apart from sex hormones, infectious diseases are another potential underlying cause of the high prevalence of an autoimmune diseases. The pathogenesis of autoimmune diseases can be activated in the effort of the body to wade off infections. Cells in the immune system that fights infections can cross-react with normal tissues. Some conditions, such as COVID-19 infections, have some implications for the development of autoimmune diseases. Experts continually understand the contribution of the immune system to the defenses against the new strain of coronavirus. Autoantibodies (immune system proteins) that attack healthy tissues could be implicated in the progression of COVID-19. Those present before the infection could be responsible for 20% or more severe or fatal COVID-19 cases (“Autoimmune response found in many with COVID-19,” 2021). However, research remains inconclusive in establishing whether SARS-CoV-2 could be responsible for the production of autoantibodies. According to Michael Oldstone, head of the Viral Immunobiology Laboratory at the Scripps Research Institute, “in molecular mimicry, a small number of self-reactive T-cells are expanded with cross-reactive epitopes to produce a quantity of T-cells sufficient to create disease” (Brower, 2004, p. 759). In addition, the author confirms that “The initial insult is often an infection, which affects a target tissue, such as the brain or pancreas, but does not cause disease. The infection may be cleared, but when the insult is repeated, self-reactive cells are expanded from a few autoreactive cells” (Brower, 2004, p. 759). For instance, there is a potential connection between the lymphocytic choriomeningitis virus and type 1 diabetes.


Overall, the body’s immune system is vital in protecting the body against pathogens and infections. The immune response mode is activated when the system senses invasions to fight and eliminate infections or diseases. However, a condition may occur where the immune system attacks itself and other healthy cells and tissues instead of focusing on infections. The situation arises if the immune system suffers from an autoimmune condition that distracts normal functioning. Understanding the genetic and environmental factors that cause the state is essential in addressing autoimmune disease’s early onset and progression. 



Autoimmune response found in many with COVID-19 (2021). Retrieved from,them%20before%20they%20got%20sick.

Dehner, C., Fine, R., & Kriegel, M. A. (2019). The Microbiome in Systemic Autoimmune Disease–Mechanistic Insights from Recent Studies. Current Opinion in Rheumatology31(2), 201.

Janeway Jr, C. A., Travers, P., Walport, M., & Shlomchik, M. J. (2001). Autoimmune responses are directed against self antigens. In Immunobiology: The Immune System in Health and Disease. 5th edition. Garland Science.

Khan, M. F., & Wang, G. (2018). Environmental agents, oxidative stress, and autoimmunity. Current opinion in Toxicology7, 22-27.

Khan, M. F., & Wang, H. (2020). Environmental exposures and autoimmune diseases: Contribution of gut microbiome. Frontiers in Immunology10, 3094.

Kumar, P., Saini, S., Khan, S., Lele, S. S., & Prabhakar, B. S. (2019). Restoring self-tolerance in autoimmune diseases by enhancing regulatory T-cells. Cellular Immunology339, 41-49.

Latorre, D., Kallweit, U., Armentani, E., Foglierini, M., Mele, F., Cassotta, A., … & Sallusto, F. (2018). T cells in patients with narcolepsy target self-antigens of hypocretin neurons. Nature562(7725), 63-68.

Mackay, I. R., & Rose, N. R. (2014). The autoimmune diseases. Elsevier Inc..

Vojdani, A. (2014). A potential link between environmental triggers and autoimmunity. Autoimmune diseases2014.

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