The immune system’s primary role is to protect the body from infection. It achieves this by recognising cells that do not belong to the body and setting off a series of physiological events that lead to the non-self cell removal. The non-self cell could be a pathogen, such as a virus, bacteria or fungi. Alternatively, it could be a mutated cell, such as a cancer cell. It is this ability to recognise non-self cells that is fundamental to the function of the immune system. When this recognition is lost, the ability of the immune system to discern self-cells from non-self-cells is hindered. Autoimmune diseases are disorders whereby the immune system attacks self-cells – the body’s cells. The complex genetic and environmental nature of autoimmune diseases have made them difficult to treat; however, in recent times, breakthroughs in the understanding of autoimmune diseases have led to new innovative therapies that provide great promise. This article will focus on one of these promising therapies, interferon therapy.
Understanding autoimmune diseases
Definition and prevalence
Autoimmune diseases are disorders whereby your immune system mistakenly attacks your body’s cells.
Mechanism of autoimmune diseases
The immune response is a specialised and complex process that relies on the coordinated activity of many immune cells. The immune cells are diverse and specific to many different non-self cells (cells/organisms that do not belong to the body). This specificity is important for developing immunity, particularly against pathogens (harmful organisms). The specificity enables an adaptive immune response, whereby many specialised cells that are specific and targeted to a particular non-self cell are produced. B-cells and T-cells, two different types of immune cells, are largely responsible for autoimmunity. When errors occur in the development of these cells in the bone marrow and thymus, it produces irregular cells that do not function appropriately. Thus, the ability of these cells to differentiate between self-cells and non-self-cells is non-existent, leading to the immune system attacking self-cells.1
Common autoimmune diseases
Type I diabetes
Type I diabetes is a disorder characterised by an inability to produce insulin. Insulin is critical in stimulating cell blood glucose uptake, preventing high blood glucose levels. In type I diabetes, an autoimmune reaction destroys beta cells in the pancreas. Beta cells in the Pancreas are responsible for insulin production.2
Multiple sclerosis
Multiple sclerosis (MS) is a neurodegenerative disorder whereby the fatty insulating layer that covers the nerves, known as myelin sheath, becomes damaged through autoimmunity. Myelin sheath enables nerves to communicate more rapidly and effectively.3
Lupus
Lupus is a systemic disorder whereby the immune system attacks tissues and organisms throughout the body. It can lead to problems with joints, kidneys, and other organs.
Rheumatoid arthritis
Rheumatoid arthritis is an autoimmune disorder which affects the lining of joints. The inflammation can also lead to complications in other organs and tissues.4
Interferon: the body's natural defence
What is an interferon?
Interferons (IFNs) are signalling proteins cells release in response to infection. Upon infection, IFNs are released and act on neighbouring cells to warn them so they can prepare their defences against infection. They can also recruit other immune cells to the site of infection.
Types of interferons
There are three main types of IFNs - alpha, beta and gamma. These three IFNs can then be subdivided into two classes: type I and type II; type I interferons include alpha and beta, and type II includes gamma.
Type I IFNs can be released in any cell upon infection by a virus. Their primary role is to induce viral resistance in cells.
Two specific immune cells primarily release Type II IFNs: natural killer (NK) cells and T lymphocytes. They are responsible for signalling to the immune system to induce a response to infection.5
The role of interferon in autoimmune diseases
Research findings
Mounting research has suggested the involvement of IFNs (particularly type I) in the development of autoimmune diseases such as Lupus, Sjögren syndrome, inflammatory myotis and rheumatoid arthritis.6
Type I IFNs contribute to the development of lupus primarily through genetics and IFN therapy. The disruption of the type I IFN pathway can lead to autoimmune disease. Normally, type I IFNs are activated when in the presence of viral genetic material (DNA and RNA) and act on immune cells to stimulate the activation of IFN genes, which activate antiviral immune responses in the body. In autoimmune diseases such as lupus, the IFN pathway becomes dysregulated, and variants of interferon-related genes perform abnormal functions, leading to autoimmunity's characteristic immune tolerance.7,8,9
Applications of interferon therapy in autoimmune diseases
Current uses and treatments
The regulatory effects of IFNs on the immune system have made them a target for therapy. Primarily used as an anti-viral, they have more recently been used in treatment for autoimmunity. As autoimmune diseases commonly result in inflammation, IFNs can help target this and have thus been used in treating MS.
Efficacy and limitations
Most research assessing the efficacy of IFN therapy as a treatment for autoimmune disease has looked at MS. Results suggest that IFN therapy is an effective treatment that can help prevent MS relapse and disease progression. One study involving 1512 patients found that those treated with interferon therapy had significantly reduced relapses compared to placebo. Research on its role and efficacy in rheumatoid disorders is only in its early stages and has not yet reached clinical testing. The drawback of this therapy is that it can exacerbate the symptoms of certain diseases and cause unwanted side effects, such as flu-like symptoms.8,9
Risks and side effects of interferon therapy
Before taking any medication, it is important to consult with your GP to ensure that you can take the medication safely.
Common side effects
Less common side effects
Patient management and care
Patient cases vary significantly and, therefore, determine the management plan. Medical history, age and gender are just a few of the considerations when addressing a patient's needs. This ensures that the treatment is carefully tailored to the individual's needs. It is also important to consider potential interactions with other medications.
Summary
Autoimmune diseases are disorders whereby the immune system mistakenly attacks the body’s cells. The inability of the immune system to differentiate between self and non-self cells is often a result of genetics and environmental factors leading to abnormal immune cell development. Many treatments have been developed to help tackle the complex nature of autoimmunity; one of these treatments is interferon therapy. Recent research has shed light on the importance of interferons in regulating immune processes. Genetic variants of interferons can lead to an overstimulated immune response, eventually resulting in immune tolerance, a hallmark of autoimmunity. A desirable effect of interferons is their ability to act as an anti-inflammatory, which has proven to be effective in treating MS. However, doubts about their safety and side effects in certain individuals have raised concerns, and therefore, alternative treatments are being considered.
FAQs
Can autoimmune diseases be cured?
There is currently no cure for autoimmune diseases; however, there are treatments that can help manage symptoms.
Is autoimmune disease serious?
Systemic autoimmune diseases such as lupus and multiple sclerosis can lead to complications and are considered serious. However, with the correct treatment, many people can continue to engage in their daily activities.
What is the hardest autoimmune disease to diagnose?
Autoimmune diseases such as lupus, vasculitis, Addison’s disease and rheumatic disorders are considered the hardest to diagnose. Collaboration with primary care physicians and specialists, such as rheumatologists, immunologists and endocrinologists, can help diagnose and treat these conditions appropriately.
How long can you be on interferon therapy?
Interferon therapy tends to be more short-term. This is due to the unwanted side effects that accompany long-term use.
References
- Wang L, Wang FS, Gershwin ME. Human autoimmune diseases: a comprehensive update. Journal of internal medicine. 2015 Oct;278(4):369-95.
- Popoviciu MS, Kaka N, Sethi Y, Patel N, Chopra H, Cavalu S. Type 1 diabetes mellitus and autoimmune diseases: a critical review of the association and the application of personalized medicine. Journal of Personalized Medicine. 2023 Feb 26;13(3):422.
- Barkhane Z, Elmadi J, Kumar LS, Pugalenthi LS, Ahmad M, Reddy S. Multiple sclerosis and autoimmunity: a veiled relationship. Cureus. 2022 Apr 19;14(4).
- Weyand CM, Goronzy JJ. The immunology of rheumatoid arthritis. Nature immunology. 2021 Jan;22(1):10-8.
- Cao L, Zhang L, Zhang X, Liu J, Jia MA, Zhang J, Liu J, Wang F. Types of interferons and their expression in plant systems. Journal of Interferon & Cytokine Research. 2022 Feb 1;42(2):62-71.
- Londe AC, Fernandez-Ruiz R, Julio PR, Appenzeller S, Niewold TB. Type I interferons in autoimmunity: Implications in clinical phenotypes and treatment response. The Journal of rheumatology. 2023 Sep 1;50(9):1103-13.
- Greth W, Robbie GJ, Brohawn P, Hultquist M, Yao B. Targeting the interferon pathway with sifalimumab for the treatment of systemic lupus erythematosus. Immunotherapy. 2017 Jan;9(1):57-70.
- Eloranta ML, Rönnblom L. Cause and consequences of the activated type I interferon system in SLE. Journal of molecular medicine. 2016 Oct;94:1103-10.
- Fernandez-Ruiz R, Niewold TB. Type I interferons in autoimmunity. Journal of Investigative Dermatology. 2022 Mar 1;142(3):793-803.
- Torkildsen Ø, Myhr KM, Bø L. Disease‐modifying treatments for multiple sclerosis–a review of approved medications. European journal of neurology. 2016 Jan;23:18-27.
- Silva MO. Risk of autoimmune complications associated with interferon therapy. Gastroenterology & Hepatology. 2012 Aug;8(8):540.

