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Living With an Autoimmune Disease

Find information to better understand your autoimmune disease

Scientists have spent decades exploring how the immune system normally develops and functions. This allows scientists to define what changes occur in autoimmunity. These differences form the basis for therapies to treat autoimmune diseases.

Educating yourself about your condition and the underlying mechanisms of autoimmune diseases can also help you better understand your health and make informed decisions.

How does the immune system typically work?

The immune system consists of two main branches: innate and adaptive immunity. Innate immunity is a rapid, nonspecific defense against pathogens, while adaptive immunity involves specialized cells that learn to fight specific threats. Inside the adaptive immune system are white blood cells, also known as lymphocytes, including B and T cells.

As these lymphocytes develop, each B and T cell is unique. This diversity helps the immune system recognize and fight off different viruses, bacteria, and other harmful pathogens it encounters. It’s like a locksmith creating many “keys” in advance in case bacteria enters the body, so it can be locked down.

These lymphocytes are also good at fighting bacteria by causing inflammation, a vital part of the body’s immune response that serves as a defense mechanism against harmful stimuli. T cells, for example, help control the bacteria that causes tuberculosis by releasing a substance called tumor necrosis factor alpha (TNFα). This substance signals for cell death in infected cells, helping to eliminate the bacteria and contain the spread of infection.

What causes autoimmunity?

The immune system is great at defending us from pathogens, but sometimes, the “keys” can get mixed up and attack our own cells by mistake. We call these mistaken keys “‘self-reactive” cells because they react against our own cells and tissues.

As the immune system generates newly formed T and B cells, there is a complex system of cellular interactions that occur in the bone marrow (for B cells) and in the thymus (for T cells) that tries to ensure that any cells that strongly react against your own cells and tissues get deleted before they get out into the body where they could encounter the rest of your tissues.

While it eliminates many self-reactive cells, the system isn’t perfect, and some of these self-reactive cells slip through. The self-reactive cells are actually a normal part of everyone’s immune system (even without autoimmunity) and can be very important in protecting us against multiple, closely related viruses 1, 2, 3 Though, these cells are triggered and direct their action against your own tissues, resulting in autoimmune disease. For example, in rheumatoid arthritis, self-reactive cells attack joints, as if they were harmful pathogens. This triggers the production of substances like TNFα, which normally fight bacteria but in the case of rheumatoid arthritis end up hurting our own cells.4

We’re not always sure why self-reactive cells are triggered, but it is often linked to infections that people had before their autoimmune diseases begin.5

Spotlight

Turning knowledge into treatment for rheumatoid arthritis

Rheumatoid arthritis is an example of how advancing our understanding of the immune system has led to effective treatments. Scientists have created therapies that directly block TNFα, a key player in inflammation. These therapies have proven successful in slowing or halting damage to the joints.6

By aiming at a specific target, these treatments often cause fewer side effects. Although people getting these treatments need to be cautious about certain infections like tuberculosis. Other types of immune responses, such as to the COVID-19 vaccines, do not appear to be affected by these therapies.7, 8

How are scientists combating autoimmune diseases?

Scientists are making important strides in understanding and treating autoimmune diseases. For example, after uncovering the crucial role B cells play in diseases like lupus, researchers are testing methods in ongoing clinical trials to temporarily remove B cells in people living with lupus. Early data from these trials show promise, suggesting that slowing or stopping lupus progression may be possible by eliminating B cells and their antibodies.9

Additionally, scientists have discovered that infections caused by the Epstein-Barr virus can trigger multiple sclerosis in some people.10 These infections activate self-reactive immune cells, perhaps due to the inflammatory conditions induced by the virus.11, 12 This phenomenon, known as “molecular mimicry,”13 occurs when a protein in our body looks like a protein on a pathogen’s surface.

As a result, scientists are currently working on developing vaccines and antiviral treatments to target the Epstein-Barr virus, hoping to prevent or mitigate its role in triggering autoimmune diseases like multiple sclerosis.14

While we’re still piecing together the puzzle of autoimmune diseases, scientists are working to deepen their understanding of the immune system. By examining how it operates when it’s functioning properly—and when it’s not—we’re steadily uncovering new insights to expand our options to help manage autoimmunity.

If you’re living with an autoimmune disease and want to learn more, talk to your healthcare provider to get disease-specific insights into your condition, discuss treatment options, and address any concerns you may have.

Resources
For more information to help understand your autoimmune disease, explore the following resources from the American Association of Immunologists and other trusted sources:

Sources

  1. J Exp Med. 2017 Aug 7;214(8):2283-2302. doi: 10.1084/jem.20161190. Epub 2017 Jul 11. PMID: 28698284. https://pubmed.ncbi.nlm.nih.gov/28698284/ 
  2. 2020 Dec 15;53(6):1230-1244.e5.doi: 10.1016/j.immuni.2020.10.005. https://pubmed.ncbi.nlm.nih.gov/33096040/
  3. J Exp Med (2013) 210 (2): 389–399. https://doi.org/10.1084/jem.20121970
  4. Husby G, Williams RC Jr. Synovial localization of tumor necrosis factor in patients with rheumatoid arthritis. J Autoimmun. 1988 Aug;1(4):363-71. doi: 10.1016/0896-8411(88)90006-6. PMID: 3075463. https://pubmed.ncbi.nlm.nih.gov/3075463/
  5. Getts DR, Chastain EM, Terry RL, Miller SD. Virus infection, antiviral immunity, and autoimmunity. Immunol Rev. 2013 Sep;255(1):197-209. doi: 10.1111/imr.12091. PMID: 23947356; PMCID: PMC3971377. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3971377/
  6. Lipsky, P. E., Van Der Heijde, D. M., St Clair, E. W., Fürst, D. E., Breedveld, F. C., Kalden, Smolen, J. S., Weisman, M. H., Emery, P., Feldmann, M., Harriman, G. R., & Maini, R. N. (2000). Infliximab and methotrexate in the treatment of rheumatoid arthritis. The New England Journal of Medicine, 343(22), 1594–1602. https://doi.org/10.1056/nejm200011303432202
  7. Keane, J., Gershon, S. K., Wise, R. P., Mirabile-Levens, E., Kasznica, J., Schwieterman, W. D., Siegel, J., & Braun, M. M. (2001). Tuberculosis Associated with Infliximab, a Tumor Necrosis Factor α–Neutralizing Agent. The New England Journal of Medicine, 345(15), 1098–1104. https://doi.org/10.1056/nejmoa011110
  8. Deepak, P., Kim, W., Paley, M., Yang, M., Carvidi, A., Demissie, E., El-Qunni, A. A., Haile, A., Huang, K., Kinnett, B., Liebeskind, M. J., Liu, Z., McMorrow, L., Paez, D., Pawar, N., Perantie, D. C., Schriefer, R. E., Sides, S. E., Thapa, M., Kim, A. H. (2021). Effect of immunosuppression on the immunogenicity of mRNA vaccines to SARS-COV-2. Annals of Internal Medicine, 174(11), 1572–1585. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8407518/
  9. Mackensen, A., Müller, F., Mougiakakos, D. et al. Anti-CD19 CAR T cell therapy for refractory systemic lupus erythematosus. Nat Med 28, 2124–2132 (2022). https://pubmed.ncbi.nlm.nih.gov/36109639/
  10. Kjetil Bjornevik et al. ,Longitudinal analysis reveals high prevalence of Epstein-Barr virus associated with multiple sclerosis.Science375,296-301(2022).DOI:10.1126/science.abj8222 https://pubmed.ncbi.nlm.nih.gov/35025605/
  11. J Exp Med. 2022 Jun 6;219(6):e20212553. doi: 10.1084/jem.20212553. Epub 2022 Apr 14. PMID: 35420627. https://pubmed.ncbi.nlm.nih.gov/35420627/
  12. J Exp Med. 2017 Vol. 214 No. 8 2283–2302. https://doi.org/10.1084/jem.20161190
  13. Clin Microbiol Rev. 2006 Jan;19(1):80-94. doi: 10.1128/CMR.19.1.80-94.2006. https://pubmed.ncbi.nlm.nih.gov/16418524/
  14. NIH launches clinical trial of Epstein-Barr virus vaccine. (2022, May 6). National Institutes of Health (NIH). https://www.nih.gov/news-events/news-releases/nih-launches-clinical-trial-epstein-barr-virus-vaccine
  15. Allie, N., Grivennikov, S., Keeton, R. et al. Prominent role for T cell-derived Tumour Necrosis Factor for sustained control of Mycobacterium tuberculosis infection. Sci Rep 3, 1809 (2013). https://pubmed.ncbi.nlm.nih.gov/23657146/
  16. Gardam MA, Keystone EC, Menzies R, Manners S, Skamene E, Long R, Vinh DC. Anti-tumour necrosis factor agents and tuberculosis risk: mechanisms of action and clinical management. Lancet Infect Dis. 2003 Mar;3(3):148-55. doi: 10.1016/s1473-3099(03)00545-0. PMID: 12614731. https://pubmed.ncbi.nlm.nih.gov/12614731/
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