interleukin 1 alpha
Last updated 23 Mar 2022
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The IL1A gene provides instructions for making a protein called interleukin-1 alpha. Interleukins are a group of proteins that are made primarily in immune system cells. They are involved in cell-to-cell communication and have a wide variety of functions within the immune system. Interleukin-1 alpha is described as "pro-inflammatory" because it stimulates the activity of genes involved in inflammation and immunity. This protein plays a critical role in protecting the body from foreign invaders such as bacteria and viruses. It is also involved in bone resorption, the breakdown and removal of bone tissue that is no longer needed.
Normal function
The IL1A gene provides instructions for making a protein called interleukin-1 alpha. Interleukins are a group of proteins that are made primarily in immune system cells. They are involved in cell-to-cell communication and have a wide variety of functions within the immune system. Interleukin-1 alpha is described as "pro-inflammatory" because it stimulates the activity of genes involved in inflammation and immunity. This protein plays a critical role in protecting the body from foreign invaders such as bacteria and viruses. It is also involved in bone resorption, the breakdown and removal of bone tissue that is no longer needed.
Interleukin-1 alpha is initially produced as a relatively long protein that is trapped within cells. Another protein, called calpain, cuts (cleaves) this precursor protein to create a shorter, mature version of interleukin-1 alpha. The shorter form of this protein is secreted by immune system cells to influence the functions of other cells.
Conditions referring to this gene or chromosome
Other names
hematopoietin-1
IL-1 alpha
IL-1A
IL1
IL1-ALPHA
IL1A_HUMAN
IL1F1
interleukin 1, alpha
Interleukin-1 alpha
preinterleukin 1 alpha
pro-interleukin-1-alpha
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Further reading and references
- interleukin 1 alpha; MedlinePlus, National Library of Medicine.
- Asensi V, Alvarez V, Valle E, Meana A, Fierer J, Coto E, Carton JA, Maradona JA, Paz J, Dieguez MA, de la Fuente B, Moreno A, Rubio S, Tuya MJ, Sarasua J, Llames S, Arribas JM. IL-1 alpha (-889) promoter polymorphism is a risk factor for osteomyelitis. Am J Med Genet A. 2003 Jun 1;119A(2):132-6. doi: 10.1002/ajmg.a.20137.
- Brown MA, Xu H, Li Z. Genetics and the axial spondyloarthritis spectrum. Rheumatology (Oxford). 2020 Oct 1;59(Suppl4):iv58-iv66. doi: 10.1093/rheumatology/keaa464.
- Graves DT, Cochran D. The contribution of interleukin-1 and tumor necrosis factor to periodontal tissue destruction. J Periodontol. 2003 Mar;74(3):391-401. doi: 10.1902/jop.2003.74.3.391.
- Kawaguchi Y, Tochimoto A, Hara M, Kawamoto M, Sugiura T, Saito S, Kamatani N. Contribution of single nucleotide polymorphisms of the IL1A gene to the cleavage of precursor IL-1alpha and its transcription activity. Immunogenetics. 2007 Jun;59(6):441-8. doi: 10.1007/s00251-007-0213-y. Epub 2007 Apr 18.
- Lee S, Temple S, Roberts S, Price P. Complex effects of IL1A polymorphism and calpain inhibitors on interleukin 1 alpha (IL-1 alpha) mRNA levels and secretion of IL-1 alpha protein. Tissue Antigens. 2008 Jul;72(1):67-71. doi: 10.1111/j.1399-0039.2008.01052.x. Epub 2008 May 20.
- Sims AM, Timms AE, Bruges-Armas J, Burgos-Vargas R, Chou CT, Doan T, Dowling A, Fialho RN, Gergely P, Gladman DD, Inman R, Kauppi M, Kaarela K, Laiho K, Maksymowych W, Pointon JJ, Rahman P, Reveille JD, Sorrentino R, Tuomilehto J, Vargas-Alarcon G, Wordsworth BP, Xu H, Brown MA; International Genetics of Ankylosing Spondylitis. Prospective meta-analysis of interleukin 1 gene complex polymorphisms confirms associations with ankylosing spondylitis. Ann Rheum Dis. 2008 Sep;67(9):1305-9. doi: 10.1136/ard.2007.081364. Epub 2007 Dec 6.
- Tsezou A, Poultsides L, Kostopoulou F, Zintzaras E, Satra M, Kitsiou-Tzeli S, Malizos KN. Influence of interleukin 1alpha (IL-1alpha), IL-4, and IL-6 polymorphisms on genetic susceptibility to chronic osteomyelitis. Clin Vaccine Immunol. 2008 Dec;15(12):1888-90. doi: 10.1128/CVI.00209-08. Epub 2008 Oct 29.
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