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. Author manuscript; available in PMC: 2014 Sep 25.
Published in final edited form as: Nat Immunol. 2010 Nov;11(11):973. doi: 10.1038/ni1110-973

IL-1 family nomenclature

Charles Dinarello 1, William Arend 2, John Sims 3, Dirk Smith 4, Hal Blumberg 5, Luke O'Neill 6, Raphaela Goldbach-Mansky 7, Theresa Pizarro 8, H Hoffman 9, Philip Bufler 10, Marcel Nold 11, Pietro Ghezzi 12, Alberto Mantovani 13, Cecilia Garlanda 14, Diana Boraschi 15, Anna Rubartelli 16, Mihai Netea 17, Jos van der Meer 18, Leo Joosten 19, Tom Mandrup-Poulsen 20, Marc Donath 21, Eli Lewis 22, Josef Pfeilschifter 23, Michael Martin 24, Michael Kracht 25, H Muehl 26, Daniela Novick 27, Miodrag Lukic 28, Bruno Conti 29, Alan Solinger 30, Peyman Kelk 31, Frank van de Veerdonk 32, Chiristopher Gabel 33
PMCID: PMC4174560  NIHMSID: NIHMS629099  PMID: 20959797

To the Editor:

Newly cloned interleukin 1 (IL-1) family members13 were originally given an IL-1 family (IL-1F) designation4, but as functions have now been elucidated for several of these5,6, we propose that each now be assigned an individual interleukin designation. IL-1F6, IL-1F8 and IL-1F9 are encoded by distinct genes but use the same receptor complex (IL-1Rrp2 and AcP), are proinflammatory and deliver nearly identical signals712. We propose these be designated IL-36α, IL-36β and IL-36γ, respectively. IL-1F5 also binds to IL-1Rrp2 but antagonizes those cytokines in a manner analogous to that used by IL-1Ra to antagonize IL-1α and IL-1β79. We propose that IL-1F5 be renamed IL-36Ra (for ‘receptor antagonist’). In the IL-1 nomenclature, IL-1Ra is used for the natural product, whereas IL-1ra is used for the recombinant product; therefore, IL-36Ra is appropriate for natural IL-1F5.

IL-1F7 produces anti-inflammatory effects by suppressing innate immune responses; it does this by decreasing the production of inflammatory cytokines induced by Toll-like receptor agonists as well as that of IL-1 and tumor necrosis factor13,14. We propose this IL-1 family member be renamed IL-37. IL-1F7 has various splice forms1,2,15,16, of which IL-1F7b is the most studied. We propose that IL-1F7a, IL-1F7b and so on be renamed IL-37a, IL-37b and so on. The one remaining IL-1 family member, for which no function has yet been demonstrated, is IL-1F10; however, as evidence of its properties remains limited, we suggest that it retain its IL-1F designation until a function is clearly identified, although it might be prudent to reserve the designation IL-38 for this eventuality.

Contributor Information

Charles Dinarello, Department of Medicine, University of Colorado Denver, Aurora, Colorado, USA..

William Arend, Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado, USA..

John Sims, Molecular Immunology, Amgen, Seattle, Washington, USA..

Dirk Smith, Amgen, Seattle, Washington, USA..

Hal Blumberg, Department of Cellular Immunology, Novo Nordisk Inflammation Research Center, Seattle, Washington, USA..

Luke O'Neill, Department of Biochemistry, Trinity College, Dublin, Ireland..

Raphaela Goldbach-Mansky, Translational Autoinflammatory Disease Section, National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA..

Theresa Pizarro, Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA..

H. Hoffman, University of California-San Diego, San Diego, California, USA.

Philip Bufler, Department of Pediatrics, Ludwig-Maximilians University, Munich, Germany..

Marcel Nold, Monash Institute of Medical Research, Monash University, Melbourne, Australia..

Pietro Ghezzi, Division of Clinical and Laboratory Investigation, Brighton & Sussex Medical School, Falmer, UK..

Alberto Mantovani, Department of Inflammation, Istituto Clinico Humanitas, Milan, Italy..

Cecilia Garlanda, Department of Inflammation, Istituto Clinico Humanitas, Milan, Italy..

Diana Boraschi, Unit of Immunobiology, Institute of Biomedical Technologies, National Research Council, Pisa, Italy..

Anna Rubartelli, National Cancer Research Institute, Genoa, Italy..

Mihai Netea, Department of Medicine, Radboud University Medical Center, Nijmegen, The Netherlands..

Jos van der Meer, Department of Medicine, Radboud University Medical Center, Nijmegen, The Netherlands..

Leo Joosten, Department of Rheumatology, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands..

Tom Mandrup-Poulsen, Steno Diabetes Center, Copenhagen, Denmark..

Marc Donath, Department of Endocrinology Diabetes & Metabolism, University Hospital Basel, Basel, Switzerland..

Eli Lewis, Ben-Gurion University of the Negev, Be'er Sheva, Israel..

Josef Pfeilschifter, University of Frankfurt, Frankfurt, Germany..

Michael Martin, Department of Biology and Chemistry, Justus-Liebig-University, Giessen, Germany..

Michael Kracht, Rudolf-Buchheim Institute of Pharmacology, Justus Liebig University, Giessen, Germany..

H. Muehl, Pharmazentrum Frankfurt, University Hospital Goethe-Universität Frankfurt, Frankfurt, Germany.

Daniela Novick, Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel..

Miodrag Lukic, Department of Microbiology & Immunology, United Arab Emirates University, Al Ain, United Arab Emirates..

Bruno Conti, Department of Molecular and Integrative Neurosciences, The Scripps Research Institute, La Jolla, California, USA..

Alan Solinger, XOMA, Berkeley, California, USA..

Peyman Kelk, Umea University, Umea, Sweden..

Frank van de Veerdonk, Radboud University Medical Center, Nijmegen, The Netherlands..

Chiristopher Gabel, Amgen, Seattle, Washington, USA..

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