Abstract
To the Editor:
Newly cloned interleukin 1 (IL-1) family members1,2,3 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 signals7,8,9,10,11,12. 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-1β7,8,9. 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.
Newly cloned interleukin 1 (IL-1) family members1,2,3 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 signals7,8,9,10,11,12. 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-1β7,8,9. 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.
Original language | English |
---|---|
Pages (from-to) | 973 |
Number of pages | 1 |
Journal | Nature Immunology |
Volume | 11 |
Issue number | 11 |
DOIs | |
State | Published - 2010 |
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology