Human interleukin-12α and EBI3 are cytokines with anti-inflammatory functions.

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State: Public
Version: Final published version
License: CC BY 4.0
Serval ID
serval:BIB_67C40EE6710B
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Human interleukin-12α and EBI3 are cytokines with anti-inflammatory functions.
Journal
Science advances
Author(s)
Hildenbrand K., Bohnacker S., Menon P.R., Kerle A., Prodjinotho U.F., Hartung F., Strasser P.C., Catici DAM, Rührnößl F., Haslbeck M., Schumann K., Müller S.I., da Costa C.P., Esser-von Bieren J., Feige M.J.
ISSN
2375-2548 (Electronic)
ISSN-L
2375-2548
Publication state
Published
Issued date
27/10/2023
Peer-reviewed
Oui
Volume
9
Number
43
Pages
eadg6874
Language
english
Notes
Publication types: Journal Article
Publication Status: ppublish
Abstract
Interleukins are secreted proteins that regulate immune responses. Among these, the interleukin 12 (IL-12) family holds a central position in inflammatory and infectious diseases. Each family member consists of an α and a β subunit that together form a composite cytokine. Within the IL-12 family, IL-35 remains particularly ill-characterized on a molecular level despite its key role in autoimmune diseases and cancer. Here we show that both IL-35 subunits, IL-12α and EBI3, mutually promote their secretion from cells but are not necessarily secreted as a heterodimer. Our data demonstrate that IL-12α and EBI3 are stable proteins in isolation that act as anti-inflammatory molecules. Both reduce secretion of proinflammatory cytokines and induce the development of regulatory T cells. Together, our study reveals IL-12α and EBI3, the subunits of IL-35, to be functionally active anti-inflammatory immune molecules on their own. This extends our understanding of the human cytokine repertoire as a basis for immunotherapeutic approaches.
Keywords
Humans, Cytokines/metabolism, Interleukin-12/metabolism, Interleukins/metabolism, Minor Histocompatibility Antigens/metabolism, T-Lymphocytes, Regulatory
Pubmed
Open Access
Yes
Create date
26/10/2023 13:59
Last modification date
08/08/2024 6:26
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