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Oberle, N.* ; Eberhardt, N.* ; Falk, C.S. ; Krammer, P.H.* ; Suri-Payer, E.*

Rapid suppression of cytokine transcription in human CD4⁺CD25ˉ T cells by CD4⁺Foxp3⁺ regulatory T cells: Independence of IL-2 consumption, TGF-β, and various inhibitors of TCR signaling.

J. Immunol. 179, 3578-3587 (2007)
Zum Artikel PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
CD4+CD25(high) forkhead box P3+ regulatory T cells (Treg) are critical mediators of peripheral self-tolerance and immune homeostasis. Treg suppress proliferation and cytokine production of conventional T cells (Tcon). The exact mechanism of suppression, however, is still unknown. To gain a better understanding of Treg function, we investigated the kinetics of cytokine suppression in Tcon reisolated from cocultures with preactivated human Treg. Treg inhibited induction of Th1 cytokine mRNA as early as 1 h after stimulation, whereas induction/suppression of Th2 cytokines was delayed to 10-15 h. We show that immediate cytokine mRNA suppression in Tcon was neither dependent on TGF-beta/IL-10 or IL-2 consumption, nor on induction of the transcriptional-repressor forkhead box P3 or other anergy-related genes (e.g., gene related to anergy, transducer of ErbB-2, forkhead homolog-4, repressor of GATA, inducible cAMP early repressor). In contrast, lymphocyte activation gene 3, suppressor of cytokine signaling 1, and suppressor of cytokine signaling 3 mRNA were strongly up-regulated in Tcon in the presence of Treg. However, protein analysis did not confirm a role for these proteins in early suppression. Thus, the identification of a fast inhibitory mechanism in Tcon induced by Treg constitutes an important step for future efforts to unravel the entire elusive suppressive mechanism.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
ISSN (print) / ISBN 0022-1767
e-ISSN 1550-6606
Zeitschrift Journal of Immunology
Quellenangaben Band: 179, Heft: 6, Seiten: 3578-3587 Artikelnummer: , Supplement: ,
Verlag American Association of Immunologists
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Molecular Immunology (IMI)