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Cited by 439

The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.

Mutations in STAT3 and IL12RB1 impair the development of human IL-17–producing T cells

Open access
de Beaucoudrey, Ludovic, Puel, Anne, Filipe-Santos, Orchidée, Cobat, Aurélie, Ghandil, Pegah, Chrabieh, Maya, Feinberg, Jacqueline, von Bernuth, Horst, Samarina, Arina, Jannière, Lucile, Fieschi, Claire, Stéphan, Jean-Louis, Boileau, Catherine, Lyonnet, Stanislas, Jondeau, Guillaume, Cormier-Daire, Valérie, Le Merrer, Martine, Hoarau, Cyrille, Lebranchu, Yvon, Lortholary, Olivier, Chandesris, Marie-Olivia, Tron, François, Gambineri, Eleonora, Bianchi, Lucia, Rodriguez-Gallego, Carlos, Zitnik, Simona E., Vasconcelos, Julia, Guedes, Margarida, Vitor, Artur Bonito, Marodi, Laszlo, Chapel, Helen, Reid, Brenda, Roifman, Chaim, Nadal, David, Reichenbach, Janine, Caragol, Isabel, Garty, Ben-Zion, Dogu, Figen, Camcioglu, Yildiz, Gülle, Sanyie, Sanal, Ozden, Fischer, Alain, Abel, Laurent, Stockinger, Birgitta, Picard, Capucine, Casanova, Jean-Laurent·2008·The Journal of Experimental Medicine

Abstract

The cytokines controlling the development of human interleukin (IL) 17–producing T helper cells in vitro have been difficult to identify. We addressed the question of the development of human IL-17–producing T helper cells in vivo by quantifying the production and secretion of IL-17 by fresh T cells ex vivo, and by T cell blasts expanded in vitro from patients with particular genetic traits affecting transforming growth factor (TGF) β, IL-1, IL-6, or IL-23 responses. Activating mutations in TGFB1, TGFBR1, and TGFBR2 (Camurati-Engelmann disease and Marfan-like syndromes) and loss-of-function mutations in IRAK4 and MYD88 (Mendelian predisposition to pyogenic bacterial infections) had no detectable impact. In contrast, dominant-negative mutations in STAT3 (autosomal-dominant hyperimmunoglobulin E syndrome) and, to a lesser extent, null mutations in IL12B and IL12RB1 (Mendelian susceptibility to mycobacterial diseases) impaired the development of IL-17–producing T cells. These data suggest that IL-12Rβ1– and STAT-3–dependent signals play a key role in the differentiation and/or expansion of human IL-17–producing T cell populations in vivo.

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Metadata

Authors
de Beaucoudrey, L., Puel, A., Filipe-Santos, O., Cobat, A., Ghandil, P., Chrabieh, M., Feinberg, J., von Bernuth, H., Samarina, A., Jannière, L., Fieschi, C., Stéphan, J.-L., Boileau, C., Lyonnet, S., Jondeau, G., Cormier-Daire, V., Le Merrer, M., Hoarau, C., Lebranchu, Y., Lortholary, O., Chandesris, M.-O., Tron, F., Gambineri, E., Bianchi, L., Rodriguez-Gallego, C., Zitnik, S. E., Vasconcelos, J., Guedes, M., Vitor, A. B., Marodi, L., Chapel, H., Reid, B., Roifman, C., Nadal, D., Reichenbach, J., Caragol, I., Garty, B.-Z., Dogu, F., Camcioglu, Y., Gülle, S., Sanal, O., Fischer, A., Abel, L., Stockinger, B., Picard, C., & Casanova, J.-L.
Venue
The Journal of Experimental Medicine
Published
2008-06-30
Volume
205
Issue
7
Pages
1543-1550
ISSN
  • 0022-1007 (ISSN-L)
  • 1540-9538
OpenAlex
W1965206234
Cited by
439
References
9
FWCI
17.68
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Mutations in STAT3 and IL12RB1 impair the development of human IL-17–producing T cells. https://app.cochat.ai/papers/10.1084/jem.20080321
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de Beaucoudrey, L., Puel, A., Filipe-Santos, O., Cobat, A., Ghandil, P., Chrabieh, M., Feinberg, J., von Bernuth, H., Samarina, A., Jannière, L., Fieschi, C., Stéphan, J.-L., Boileau, C., Lyonnet, S., Jondeau, G., Cormier-Daire, V., Le Merrer, M., Hoarau, C., Lebranchu, Y., . . . Casanova, J.-L. (2008). Mutations in STAT3 and IL12RB1 impair the development of human IL-17–producing T cells. The Journal of Experimental Medicine. https://doi.org/10.1084/jem.20080321

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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