"TGF[beta] in the context of an inflammatory cytokine milieu
supports de novo differentiation of IL-17-producing T cells," by
Marc Veldhoen, Richard J. Hocking, Christopher J. Atkins, Richard M.
Locksley, and Brigitta Stockinger, Immunity, 24(2): 179-89,
February 2006.
[Authors' affiliations: National Institute for Medical Research, Mill Hill,
London, U.K.; Howard Hughes Medical
Institute, University of California, San Francisco]
Abstract: "We describe de novo generation of
IL-17-producing T cells from naive CD4 T cells, induced in cocultures of
naive CD4 T cells and naturally occurring CD4(+) CD25(+) T cells (Treg) in
the presence of TLR3, TLR4, or TLR9 stimuli. Treg can be substituted by
TGF[beta]1, which, together with the proinflammatory cytokine IL-6,
supports the differentiation of IL-17-producing T cells, a process that is
amplified by IL-1[beta] and TNF[alpha]. We could not detect a role for
IL-23 in the differentiation of IL-17-producing T cells but confirmed its
importance for their survival and expansion. Transcription factors GATA-3
and T-bet, as well as its target Hlx, are absent in IL-17-producing T
cells, and they do not express the negative regulator for TGF[beta]
signaling, Smad7. Our data indicate that, in the presence of IL-6,
TGF[beta]1 subverts Th1 and Th2 differentiation for the generation of
IL-17-producing T cells."
This 2006 report from Immunity was cited 48 times
in current journal articles indexed by Clarivate during
January-February 2008. During that two-month period, this was the
third-most-cited biology published in the last two years (excluding
reviews). Prior to the most recent bimonthly count, citations to the paper
have accrued as follows:
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