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"Reciprocal developmental pathways for the
generation of pathogenic effector TH17 and regulatory T cells," by
Estelle Bettelli and 7 others, Nature, 441(7090): 235-8, 11 May 2006.
[Authors' affiliations: Brigham and Women's
Hospital and Harvard Medical School, Boston, MA]
Abstract: "On activation, T cells
undergo distinct developmental pathways, attaining specialized properties
and effector functions. T-helper (T-H) cells are traditionally thought to
differentiate into T(H)1 and T(H)2 cell subsets. T(H)1 cells are necessary
to clear intracellular pathogens and T(H)2 cells are important for clearing
extracellular organisms. Recently, a subset of interleukin (IL)-17-producing
T (T(H)17) cells distinct from T(H)1 or T(H)2 cells has been described and
shown to have a crucial role in the induction of autoimmune tissue injury.
In contrast, CD4(+) CD25(+) Foxp3(+) regulatory T (T-reg) cells inhibit
autoimmunity and protect against tissue injury. Transforming growth
factor-beta (TGF-beta) is a critical differentiation factor for the
generation of T-reg cells. Here we show, using mice with a reporter
introduced into the endogenous Foxp3 locus, that IL-6, an acute phase
protein induced during inflammation, completely inhibits the generation of
Foxp3(+) T-reg cells induced by TGF-beta. We also demonstrate that IL-23 is
not the differentiation factor for the generation of T(H)17 cells. Instead,
IL-6 and TGF-beta together induce the differentiation of pathogenic T(H)17
cells from naive T cells. Our data demonstrate a dichotomy in the generation
of pathogenic (T(H)17) T cells that induce autoimmunity and regulatory
(Foxp3(+)) T cells that inhibit autoimmune tissue injury."
This 2006 report from Nature was
cited 31 times in current journal articles indexed by Thomson
Scientific during May-June 2007. Matching its placement after the previous
count for March-April, the paper retains its spot as the second-most-cited
biology paper published in the last two years, aside from reviews. Prior to
the most recent bimonthly count, citations to the paper have accrued as
follows:
March-April 2007: 30 citations
January-February 2007: 23
November-December 2006: 16
September-October 2006: 18
July-August 2006: 4
May-June 2006: 1
Total citations to date: 123
SOURCE: Hot
Papers Database (Included with a subscription to the print newsletter Science
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Research Services Group. Packaged on a CD that is mailed with each Science
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Papers Database contains data on hundreds of highly cited papers published
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organization, journal, field, and more. Total citations, as well as citations
accrued during successive bimonthly periods, can be assessed and graphed. An
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