The paper:
X. O. Yang et al., "STAT3 regulates cytokine-mediated generation of inflammatory helper T cells," J Biol Chem, 282:9358–63, 2007. (Cited in 118 papers)
The finding:
Chen Dong and his colleagues at the M.D. Anderson Cancer Center in Houston, Texas, modulated the expression levels of a transcription factor called STAT3 in undifferentiated helper T cells from mice spleen and lymph nodes. They showed that STAT3 is essential for the differentiation of TH17, a recently discovered helper T cell so-named because it produces the cytokine interleukin-17 (IL-17).
The application:
IL-17 has been implicated in a variety of inflammatory diseases, including multiple sclerosis, psoriasis, and rheumatoid arthritis. The recognition of STAT3's role in TH17's development "identifies a clear drug target to inhibit TH17 differentiation," says Jay Kolls, an immunologist at Louisiana State University in New Orleans.
The danger:
"The genome-wide targets of STAT3 are turning out to be immense," says John ...
