Interleukin 17–producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2005-11

AUTHORS

Laurie E Harrington, Robin D Hatton, Paul R Mangan, Henrietta Turner, Theresa L Murphy, Kenneth M Murphy, Casey T Weaver

ABSTRACT

CD4(+) T cells producing interleukin 17 (IL-17) are associated with autoimmunity, although the precise mechanisms that control their development are undefined. Here we present data that challenge the idea of a shared developmental pathway with T helper type 1 (T(H)1) or T(H)2 lineages and instead favor the idea of a distinct effector lineage we call 'T(H)-17'. The development of T(H)-17 cells from naive precursor cells was potently inhibited by interferon-gamma (IFN-gamma) and IL-4, whereas committed T(H)-17 cells were resistant to suppression by T(H)1 or T(H)2 cytokines. In the absence of IFN-gamma and IL-4, IL-23 induced naive precursor cells to differentiate into T(H)-17 cells independently of the transcription factors STAT1, T-bet, STAT4 and STAT6. These findings provide a basis for understanding how inhibition of IFN-gamma signaling enhances development of pathogenic T(H)-17 effector cells that can exacerbate autoimmunity. More... »

PAGES

1123-1132

Journal

TITLE

Nature Immunology

ISSUE

11

VOLUME

6

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ni1254

DOI

http://dx.doi.org/10.1038/ni1254

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1051485127

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/16200070


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