Orphans against autoimmunity.
In this issue of Immunity, Hermann-Kleiter et al. (2008) identify a nuclear orphan receptor, NR2F6, as a negative regulator of the T helper 17 cell subset and report that NR2F6-deficient mice develop late-onset autoimmune disease.
Bandukwala
Hozefa
H
Department of Pathology, Harvard Medical School and Immune Disease Institute, 200 Longwood Avenue, Boston, MA 02115, USA.
Sundrud
Mark S
MS
Rao
Anjana
A
D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology* / Q000378:metabolism; D015551:Autoimmunity; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology* / Q000378:metabolism; D051836:COUP Transcription Factors; D004268:DNA-Binding Proteins / Q000378:metabolism*; D020381:Interleukin-17 / Q000096:biosynthesis / Q000276:immunology; D007376:Interleukin-2 / Q000096:biosynthesis / Q000276:immunology; D008213:Lymphocyte Activation; D051379:Mice; D018345:Mice, Knockout; D010766:Phosphorylation; D011493:Protein Kinase C / Q000378:metabolism*; D018160:Receptors, Cytoplasmic and Nuclear / Q000378:metabolism*; D012097:Repressor Proteins
D051836:COUP Transcription Factors; D004268:DNA-Binding Proteins; D020381:Interleukin-17; D007376:Interleukin-2; C484221:Nr2f6 protein, mouse; D018160:Receptors, Cytoplasmic and Nuclear; D012097:Repressor Proteins; D011493:Protein Kinase C