Transcriptome analysis of TH2 CD4(+) T cells differentiated from wild-type and NLRP3KO mice.
The Nod-like receptor NLRP3 is involved in the formation of NLRP3. Up to now, the immunological functions of NLRP3 independently of inflammasome is unclear. In this dataset containing 6 samples (TH0, TH2 cells at day 3 and day 6 in wild type or Nlrp3 deficient cells), we show that NLRP3 expression in CD4(+) T cells supports a T helper 2 (TH2) transcriptional program in a cell-intrinsic manner (raw and normalized data are accessible on Gene Expression Omnibus database under the number GSE54561, http://www.dtd.nlm.nih.gov/geo/query/acc.cgi?acc=GSE54561). Indeed, NLRP3 positively-regulated TH2 program independently of inflammasome formation. These data indicated that TH2 specific genes such as cMaf or Il4 were not induced in Nlrp3 deficient cells. These results demonstrate the capacity of NLRP3 to act as a key transcription factor in TH2 differentiation.
Inserm U866, Dijon, France.
Mélanie
M
Bruchard
Inserm U866, Dijon, France ; Centre Georges-François Leclerc, Platform of Transfer in Cancer Biology, Dijon, France.
Romain
R
Boidot
Inserm U866, Dijon, France ; Centre Georges-François Leclerc, Platform of Transfer in Cancer Biology, Dijon, France.
François
F
Ghiringhelli
Inserm U866, Dijon, France ; Centre Georges-François Leclerc, Platform of Transfer in Cancer Biology, Dijon, France.
Frédérique
F
Végran
NLRP3; Th2 differentiation; Transcriptome