Tracking the fate of pathogenic CD4 T helper cells in vivo.

ABSTRACT: Inflammation is a beneficial host response to infection, but it also contributes to inflammatory disease if unregulated. The Th17 lineage of T helper (Th) cells can cause severe human inflammatory diseases. These cells exhibit both instability (i.e., they can cease to express their signature cytokine, IL-17A) and plasticity (i.e., they can start expressing cytokines typical of other lineages) upon in vitro re-stimulation. However technical limitations prevented the transcriptional profiling of pre- and post-conversion Th17 cells ex vivo during immune responses. Thus, it is unknown whether Th17 cell plasticity merely reflects change in expression of a few cytokines, or if Th17 cells physiologically undergo global genetic reprogramming driving their conversion from one T helper cell type t

ORGANISM(S): Mus musculus

SUBMITTER: Travers Ching 

PROVIDER: E-GEOD-68242 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress