The nuclear receptor REV-ERBα modulates Th17 cell-mediated autoimmune disease is a research paper published in Proceedings of the National Academy of Sciences (2019). On theSindex it has a DataRank of 2.4. It has been cited 86 times, with 75 citing works in its 1-hop citation network.
T helper 17 (Th17) cells produce interleukin-17 (IL-17) cytokines and drive inflammatory responses in autoimmune diseases such as multiple sclerosis. The differentiation of Th17 cells is dependent on the retinoic acid receptor-related orphan nuclear receptor RORγt. Here, we identify REV-ERBα (encoded by Nr1d1 ), a member of the nuclear hormone receptor family, as a transcriptional repressor that antagonizes RORγt function in Th17 cells. REV-ERBα binds to ROR response elements (RORE) in Th17 cells and inhibits the expression of RORγt-dependent genes including Il17a and Il17f . Furthermore, elevated REV-ERBα expression or treatment with a synthetic REV-ERB agonist significantly delays the onset and impedes the progression of experimental autoimmune encephalomyelitis (EAE). These results suggest that modulating REV-ERBα activity may be used to manipulate Th17 cells in autoimmune diseases.
FAIR checklist signals are shown for context only and do not affect DataRank scoring.
Base Score Contribution
0.670
From this paper's citation signal
Citation Network Contribution
1.7
From 68 citing papers with measurable signal
Ranked by citation count — the same ordering the engine uses when summing log1p(Cq) over citers.
DataRank blends this paper's own citation count with the influence of the papers that cite it. Here, roughly 28% comes from its base citations and 72% from the citation network (68 citing papers contributed measurable signal).
Citers are pulled from OpenAlex sorted by cited_by_count:descand capped per paper, so when the cap binds we keep the highest-signal references and the score is reproducible across reruns.
Click a node to highlight its connections. Use scroll to zoom. Drag to pan.