Th17 plasticity and its changes associated with inflammatory bowel disease

Table 2 Transcription factors related to 17 secreting helper T development and plasticity

Transcription factor	Effect	Ref.
Fosl2	A key determinant of cellular plasticity	[30]
IRF4	Th17 differentiation via RORγt dependent and independent pathways	[115]
	Augmented in patients with IBD and correlated with enhanced production of IL-17 and IL-22 mRNA	[70]
BATF	Required for differentiation of Th17 via induction of RORγt, and bound to IL-17, IL-21 and IL-22 promoters	[116]
	BATF+ RORc- Th17 cells are found in gut tissues from UC but not CD patients.	[73]
HIF-1	A key transregulator of Th17 polarization and suppressor of Foxp3 in Treg	[33,81]
	Reciprocal regulation between HIF-1 and miR210	[81]
Jmjd3	H3K27 demethylase, important for Th1/Th17 plasticity	[101]
RORc (human)	Essential for Th17 differentiation induced by TGF-β1 and IL-6 or IL-21	[35]
RORγt (mouse)
IKZF3 (Aiolos)	Promotes Th17 differentiation via silencing of the IL-2 locus	[74]
	Aiolos+ iTreg respond to IL-1β and downregulate their suppressor functions	[75]

RORγt: Related orphan receptor γ thymus in mouse; IL: Interleukin; TGF: Transforming growth factor; CD: Crohn's disease; UC: Ulcerative colitis; HIF: Hypoxia-inducible factor; IRF4: Interferon regulatory factor 4; IBD: Inflammatory bowel diseases.