Cell state · L2
ILC2.activated
181 cells in the full atlas (not the displayed sample).
These are the cell-population annotations shown in the SCREATE Cell Browser.
Read trait, study and gene evidence reports for this population →
Explore this population in Cell Browser →
Marker genes
ATF3, BTG2, CD69, DUSP1, FOS, HSPA1B, JUN, JUNB, LST1, LTB, MYLIP, NFKBIA, NR4A1, TAGAP, TMIGD2, TNF, WDR74, ZFP36L1
Annotation genes
ATF3, CD69, FOS, HSPA1B, JUN, JUNB, NFKBIA, TNF, ZFP36L1
Annotation rationales
The combination of CD69 (early activation/retention), AP-1 components FOS/JUN/JUNB, and stress-adaptive brakes ATF3, NFKBIA (IκBα), and DUSP1 reflects an ILC2 that has just sensed alarmins (e.g., IL-33/TSLP/IL-25) and rapidly engaged its transcriptional ignition program. Heat-shock chaperone HSPA1B supports proteostasis under acute cytokine signaling, while TNF indicates crosstalk with dendritic cells/endothelium. Post-transcriptional dampener ZFP36L1 limits overproduction of type-2 cytokine mRNAs, preventing runaway inflammation. Together these Annotation genes—ATF3, CD69, FOS, HSPA1B, JUN, JUNB, NFKBIA, TNF, ZFP36L1—capture the classic acutely activated ILC2 phenotype poised for rapid effector release yet equipped with intrinsic negative feedback.
Functional implications
Launches swift type-2 immunity at barrier sites: bursts of IL-5/IL-13 (and auxiliary TNF) to recruit eosinophils, activate mucus production, and promote smooth-muscle tone and vascular addressins for leukocyte entry. Coordinates epithelial repair (goblet-cell hyperplasia, tuft-cell feedback) while NFKBIA/ATF3/ZFP36L1 constrain the response to avoid tissue damage, enabling quick on/off control of allergic-like and wound-healing programs.
Marker and functional descriptions are atlas annotations. Explore gene expression, trait associations and regulatory elements in the interactive browsers; see the browser guide.