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Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
We have reported a predominant Th2 immune response in steroid-dependent nephrotic syndrome (SDNS). This study aimed to study ILC2s contribution to the Th2-biased phenotype in idiopathic nephrotic syndrome (INS) patients in relapse as well as recapitulate INS through adoptive cell transfer of patient-specific ILC2s in immunocompromised mice.
A total of 14 patients with childhood-onset INS (relapse and remission paired samples) and 7 age-matched healthy controls were recruited. ILC2s were isolated through removal (positive selection) of CD19, CD4, CD8, CD14 followed by ILC2s negative selection (Miltenyi). To investigate ILC2-induced proteinuria in vivo, ILC2s from SDNS patients in relapse were adoptive transferred to NOD scid-gamma (NSG) mice. For in vitro study, ILC2 cells were cultured for 72 hours with IL-33, IL-25, TSLP (10ng/ml) and IL-2 (20ng/ml) and the culture supernatants were collected for cytokine measurement. GATA3 expression levels were examined in ILC2s though incubation of PBMC with IL-33 (10ng/ml) for 72h, with or without Dexamethasone (Dex) (0.1µmol/ml). ILC subsets and GATA3 were analysed using flow cytometry, with ILC2s defined as CD45+Lin-CD127+CRTH2+. Statistical analysis was done using Mann-Whitney U tests and Wilcoxon signed-rank test for paired samples.
INS patients in relapse had higher ILC2s levels compared to controls (19.0±2.2% vs 9.6±2.3%, P=0.01) with concomitant elevated production of Th2 and Th2-related cytokines (IL-5, IL-13, IL-9, IL-10 and Eotaxin (P<0.04)). This was associated with higher GATA3 expression in ILC2s in SDNS patients compared to controls (18.13%±3.46% vs 2.50%±2.50%, P=0.02), which was not seen in SRNS patients (3.70%±3.70%, P>0.99), in keeping with Th2 polarisation in steroid-dependent disease. Following remission, ILC2s levels were significantly decreased (P=0.01, paired). Dexamethasone incubation of PBMC in relapsed SDNS patients resulted in downregulation of ILC2 GATA3 levels (mean difference 13.96%±3.21%, P=0.02, paired), but paradoxically increased ILC2 cell numbers (mean difference 5.8±1.1%, P<0.001). Mice transfused with ILC2 cells from SDNS patients in relapse (736±113 µg/6h, n=6) showed significant increase in 6-hour urine albumin excretion compared to mice transfused with ILC2 cells from healthy controls (291±76 µg/6h, n=7, P=0.02) 14 days following adoptive transfer.
ILC2s are expanded with greater Th2 cytokine production in relapse compared to healthy controls, associated with GATA3 expression in steroid-dependent disease. Adoptive transfer of patients’ ILC2 cells in mice was able to induce glomerular injury. Steroid therapy constrains ILC2 GATA3 expression and Th2 polarisation, but does not effectively decrease ILC2 cell number directly. ILC2 expansion may instead be reversed indirectly by the effects of steroids on other cell types and mediators in vivo.
