Journal: iScience

Article Title: An atom-edged magnetic nanomotor for cancer mechanotherapy

doi: 10.1016/j.isci.2026.114994

Figure Lengend Snippet: MagGO primarily induces pyroptosis as the mode of cell death (A–C) CLSM images of CTSB release of U87 (A), MDA-MB-231 (B), and A549 (C) cells after MagGO treatment under 3D MF. The applied field strength is 75 mT. The duration of magnetic field application is 30 min. Scale bars, 20 μm. (D–F) The cell viabilities of U87 (D), MDA-MB-231 (E), and A549 (F) cells treated with MagGO were assessed after pre-treatment with z-VAD-FMK (10 μM), Necrostatin-1 (10 μM), 3-Methyladenine (10 μM), Ferrostatin-1 (2 μM), and MCC950 (10 nM) for 4 h, followed by exposure to 3D MF at 5 Hz for 30 min. The applied field strength was 75 mT. The data were presented as the mean ± SD. Data were analyzed by one-way ANOVA with Tukey’s post hoc test. (G and H) Quantification of IL-1β (G) and IL-18 (H) release from U87 cells for control, MagGO, and MagGO+3D MF ( n = 3). The data were presented as the mean ± SD. Data were analyzed by one-way ANOVA with Tukey’s post-hoc test. (I and J) Western blot analysis of Casp-1 (I) and GSDMD (J) in U87 cells for control, MagGO, and MagGO+3D MF.

Article Snippet: Human IL-18 (Interleukin 18) ELISA Kit , Elabscience , Cat#E-EL-H0253.

Techniques: Control, Western Blot

Journal: Science Advances

Article Title: Identification of the niche and mobilization mechanism for tissue-protective multipotential bone marrow ILC progenitors

doi: 10.1126/sciadv.abq1551

Figure Lengend Snippet: ( A ) Frequency of ILCPs in the BM, blood, and colon of control and DSS-treated mice. ( B ) Emigration rate of BM ILCPs in control and DSS-treated mice. The distribution of CellTracker + cells was examined 48 hours after the labeling in control and DSS-treated mice. ( C ) Expression of IL18r1 on ILCPs in the BM parenchyma and sinusoids. Violin plots of scRNA-seq data are shown. ( D ) Expression of IL-18R1 on pILCPs versus sILCPs. Ab, antibody. ( E ) Effects of IL-18 treatment on the frequency of pILCPs and sILCPs in the BM. ( F ) Effects of IL-18 treatment on the frequency of ILC progenitors in the peripheral blood. Mice were treated (intraperitoneally) with IL-18 for 4 days and then euthanized 48 hours after the last injection (E and F). ( G ) Effect of IL-18 on the expression of S1PR1. ( H ) Effect of IL-18 on the chemotaxis of ILCP to S1P (+) and CXCL12 (−) gradients. The ILCPs were treated in vitro with IL-18 in the presence of cytokines (stem cell factor and IL-7 at 20 ng/ml) on OP9-DL1 cells as the feeder layer (G and H). Pooled data obtained from at least three different experiments ( n = 4 to 6) are shown. * P < 0.05.

Article Snippet: Mice were injected intraperitoneally with a neutralizing anti–IL-18 (YIGIF74-1G7, BioXcell) or isotype control on days 1 and 4 during the experiment, and mice were euthanized on day 7.

Techniques: Labeling, Expressing, Injection, Chemotaxis Assay, In Vitro

Journal: Science Advances

Article Title: Identification of the niche and mobilization mechanism for tissue-protective multipotential bone marrow ILC progenitors

doi: 10.1126/sciadv.abq1551

Figure Lengend Snippet: ( A ) Effect of IL-18 neutralization on the emigration of ILCPs in the blood and colon of wild-type (WT) C57BL/6 mice treated with DSS. BM CellTracker microinjection was performed on tibia BM cells, and mice were euthanized 48 hours later. ( B to G ) Effect of sILCPs on the intestinal inflammation and ILC activity under the suppressed ILCP mobilization condition in DSS-treated Rag1 −/− mice. Shown are gross morphology and body weight change (B), histological changes (C), histological and stool scores (D), numbers of colon ILCPs (E), numbers of colon ILC3 (F), and IL-22 production by colon ILCs (G). Pooled data obtained from at least three different experiments ( n = 4 to 8) are shown. * P < 0.05.

Article Snippet: Mice were injected intraperitoneally with a neutralizing anti–IL-18 (YIGIF74-1G7, BioXcell) or isotype control on days 1 and 4 during the experiment, and mice were euthanized on day 7.

Techniques: Neutralization, Activity Assay

Journal: Science Advances

Article Title: Identification of the niche and mobilization mechanism for tissue-protective multipotential bone marrow ILC progenitors

doi: 10.1126/sciadv.abq1551

Figure Lengend Snippet: pILCPs are developed from early lymphoid progenitors and located in the parenchyma of the BM. Many of these cells are active in cell cycling. pILCPs express CXCR4 and Itg-α4β1, which confer them the microenvironmental tropism within the BM parenchyma. pILCPs developmentally down-regulate Itg-α4β1 to weaken the interaction with parenchymal niche cells and up-regulate S1PR1 to become sILCPs, allowing them to migrate from the parenchyma to the sinusoid niche for emigration. Most sILCPs are in the resting phase of cell cycling and highly expressing IL-18R1 and ICOS. In inflammatory conditions, peripheral signals, such as IL-18, would stimulate IL-18R1 + BM ILCPs or sILCPs. This signal further induces the expression of S1PR1 to increase the chemotactic sensitivity of ILCPs to the bloodborne chemoattractant for emigration. Therefore, mobilization of BM ILCPs is controlled in the steady state and further regulated in inflammatory conditions. Mobilized ILCPs in the blood circulation have the Itg-α4β1 low S1PR1 − phenotype, and these ILCPs can migrate to various peripheral tissues to generate mature ILC1, ILC2, and non-LTi ILC3. The ILCPs, mobilized in inflammatory conditions, have the potential to regulate inflammatory responses and ameliorate tissue damages.

Article Snippet: Mice were injected intraperitoneally with a neutralizing anti–IL-18 (YIGIF74-1G7, BioXcell) or isotype control on days 1 and 4 during the experiment, and mice were euthanized on day 7.

Techniques: Expressing