Fig 2: Combination of primary NK cells and doxorubicin increases MCF7 cell death. (A) Primary NK cells from two healthy donors were expanded and characterized for the expression of CD45, CD56, CD3 and CD16 using flow cytometric analysis. (B) The ability of primary NK cells to kill the MCF7 cells in the presence or absence of doxorubicin. Data are presented as the mean ± SEM. NK, natural killer; ns, not significant.

Fig 3: TLR2 Deficiency Reduces Oxidative Stress-Induced Iba1 Positive Mononuclear Cell Infiltration(A and B) ARPE-19 cells were treated with 10% NHS, CEP-HSA, or NHS plus CEP-HSA and (A) LDH activity.(B) MCP-1 was assayed.(C) MCP-1 secretion from ARPE-19 cells untreated or treated with anti-TLR2 0.1 mg for 1 h prior to 10% NHS, CEP, or both for 24 h.(D–G) WT and TLR2–/– mice were injected IV, with 50 mg/kg of NaIO3 (n > 5). Retinal cryosections (D and F) were stained for IBA1 (green) and DAPI (blue) at 72 h (white arrows indicate iba1+cells subjacent to the RPE). Quantification of Iba1+ cells per 203 frame in the ONL (E) and photoreceptor OS (G), mean ± SEM; p value determined by nonparametric t test, minimum of eight frames counted/mouse (n = 10).(H) THP-1 monocyte migration (after 120 min) from top chamber (8-µm pore transwells), toward fresh complete media, or conditioned media from RPE cells that were untreated, treated with CEP for 24 h, or treated with CEP + NHS, mean ± SEM for 4–5 counts; *p < 0.05.(I) MCP_1 secreted from ARPE-19 cells treated with CEP-HSA or CEP-HSA in the presence of NHS for 24 h.(J) CD86 MFI in CD45+CD66b-CD14+CD16+ monocytes treated with MCP-1 for 24 h. Experiments were carried out in triplicate and data are mean ± SE for three separate experiments. The p value was determined by nonparametric t test.(K) Polarized ARPE-19 cells treated with NHS, CEP, or both NHS and CEP were assayed for secretion of MCP-1 by ELISA in both apical and basolateral supernatants. In all images, scale bars represent 20 µm.

Fig 4: Characterization of purified ES-MSCs derived from GDF6-treated H1 hESCs. Proportions of CD73+CD146+CD271+CD45- H1-MSC-V (a) and H1-MSC-G (b) were compared by FACS. c ALP staining and quantitative ALP activity assay in H1-MSC-V and H1-MSC-G cells after 14 days of OI. d ARS staining and quantification in H1-MSC-V and H1-MSC-G cells after 14 days of OI. e Alcian blue staining and quantification in H1-MSC-V and H1-MSC-G cells after 21 days of CI. f Oil Red O staining and quantification after 21 days of adipogenic induction (AI) in H1-MSC-V and H1-MSC-G cells. Bar indicates 40 µm. qRT-PCR gene expression analysis of osteogenic (ALPL, RUNX2, IBSP, OCN) (g), chondrogenic (SOX9 and COL2a1) (h), and adipogenic markers (PPAR? and LPL) (i) after lineage-specific differentiation in H1-MSC-V and H1-MSC-G cells. j, k In vivo bone formation of H1-MSC-V and H1-MSC-G cells in immunocompromised mice. Representative H&E staining of transplants (j) and quantitative analysis of mineralized tissue versus total area (k). n = 5. Bar indicates 40 µm. All in vitro experiments were performed three times independently. *P < 0.05, **P < 0.01, ***P < 0.001. For c–f and k, Student’s t test; for g–i, two-way ANOVA with Tukey’s post hoc test

Fig 5: mRNA and protein expression of key functional molecules of ILC2s. (A–C) ILC2s were marked as CD45+Lin-CD127+CRTH2+ and sorted via FACS. (A) A heatmap showing representative results of mRNA expression of the key functional molecules of ILC2s obtained from HD-PB, LU-PB, and LU-CA samples. (B, C) The relative mRNA expressions of IL4 (B) and IL13 (C) in ILC2s from HD-PB, LU-PB, and LU-CA samples (for each group, n=18). (D–G) Protein expression of IL-4 (D, E) and IL-13 (F, G) in ILC2s from HD-PB, LU-PB, and LU-CA samples assessed via flow cytometry (for each group, n=20). HD-PB: PBMCs from healthy donors, LU-PB: PBMCs from NSCLC patients, and LU-CA: tumor single cell suspension from NSCLC patients. NS, not significant; *P<0.05, ***P<0.001, ****P<0.0001. P values were calculated by one-way ANOVA and post hoc comparisons were performed via Tukey’s test.