Fig 1: The Fab fragment of serum IgG cannot induce microglial activation. Note that the expression of CD11b and NO was not significantly changed in cerebral cortical microglias (a, b) and cerebellar microglias (c, d) incubated with the Fab fragment of IgG from children with OMS and NB compared with that from NB patients and healthy control. p > 0.05, one-way ANOVA, n = 10 (health control), n = 20 (NB), and n = 10 (OMS + NB)
Fig 2: AB23A targets CD11b/CD18 and improves polarization of TAMs, thereby affecting tumor apoptosis. (A and B) IHC detected the expressions of iNOS and Arg-1. (C) ELISA was used to detect the levels of related markers in tumor tissue. (D) Tunel assay detected apoptosis. (E) Statistical analysis diagram of apoptosis rate. ***p < 0.001 vs A549; #p < 0.05, ###p < 0.001 vs A549+shRNA-NC; ΔΔΔp < 0.001 vs A549+shRNA-ITGB2.
Fig 3: ITGAM deficiency attenuates the development of experimental AAA, vascular structural injury, and the inflammatory response. A, Representative photographs of the infrarenal abdominal aortas in saline‐ or CaCl2‐treated WT and ITGAM(‐/‐) male mice. The black dotted lines indicate the edge of abdominal aortas. B, Kaplan–Meier survival curves of WT (n=15) and ITGAM(‐/‐) mice (n=15). No significant difference was found regarding the survival rate. C, Incidence of AAA formation in WT and ITGAM(‐/‐) mice in response to CaCl2. D, Maximal abdominal aortic diameter of WT (n=15) and ITGAM(‐/‐) mice (n=13) 6 weeks after being exposed to CaCl2 and the sham‐treated mice (n=15). The data represent the mean±SEM. **P<0.01, ***P<0.001. E, Representative H&E, EVG, and Masson trichrome staining of the abdominal aortic tissues from the sham‐treated, WT, and ITGAM(‐/‐) mice. Scale bar=100 μm. F and G, Quantification of elastin fragmentation and collagen deposition in the experimental groups (n=6), *P<0.05, **P<0.01, ****P<0.0001. H through K, Serum CCL2, TNF‐α, IL‐6, and IL‐1β levels in the experimental groups (n=6 for each group) detected by ELISA, *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. AAA indicates abdominal aortic aneurysm; EVG, Elastica Van Gieson; H&E, hematoxylin and eosin; ITGAM, integrin subunit alpha M; and WT, wild‐type.
Fig 4: Verification of the immunotype in mouse and patient samples by IHC staining. (a, c) Representative IHC images of CD206+ M2 macrophages (a) and FoxP3+ Tregs (c) in mouse PDAC samples (400×). (b, d) Statistics of the number of M2 macrophages (b) and Tregs (d) in a 400× field, each dot represents the mean of three random field in one sample. (e) Representative IHC images of CD3, CD11b, CD11c, CD19, CD163 and FoxP3 staining using human PDAC sample (400×, n = 8 in each group). (f) Statistics of the number of T cells, myeloid cells, DCs, B cells, M2 macrophages and Tregs in a 400× field, each dot represents the mean of three random field in one sample. n = 8 in each group. Donor pancreas: pancreas from organ donors, RPC: resectable pancreatic cancer, MPC: metastatic pancreatic cancer. For (b), (d) and (f), bar indicates mean ± SD, * p < 0.05, ** p < 0.01, *** p < 0.001, one-way ANOVA, multiple comparisons.
Fig 5: Has_ circ_ 0001326 regulates macrophages polarization via has-miR-136-5p/USP4 axis in THP-1 induced macrophages. (a) qRT-PCR was used to detect the expression of hsa-miR-136-5p, USP4, CD11B, INOS, ARG1, and FIZZ1 in CON (cotransfected si-NC and inhibitor NC), si-circ (cotransfected si-circ-3 and inhibitor NC), and si-circ+hsa-miR-136-5p inhibitor group. (b) Western blot assay was used to determine the expression of USP4, CD11B, INOS, ARG1, and FIZZ1 in CON, si-circ, and si-circ+hsa-miR-136-5p inhibitor group. (c) ELISA was used to evaluate the secretion of TNF-α, IL-6, IL-10 and IL-RA in CON, si-circ, and si-circ+hsa-miR-136-5p inhibitor group. (d) Dual luciferase reporter assay was used to further confirm the relationship between hsa_ circ_ 0001326 and hsa-miR-136-5p, the relationship between hsa-miR-136-5p and USP4; * indicates the p value less than 0.05.
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