Journal: Journal of Cellular and Molecular Medicine

Article Title: TREM2 expression promotes liver and peritoneal M2 macrophage polarization in mice infected with Schistosoma japonicum

doi: 10.1111/jcmm.17842

Figure Lengend Snippet: Primers for genotype identification.

Article Snippet: B6/JGpt‐ Trem2 em1Cd3332in1 /Gpt knockout mice ( Trem2 −/− mice) were established by Gempharmatech Co., Ltd (Jiangsu, China) and wild‐type C57BL/6 mice were purchased from Laboratory Animal Centre of Nantong University.

Techniques:

Journal: Journal of Cellular and Molecular Medicine

Article Title: TREM2 expression promotes liver and peritoneal M2 macrophage polarization in mice infected with Schistosoma japonicum

doi: 10.1111/jcmm.17842

Figure Lengend Snippet: Primers used in RT‐qPCR.

Article Snippet: B6/JGpt‐ Trem2 em1Cd3332in1 /Gpt knockout mice ( Trem2 −/− mice) were established by Gempharmatech Co., Ltd (Jiangsu, China) and wild‐type C57BL/6 mice were purchased from Laboratory Animal Centre of Nantong University.

Techniques:

Journal: Journal of Cellular and Molecular Medicine

Article Title: TREM2 expression promotes liver and peritoneal M2 macrophage polarization in mice infected with Schistosoma japonicum

doi: 10.1111/jcmm.17842

Figure Lengend Snippet: TREM2 expression is upregulated in livers of mice infected with Schistosoma japonicum . (A) Trem2 mRNA expression in livers was detected by RT‐qPCR and compared to uninfected controls. ** p < 0.01. (B) TREM2 protein expression in mouse livers was detected by western blotting and compared to uninfected controls. ** p < 0.01, *** p < 0.001. (C) The expression of TREM2 in liver tissues of infected (12 W) or uninfected mice was observed by immunofluorescence staining. Green: F4/80+ cells. Red: TREM2+ cells. Yellow: F4/80 + TREM2+ cells. Bar: 100 μm.

Article Snippet: B6/JGpt‐ Trem2 em1Cd3332in1 /Gpt knockout mice ( Trem2 −/− mice) were established by Gempharmatech Co., Ltd (Jiangsu, China) and wild‐type C57BL/6 mice were purchased from Laboratory Animal Centre of Nantong University.

Techniques: Expressing, Infection, Quantitative RT-PCR, Western Blot, Immunofluorescence, Staining

Journal: Journal of Cellular and Molecular Medicine

Article Title: TREM2 expression promotes liver and peritoneal M2 macrophage polarization in mice infected with Schistosoma japonicum

doi: 10.1111/jcmm.17842

Figure Lengend Snippet: Trem2 deletion inhibits Arg1 and Ym1 expression in livers from mice infected with Schistosoma japonicum . (A) Genotype identification was detected by PCR. WT1 and WT2: Two wild‐type mice. KO1 ~ 4: Four Trem2 −/− mice. N: ddH 2 O was used as negative template DNA. Lanes 1, 3, 4, 6, 8, 10 and 12: Primers ( Trem2 ‐5S‐in‐tF1 and Trem2 ‐5S‐in‐tR1) were used and the positive products indicated that this mouse was a wild‐type. Lanes 2, 5, 7, 9, 11, 13 and 14: Primers ( Trem2 ‐5S‐in‐tF1 and Trem2 ‐3S‐in‐tR1) were used and the positive products indicated that this mouse was a Trem2 −/− mouse. (B) TREM2 expression in livers from wild‐type or Trem2 −/− mice, which were infected with Schistosoma japonicum for 6 weeks and 12 weeks, was detected by immunohistochemistry. Bar: 100 μm. (C) and (D) The expression of Arg1 mRNA and Ym1 mRNA in livers of wild‐type or Trem2 −/− mice was detected by RT‐qPCR. Expression was measured relative to the uninfected wild type mice (* p < 0.05, *** p < 0.001) or the infected wild type mice after 12 weeks ( # p < 0.05).

Article Snippet: B6/JGpt‐ Trem2 em1Cd3332in1 /Gpt knockout mice ( Trem2 −/− mice) were established by Gempharmatech Co., Ltd (Jiangsu, China) and wild‐type C57BL/6 mice were purchased from Laboratory Animal Centre of Nantong University.

Techniques: Expressing, Infection, Immunohistochemistry, Quantitative RT-PCR

Journal: Journal of Cellular and Molecular Medicine

Article Title: TREM2 expression promotes liver and peritoneal M2 macrophage polarization in mice infected with Schistosoma japonicum

doi: 10.1111/jcmm.17842

Figure Lengend Snippet: Trem2 deletion increases F4/80 + CD86+ cells in peritoneal macrophages. (A) TREM2 expression is upregulated in peritoneal macrophages from mice infected with Schistosoma japonicum . The number of TREM2+ cells in F4/80 + CD11b + peritoneal macrophages was determined by flow cytometry and compared to uninfected controls. * p < 0.05, ** p < 0.01, *** p < 0.001. (B) The number of F4/80 + CD86+ cells in total peritoneal macrophages obtained from wild‐type or Trem2 −/− mice with or without IL4/13 stimulation was determined by flow cytometry. ** p < 0.01. (C) The number of F4/80 + CD206+ cells in total peritoneal macrophages obtained from wild‐type or Trem2 −/− mice with or without IL4/13 stimulation was determined by flow cytometry. * p < 0.05. All results are relative to their respective controls.

Article Snippet: B6/JGpt‐ Trem2 em1Cd3332in1 /Gpt knockout mice ( Trem2 −/− mice) were established by Gempharmatech Co., Ltd (Jiangsu, China) and wild‐type C57BL/6 mice were purchased from Laboratory Animal Centre of Nantong University.

Techniques: Expressing, Infection, Flow Cytometry

Journal: Journal of Neuroinflammation

Article Title: Cognitive dysfunction in type 1 diabetes: role of TREM2 in microglial activation and Aβ pathology

doi: 10.1186/s12974-025-03611-3

Figure Lengend Snippet: TREM2 deletion aggravates cognitive impairment and promotes Aβ accumulation in the prefrontal cortex of T1D mice. a , b Blood glucose ( a ) and body weight ( b ) of mice in each group. n = 13. c Escape latency of each group for days 1 to 8 by Morris water maze (MWM). n = 12. d , e Time percent in the target quadrant ( d ) and representative path maps ( e ) of each group following removal of the platform. n = 12. f Swimming speeds of each group. n = 6. g Escape latency of each group in the MWM visible platform test on day 9. n = 7. h Recognition index in the novel object recognition test. n = 6. i) Grooming duration in the splash test. n = 9. j , k Mean percentage of conditioned freezing in the context test ( j ) and in the cued test ( k ). Ctrl, n = 6; T1D, n = 6; TREM2 cKO, n = 6 and T1D + TREM2 cKO, n = 5. l Representative images of Western blot showed the TREM2 expression in the prefrontal cortex. m Representative images of immunofluorescent staining of Iba1 (red), 6E10 (green) and DAPI (blue) in the prefrontal cortex. Scale bar = 20 μm. n , o , p Relative number of Iba1 positive cells (n), relative fluorescent area of 6E10 ( o ) and percentage of 6E10 area per micoglia ( p ) in the prefrontal cortex. n = 6. q The level of Aβ1–42 in the prefrontal cortex by ELISA. n = 5. WT: Wild-type. TREM2 cKO: TREM2 knockout. Ctrl: Wild-type nondiabetic group. T1D: Wild-type diabetic group. T1D + TREM2 cKO: TREM2 knockout diabetic group. Data were presented as mean ± SEM. For in vivo studies, n represents the number of animals per group. For a-d, f-k, n-q, One-way ANOVA. * p < 0.05, ** p < 0.01, *** p < 0.001. ## p < 0.01, ### p < 0.001, compared with Ctrl group. & p < 0.05, compared with T1D group.

Article Snippet: The C57BL/6J mice were purchased from Beijing Vital River Laboratory Animal Technology Co., Ltd., while TREM2 conditional knockout (TREM2 cKO) mice on a C57BL/6J background were obtained from Cyagen Biosciences Inc.

Techniques: Western Blot, Expressing, Staining, Enzyme-linked Immunosorbent Assay, Knock-Out, In Vivo

Journal: Journal of Neuroinflammation

Article Title: Cognitive dysfunction in type 1 diabetes: role of TREM2 in microglial activation and Aβ pathology

doi: 10.1186/s12974-025-03611-3

Figure Lengend Snippet: The impact of TREM2 on microglial phagocytosis of Aβ under T1D and high glucose condition. a-c Representative images of immunofluorescent staining ( a ) of Iba1 (red), CD68 (green) and DAPI (blue), CD68 mean intensity ( b ) and CD68/Iba-1 ratio ( c ) in the prefrontal cortex. Scale bar = 10 μm. n = 6. d-f Representative images of immunofluorescent staining ( d ) of Iba1 (red), CD68 (green) and DAPI (blue), CD68 mean intensity ( e ) and CD68/Iba-1 ratio ( f ) in primary cultured microglia. n = 5. g Representative images of Western blot showed the TREM2 expression in BV2 cells from different treatment groups. h, i Representative images ( h ) and mean intensity ( i ) of fluorescent Aβ (green) in BV2 cells at different time points. Scale bar = 7.8 μm. n = 3. j, k The percentage of fluorescent Aβ + BV2 cells ( j ) and representative flow cytometry dot plots ( k ). n = 5. WT: Wild-type. TREM2 cKO: TREM2 knockout. Ctrl: Wild-type nondiabetic group. T1D: Wild-type diabetic group. T1D + TREM2 cKO: TREM2 knockout diabetic group. NG: Normal glucose group. HG: High glucose group. HG + TREM2 cKO: TREM2 knockout high-glucose group. HG + Aβ: High-glucose group with Aβ. HG + Vector + Aβ: High-glucose group with empty vector and Aβ. HG + TREM2-OE + Aβ: High-glucose group with TREM2 overexpression and Aβ. HG + Vector: High-glucose group with empty-vector. HG + TREM2-OE: High-glucose group with TREM2 overexpression. NG + Aβ: Normal glucose group with Aβ. HG + TREM2-si + Aβ: High-glucose group with TREM2 knockdown and Aβ. Data were presented as mean ± SEM. For in vivo studies, n represents the number of animals per group. For in vitro studies, n represents the number of biologically independent experiments performed. For b, c, e, f, i, j, One-way ANOVA. * p < 0.05, ** p < 0.01, *** p < 0.001. # p < 0.05, ## p < 0.01, compared with NG + Aβ group. &&& p < 0.001, compared with HG + Vector + Aβ group.

Article Snippet: The C57BL/6J mice were purchased from Beijing Vital River Laboratory Animal Technology Co., Ltd., while TREM2 conditional knockout (TREM2 cKO) mice on a C57BL/6J background were obtained from Cyagen Biosciences Inc.

Techniques: Staining, Cell Culture, Western Blot, Expressing, Flow Cytometry, Knock-Out, Plasmid Preparation, Over Expression, Knockdown, In Vivo, In Vitro

Journal: Journal of Neuroinflammation

Article Title: Cognitive dysfunction in type 1 diabetes: role of TREM2 in microglial activation and Aβ pathology

doi: 10.1186/s12974-025-03611-3

Figure Lengend Snippet: The impact of TREM2 on microglial cell migration towards different forms of Aβ. a Flow chart of cell experiments. b , c Representative images ( b ) and quantitative analysis of western blot ( c ) showed the expression of TREM2 in BV2 cells. n = 3. d , e Representative images ( d ) and migration index of BV2 cells ( e ) at different time points post scratch. n = 3. f Representative images of cell migration in BV2 cells analyzed by Transwell assay. g , h Migration ratio of BV2 cells towards fAβ ( f ) and oAβ ( g ). n = 3. NG: Normal glucose group. HG: High glucose group. TREM2-si: TREM2 knockdown group. HG + Vector: High-glucose group with empty vector. HG + TREM2-si: TREM2 knockdown high-glucose group. fAβ: Aβ fibril. oAβ: Aβ oligomer. Data were presented as mean ± SEM. For in vitro studies, n represents the number of biologically independent experiments performed. For c, two-tailed unpaired t test. For e, g, h, One-way ANOVA. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: The C57BL/6J mice were purchased from Beijing Vital River Laboratory Animal Technology Co., Ltd., while TREM2 conditional knockout (TREM2 cKO) mice on a C57BL/6J background were obtained from Cyagen Biosciences Inc.

Techniques: Migration, Western Blot, Expressing, Transwell Assay, Knockdown, Plasmid Preparation, In Vitro, Two Tailed Test

Journal: Journal of Neuroinflammation

Article Title: Cognitive dysfunction in type 1 diabetes: role of TREM2 in microglial activation and Aβ pathology

doi: 10.1186/s12974-025-03611-3

Figure Lengend Snippet: Distribution and expression dynamics of Aβ-related genes in microglial subpopulations of T1D mice. a, b Bubble plot ( a ) and violin plots ( b ) showing the expression of Aβ-related genes for each microglia subpopulation. c , e , g Violin plots showing the expression of Cx3cr1 ( c ), Ccr5 ( e ) and Trem2 ( g ) in the microglial subpopulations. d , f , h Violin plots comparing the levels of Cx3cr1 ( d ), Ccr5 ( f ) and Trem2 ( h ) in microglia between the Ctrl and T1D groups. i Violin plot showing the levels of Trem2 among microglia subpopulations. j-l Smoothed expression curves of Trem2 ( j ), Cx3cr1 ( k ) and Ccr5 ( l ) along the trajectory in microglia subpopulations. M: Microglia, Ctrl: Wild-type nondiabetic group. T1D: Wild-type diabetic group. n = 3. For in vivo studies, n represents the number of animals per group. For c-i, unpaired t test. * p < 0.05, ** p < 0.01, *** p < 0.001, compared with Ctrl group

Article Snippet: The C57BL/6J mice were purchased from Beijing Vital River Laboratory Animal Technology Co., Ltd., while TREM2 conditional knockout (TREM2 cKO) mice on a C57BL/6J background were obtained from Cyagen Biosciences Inc.

Techniques: Expressing, In Vivo

Journal: Journal of Neuroinflammation

Article Title: Cognitive dysfunction in type 1 diabetes: role of TREM2 in microglial activation and Aβ pathology

doi: 10.1186/s12974-025-03611-3

Figure Lengend Snippet: Microglial activation and TREM2 expression in the prefrontal cortex and hippocampus of T1D mice. a , b Representative images of immunofluorescent staining of Iba1 (red), TREM2 (green) and DAPI (blue) in the prefrontal cortex ( a ) and hippocampus ( b ). Scale bar = 5 μm. c , j Schematic diagrams of prefrontal cortex ( c ) and hippocampus ( j ). d The relative number of Iba1-positive cells in the prefrontal cortex normalized to the control group. e The soma size of Iba1-positive cells in the prefrontal cortex. f , m The relative mRNA levels of LPL, CST7 and TREM2 in the prefrontal cortex ( f ) and hippocampus ( m ). n = 6. g , h , i Representative images ( g ) and quantitative analysis of Western blot showed the protein levels of Iba1 and TREM2 ( h ), and the TREM2/Iba1 ratio ( i ) in the prefrontal cortex. n = 6. k The relative number of Iba1-positive cells in the hippocampus normalized to the control group. n = 6. l The soma size of Iba1-positive cells in the hippocampus. n = 6. n , o , p Representative images ( n ) and quantitative analysis of Western blot showed the protein levels of Iba1 and TREM2 ( o ), and the TREM2/Iba1 ratio ( p ) in the hippocampus. n = 6. Ctrl: Wild-type nondiabetic group. 8 W, 15 W: T1D mice at 8 and 15 weeks post-STZ injection, respectively. Data were presented as mean ± SEM. For in vivo studies, n represents the number of animals per group. For d-f, h-i, k-m, o-p, One-way ANOVA. * p < 0.05, ** p < 0.01, *** p < 0.001, compared with Ctrl group.

Article Snippet: The C57BL/6J mice were purchased from Beijing Vital River Laboratory Animal Technology Co., Ltd., while TREM2 conditional knockout (TREM2 cKO) mice on a C57BL/6J background were obtained from Cyagen Biosciences Inc.

Techniques: Activation Assay, Expressing, Staining, Control, Western Blot, Injection, In Vivo

Journal: Journal of Neuroinflammation

Article Title: Cognitive dysfunction in type 1 diabetes: role of TREM2 in microglial activation and Aβ pathology

doi: 10.1186/s12974-025-03611-3

Figure Lengend Snippet: Identification and functional validation of differentially expressed genes related to TREM2 in the brain of T1D mice. a Volcano plot of differential gene expression profiles in the prefrontal cortex between T1D mice and T1D + TREM2 cKO mice. b Chord plot displaying the top 10 GO terms of differentially expressed genes. c , d Representative images of immunofluorescent staining ( c ) of TOM20 (green) and DAPI (blue), and the mitochondrial fragmentation index in BV2 cells, calculated as punctate/(punctate + rod-shaped + reticular) ( d ). Scale bar = 10 μm. n = 3. e) Representative electron microscopy images of mitochondria in BV2 cells. f Top 10 ranked hub gene networks generated by Cytohubba. g The relative mRNA levels of Ccr5, Cx3cr1, and Cxcl10 in the prefrontal cortex. n = 5. h GSEA showed significant enrichment in the PI3K/AKT/MTOR signaling pathway. i , k , l Representative images of immunofluorescent staining ( i ) of P-mTOR (green), Iba1 (red), and DAPI (blue), the intensity of P-mTOR in microglia ( k ), and normalized intensity of P-mTOR in microglia ( l ) in the prefrontal cortex. Scale bar = 10 μm. n = 8. j , m-o Representative images ( j ) and quantitative analysis of Western blot showed the levels of P-mTOR/mTOR ( m ), P-Erk1/2/Erk1/2 ( n ), and P-GSK3β/GSK3β ( o ) in BV2 cells. n = 3. Ctrl: Wild-type nondiabetic group. T1D: Wild-type diabetic group. T1D + TREM2 cKO: TREM2 knockout diabetic group. DEGs: Differentially expressed genes. GO: Gene ontology. GSEA: Gene set enrichment analysis. NG: Normal glucose group. HG: High glucose group. HG + Aβ: High-glucose group with Aβ. HG + Vector + Aβ: High-glucose group with empty vector and Aβ. HG + TREM2-OE + Aβ: High-glucose group with TREM2 overexpression and Aβ. Data were presented as mean ± SEM. For in vivo studies, n represents the number of animals per group. For in vitro studies, n represents the number of biologically independent experiments performed. For d, g, k-o, One-way ANOVA. * p < 0.05, ** p < 0.01

Article Snippet: The C57BL/6J mice were purchased from Beijing Vital River Laboratory Animal Technology Co., Ltd., while TREM2 conditional knockout (TREM2 cKO) mice on a C57BL/6J background were obtained from Cyagen Biosciences Inc.

Techniques: Functional Assay, Biomarker Discovery, Gene Expression, Staining, Electron Microscopy, Generated, Western Blot, Knock-Out, Plasmid Preparation, Over Expression, In Vivo, In Vitro

Journal: Journal of Neuroinflammation

Article Title: Cognitive dysfunction in type 1 diabetes: role of TREM2 in microglial activation and Aβ pathology

doi: 10.1186/s12974-025-03611-3

Figure Lengend Snippet: The TREM2-mTOR Axis Drives Microglial Clearance of Aβ in the Diabetic Brain. Accumulation of Aβ oligomers and upregulated TREM2 expression were observed in the prefrontal cortex of T1D mice. Under hyperglycemic conditions, Aβ activates TREM2, which phosphorylates its adaptor DAP12 and recruits Syk kinase. Syk then initiates the downstream PI3K-Akt-mTOR signaling pathway. This cascade enhances mitochondrial function and upregulates chemokines including Cxcl10, thereby enabling microglia to migrate toward, phagocytose, and clear Aβ oligomers efficiently. Collectively, these findings demonstrate that TREM2 plays a critical role in maintaining microglial homeostasis and countering Aβ pathology in T1D

Article Snippet: The C57BL/6J mice were purchased from Beijing Vital River Laboratory Animal Technology Co., Ltd., while TREM2 conditional knockout (TREM2 cKO) mice on a C57BL/6J background were obtained from Cyagen Biosciences Inc.

Techniques: Expressing