Journal: The Journal of Experimental Medicine

Article Title: Loss of SOCS3 expression in T cells reveals a regulatory role for interleukin-17 in atherosclerosis

doi: 10.1084/jem.20090545

Figure Lengend Snippet: SOCS3 deletion in T cells promotes IL-17 and IL-10 production, inhibits macrophage apoptosis, and limits atherosclerotic lesion development. (a) Atherosclerotic lesion size in the aortic root of chimeric Ldlr −/− SOCS3-WT or SOCS-cKO mice. Data are representative of four independent experiments throughout this work. Dashed lines indicate mean values. (b) Lesion T cell infiltration (red staining; mean values ± SEM). Data are representative of three experiments. (c) Reduced IFN-γ but increased IL-10 and IL-17 production in supernatants of CD3-stimulated CD4 + T cells (means ± SEM of five mice per group and two experiments; *, P < 0.05). (d) Necrotic core (nc; trichrome staining) size (means ± SEM) in the aortic root. Representative of two experiments and 13 mice per group. (e) Macrophage apoptosis (TUNEL staining) after coincubation with CD4 + cells from SOCS3-WT or SOCS-cKO mice (means ± SEM). Representative of three experiments (*, P < 0.05). Bars: (a) 250 µm; (b) 30 µm; (d) 60 µm.

Article Snippet: Membranes were probed with antibodies directed against SOCS3 (clone 1B2; MBL International), P-Stat3 and Stat3 protein (Cell Signaling Technology).

Techniques: Staining, TUNEL Assay

Journal: The Journal of Experimental Medicine

Article Title: Loss of SOCS3 expression in T cells reveals a regulatory role for interleukin-17 in atherosclerosis

doi: 10.1084/jem.20090545

Figure Lengend Snippet: SOCS3 deletion in T cells promotes an antiinflammatory macrophage phenotype. (a) IL-12 and IL-10 production by macrophages after coincubation with CD4 + cells from SOCS3-WT or SOCS-cKO mice in the presence or absence of Transwells. Mean values ± SEM of three to four mice per group are shown (*, P < 0.05). (b) TNF-α, NOS2, and arginase-1 mRNA expression (arbitrary units relative to GAPDH mRNA expression) by macrophages after coincubation with CD4 + cells. Mean values ± SEM of three to four mice per group and three independent experiments are shown (*, P < 0.05). (c and d) Quantitative analysis (relative to incubation without neutralizing antibodies) of NOS2, arginase-1, and TNF-α mRNA expression in macrophages after coincubation with CD4 + cells in the presence of either anti–IL-10 (c) or anti–IL-17 (d) neutralizing antibodies. (e) Quantitative analysis (relative to control without incubation with recombinant cytokines) of arginase-1 and TNF-α mRNA expression in macrophages after incubation with IL-10, IL-17 or IL-10, and IL-17. Values in c–e represent mean values ± SEM of three mice per group and three different experiments.

Article Snippet: Membranes were probed with antibodies directed against SOCS3 (clone 1B2; MBL International), P-Stat3 and Stat3 protein (Cell Signaling Technology).

Techniques: Expressing, Incubation, Control, Recombinant

Journal: The Journal of Experimental Medicine

Article Title: Loss of SOCS3 expression in T cells reveals a regulatory role for interleukin-17 in atherosclerosis

doi: 10.1084/jem.20090545

Figure Lengend Snippet: SOCS3-controlled IL-17 production protects against vascular inflammation and atherosclerotic lesion development. Representative photomicrographs (a and b) and quantitative analysis (c and d) of atherosclerotic lesion size (a and c) and lesion T cell infiltration (b and d) in the aortic root of chimeric Ldlr −/− SOCS3-WT or SOCS-cKO mice treated either with a neutralizing anti–IL-17A antibody (anti–IL-17) or an isotype-matched control (IgG; n = 7–8 mice per group). The anti–IL-17 in vivo experiment was repeated twice. p-values are shown in c and d. Dashed lines indicate mean values. (e) Increased IL-4 but reduced IL-10 production in supernatants of CD3-stimulated CD4 + T cells recovered at the time of sacrifice from chimeric Ldlr −/− mice treated with a neutralizing anti–IL-17A antibody. Means ± SEM of five mice per group performed in triplicates are shown (*, P < 0.05). (f) VCAM-1 expression in atherosclerotic lesions ( n = 6–8 mice per group and two separate experiments; *, P < 0.05). Bars: (a) 250 µm; (b) 100 µm; (f) 130 µm.

Article Snippet: Membranes were probed with antibodies directed against SOCS3 (clone 1B2; MBL International), P-Stat3 and Stat3 protein (Cell Signaling Technology).

Techniques: Control, In Vivo, Expressing

Journal: The Journal of Experimental Medicine

Article Title: Loss of SOCS3 expression in T cells reveals a regulatory role for interleukin-17 in atherosclerosis

doi: 10.1084/jem.20090545

Figure Lengend Snippet: Supplementation with IL-17 reduces vascular inflammation and limits atherosclerotic lesion development. (a) Atherosclerotic lesion size in the aortic root of 17-wk-old female chimeric Ldlr −/− SOCS3-WT mice fed a high fat diet and treated with rIL-17 or control serum albumin for 5 wk. Two different experiments are depicted with eight to nine animals in each group. Young animals were 12 wk old. (b) Lesion and adventitial T cell infiltration in 17-wk-old animals. Similar results were obtained in young animals (not depicted). (c) Endothelial VCAM-1 expression in IL-17–treated 17-wk-old mice. Results represent two separate experiments. (d) One representative example out of three different experiments of a Western blot showing reduction of IL-1–induced VCAM-1 expression after mouse endothelial cells are incubated with IL-17. Dashed lines indicate mean values. Bars: (a) 250 µm; (b) 50 µm; (c) 25 µm.

Article Snippet: Membranes were probed with antibodies directed against SOCS3 (clone 1B2; MBL International), P-Stat3 and Stat3 protein (Cell Signaling Technology).

Techniques: Control, Expressing, Western Blot, Incubation

Journal: The Journal of Experimental Medicine

Article Title: Loss of SOCS3 expression in T cells reveals a regulatory role for interleukin-17 in atherosclerosis

doi: 10.1084/jem.20090545

Figure Lengend Snippet: Expression of IL-17 in atherosclerotic vessels. (left) Mouse atherosclerosis. (a and b) Occasional staining for IL-17 (red, arrows) in inflammatory cells within the intima (i) and adventitia (arrows in b) of SOCS3-cKO mice. (c and d) Representative examples of staining for IL-17 (red, arrows) in the media (m) of the aortic sinus (c) and the coronary arteries (d) of SOCS3-cKO mice. Note that IL-17 staining in media was detected in plaque-free areas (right of the arrowheads) and was lost in areas where plaques have developed (left of the arrowheads). (e–g) Staining for IL-17 (red/brown) in the media of the aortic sinus of WT (e and f) or IL-17A–deficient (g) mice. Note that IL-17 staining almost disappeared after adsorption with the IL-17–specific peptide (f) or in vessels of IL-17A–deficient mice (g). Data are representative of at least 10 different mouse arteries. Bars: (a–d) 45 µm; (e–g) 90 µm. (right) Human atherosclerosis. (a) IL-17 staining in the media (m) and adventitia (adv) of carotid plaques. (b) The image is from an area underlying an advanced plaque. It shows IL-17 staining in adventitial vessels (arrows), but the media has lost its IL-17 staining. (c) The image is from an area underlying an early intimal thickening. It shows staining for IL-17 in the adventitial vessels (arrows) and still diffuse moderate IL-17 staining within the media. (d) Another example of IL-17 staining (brown) in an advanced carotid plaque. (e) Disappearance of IL-17 staining after adsorption with the IL-17–specific peptide. Data are representative of at least 10 different human arteries. Bars: (a) 250 µm; (b and c) 30 µm; (d and e) 45 µm.

Article Snippet: Membranes were probed with antibodies directed against SOCS3 (clone 1B2; MBL International), P-Stat3 and Stat3 protein (Cell Signaling Technology).

Techniques: Expressing, Staining, Adsorption

Journal: Bioresources and Bioprocessing

Article Title: Propionate-engineered probiotics reduce radiation-induced intestinal damage

doi: 10.1186/s40643-026-01020-9

Figure Lengend Snippet: Engineered probiotic PG mitigated radiation-induced intestinal injury by regulating the SOCS1/JAK2/STAT3 pathway. a Principal Component Analysis (PCA) revealed differences in gene expression levels among groups. b KEGG Enrichment BarPlot for IR vs. IR + PG displayed the number of differential genes in the pathway represented on the horizontal axis, pathway names on the vertical axis, and colors representing KEGG Level 1 classification. c KEGG-enriched bar graph displaying the top 20 KEGG pathways with the smallest P-values. d The results of the KEGG enrichment analysis werw presented as a scatter plot. (e) The heatmap illustrated the relative expression levels of JAK-STAT signaling pathway-related genes in the IR and IR + PG groups. f Western blot analysis demonstrated the protein expression levels of SOCS1, p-JAK2, JAK2, p-STAT3, and STAT3 across groups

Article Snippet: The primary antibodies included anti-SOCS1 (PSH09-68), JAK2 (SY0245), p-JAK2 (SY24-03), STAT3 (SY24-08), p-STAT3 (SZ43-01), and GAPDH (SA30-01), all purchased from HuaBio-Antibodies Co., Ltd (Hangzhou, China).

Techniques: Gene Expression, Expressing, Western Blot