anti–tgf-β ab 1d11, reactive mouse tgf-β1/β3 (EPIRUS Inc)

EPIRUS Inc anti–tgf-β ab 1d11, reactive mouse tgf-β1/β3

The protective effect of IFN-α against AIA is mediated by TGF-β signaling in the sensitization phase. (A) Schematic representation of the AIA model, as described in Materials and Methods. Briefly, AIA was induced in WT Sv129 mice and LysM Cre+/−Tgfbr2fl/fl with or without IFN-α treatment. TGF-β signaling was blocked in WT mice by daily i.p. injection of 150 μg <t>anti–TGF-β</t> Ab for the first 0–8 or 20–28 d of AIA. (B) The level of arthritis is expressed as severity score (mean ± SEM, n ≥ 4) from WT mice with or without IFN-α and anti–TGF-β treatment. (C) Representative histochemical slides showing inflammation of the knee joint from each group. (D) Level of arthritis expressed as severity score (mean ± SEM, n ≥ 6) from LysM Cre+/−Tgfbr2fl/fl mice with or without IFN-α treatment. Comparison of arthritis severity score between different treatment groups was done by Mann–Whitney U test (*p < 0.05).

Anti–Tgf β Ab 1d11, Reactive Mouse Tgf β1/β3, supplied by EPIRUS Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Journal: The Journal of Immunology Author Choice

Article Title: IDO1 and TGF-β Mediate Protective Effects of IFN-α in Antigen-Induced Arthritis

doi: 10.4049/jimmunol.1502125

Figure Lengend Snippet: The protective effect of IFN-α against AIA is mediated by TGF-β signaling in the sensitization phase. (A) Schematic representation of the AIA model, as described in Materials and Methods. Briefly, AIA was induced in WT Sv129 mice and LysM Cre+/−Tgfbr2fl/fl with or without IFN-α treatment. TGF-β signaling was blocked in WT mice by daily i.p. injection of 150 μg anti–TGF-β Ab for the first 0–8 or 20–28 d of AIA. (B) The level of arthritis is expressed as severity score (mean ± SEM, n ≥ 4) from WT mice with or without IFN-α and anti–TGF-β treatment. (C) Representative histochemical slides showing inflammation of the knee joint from each group. (D) Level of arthritis expressed as severity score (mean ± SEM, n ≥ 6) from LysM Cre+/−Tgfbr2fl/fl mice with or without IFN-α treatment. Comparison of arthritis severity score between different treatment groups was done by Mann–Whitney U test (*p < 0.05).

Article Snippet: TGF-β was neutralized by daily i.p. injection for the indicated time of 150 μg anti–TGF-β Ab (clone 1D11, reactive to mouse TGF-β1/β3; EPIRUS Biopharmaceuticals Netherlands BV).

Techniques: Injection, MANN-WHITNEY

IFN-α–induced activation of IDO1 in the sensitization phase of AIA and in vitro occurs independently of TGF-β. Female mice were immunized days 1 and 7 with mBSA with or without IFN-α treatment, with or without anti–TGF-β Abs administered i.p. days 1–8 as in Fig. 1 and as described for AIA in Materials and Methods. (A) Sera were collected at days 9 and 28 and analyzed for Trp and Kyn concentration by HPLC. Data are expressed as the ratio of serum levels of Kyn to Trp, n ≥ 7. Comparisons between groups were made by Mann–Whitney U test. (B) Splenocytes isolated day 10 from mBSA-sensitized mice were restimulated ex vivo with 50 μg/ml mBSA with or without 100 U/ml IFN-α, with or without 40 μg/ml anti–TGF-β. Data are expressed as fold change normalized to the reference gene Actb and Ido1 expression in mBSA-stimulated cultured cells from the same mice, n = 5. Paired Student t test was used to evaluate differences between treatments. *p < 0.05.

Journal: The Journal of Immunology Author Choice

Article Title: IDO1 and TGF-β Mediate Protective Effects of IFN-α in Antigen-Induced Arthritis

doi: 10.4049/jimmunol.1502125

Figure Lengend Snippet: IFN-α–induced activation of IDO1 in the sensitization phase of AIA and in vitro occurs independently of TGF-β. Female mice were immunized days 1 and 7 with mBSA with or without IFN-α treatment, with or without anti–TGF-β Abs administered i.p. days 1–8 as in Fig. 1 and as described for AIA in Materials and Methods. (A) Sera were collected at days 9 and 28 and analyzed for Trp and Kyn concentration by HPLC. Data are expressed as the ratio of serum levels of Kyn to Trp, n ≥ 7. Comparisons between groups were made by Mann–Whitney U test. (B) Splenocytes isolated day 10 from mBSA-sensitized mice were restimulated ex vivo with 50 μg/ml mBSA with or without 100 U/ml IFN-α, with or without 40 μg/ml anti–TGF-β. Data are expressed as fold change normalized to the reference gene Actb and Ido1 expression in mBSA-stimulated cultured cells from the same mice, n = 5. Paired Student t test was used to evaluate differences between treatments. *p < 0.05.

Techniques: Activation Assay, In Vitro, Concentration Assay, MANN-WHITNEY, Isolation, Ex Vivo, Expressing, Cell Culture

IFN-α induces IDO1 expression in splenic pDC in vitro and in vivo independently of TGF-β. AIA was induced in female mice with IFN-α treatment, as described in Materials and Methods. At days 4 and 28, mice were sacrificed and pDC were purified from their spleens. (A) Western blot analysis of IDO1 protein expression in pDC. (B) Real-time PCR analysis of Ido1, Tgfb1, Ifna11, and Ifnb1 transcripts in pDC isolated from spleen cells at days 4 and 28 of AIA from mice treated with IFN-α, normalized to the expression of Actb, and presented relative to results of pDC isolated from control mice not treated with IFN-α (dotted line, 1-fold). (C) Splenocytes were isolated at day 10 of AIA, stimulated with 50 μ/ml mBSA plus 250 U/ml IFN-α, with or without anti–TGF-β (40 μg/ml) for 72 h, and analyzed for IDO1-positive pDC by FACS (see Materials and Methods). The bar diagram (left) depicts the percentage of mPDCA+IDO1+ cells among the live lymphocyte population, and the FACS plots (right) show representative dot plots from one of five mice. Data in (A) are the representative of four experiments, and (B) and (C) (mean ± SD, n = 6) were analyzed by Student t test. *p < 0.05, ***p < 0.001.

Journal: The Journal of Immunology Author Choice

Article Title: IDO1 and TGF-β Mediate Protective Effects of IFN-α in Antigen-Induced Arthritis

doi: 10.4049/jimmunol.1502125

Figure Lengend Snippet: IFN-α induces IDO1 expression in splenic pDC in vitro and in vivo independently of TGF-β. AIA was induced in female mice with IFN-α treatment, as described in Materials and Methods. At days 4 and 28, mice were sacrificed and pDC were purified from their spleens. (A) Western blot analysis of IDO1 protein expression in pDC. (B) Real-time PCR analysis of Ido1, Tgfb1, Ifna11, and Ifnb1 transcripts in pDC isolated from spleen cells at days 4 and 28 of AIA from mice treated with IFN-α, normalized to the expression of Actb, and presented relative to results of pDC isolated from control mice not treated with IFN-α (dotted line, 1-fold). (C) Splenocytes were isolated at day 10 of AIA, stimulated with 50 μ/ml mBSA plus 250 U/ml IFN-α, with or without anti–TGF-β (40 μg/ml) for 72 h, and analyzed for IDO1-positive pDC by FACS (see Materials and Methods). The bar diagram (left) depicts the percentage of mPDCA+IDO1+ cells among the live lymphocyte population, and the FACS plots (right) show representative dot plots from one of five mice. Data in (A) are the representative of four experiments, and (B) and (C) (mean ± SD, n = 6) were analyzed by Student t test. *p < 0.05, ***p < 0.001.

Techniques: Expressing, In Vitro, In Vivo, Purification, Western Blot, Real-time Polymerase Chain Reaction, Isolation

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