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R&D Systems anti il 23 ab
Anti Il 23 Ab, supplied by R&D Systems, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+il+23+ab/IL-23+Antibody+(SR1328)/pm35395541-56-19-21
Average 90 stars, based on 1 article reviews

anti il 23 ab - by Bioz Stars, 2026-09

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Article Title: IL-17A produced by innate lymphoid cells is essential for intestinal ischemia reperfusion injury
Article Snippet: Control animals were given 200 μg rat IgG isotype control antibody (R&D systems) also in 3 doses 96, 48 and 24 hours prior to IR. .. To neutralize IL-23, 10 μg of goat-anti-mouse anti-IL-23 Ab (R&D Systems) were given in 3 doses by i.p. injection 96, 48 and 24 hours prior to IR as described by ( 48 ). .. Control animals were given 20 μg goat IgG isotype control antibody (R&D systems) also in 3 doses 96, 48 and 24 hours prior to IR.

Article Title: Autoreactive memory Th17 cells are principally derived from T-bet + RORγt + Th17/1 effectors.
Article Snippet: Effector Th17 cells, including IFN-γ-IL-17+ (eTh17) and IFN-γIL-17 (eTh17/1) subsets, play critical pathogenic functions in the induction of autoimmunity.. As acute inflammation subsides, a small proportion of the effectors survive and convert to memory Th17 cells (mTh17), which sustain chronic inflammation in autoimmune diseases.. Herein, we investigated the differential contributions of eTh17 versus eTh17/1 to the memory pool using an experimental model of ocular autoimmune disease.

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rhSlit2 attenuates bTSH-induced IL-23p19 while enhancing IL-12p35 induction in fibrocytes. Knocking-down Slit2 in GD-OF enhances IL-23p19 induction but attenuates the IL-12p35 response. (A and D) Fibrocytes and GD-OF were incubated with rhSlit2 (50 ng/ml) for 7–9 d, then received diluent or bTSH (5 mIU/mL) for 6 h. Cell layers were harvested, RNA extracted, reverse-transcribed and subjected to RT-PCR for the targets indicated. Values were normalized to their respective GAPDH signals. (B) Fibrocytes were treated as in A, media were harvested and subjected to IL-23 and IL-12 specific ELISAs. Values were normalized to respective cell layer protein content. (C) Fibrocytes were covered with GD-OF-conditioned medium that had been incubated for 48 h with uncoated beads or those coated with anti-Slit2 (100 μg) or isotype IgG (100μg), as described in “Methods”. Fibrocyte monolayers were processed as in (A). (D) Confluent GD-OF were transfected with scrambled (control) (3μg) siRNA or Slit2-targeting siRNA (3μg), were incubated for 3 d, and treated with diluent or bTSH for 6 h. They were then processed as in (A). (E) GD-OF were treated as in (D), media were collected and subjected to ELISAs for IL-23 and IL-12 as in (B). Data are expressed as the mean ± SD, *, p<0.05; **, p<0.01, ***, p<0.001 of three independent determinations.

Journal: Journal of immunology (Baltimore, Md. : 1950)

Article Title: Slit2 may underlie divergent induction by thyrotropin of IL-23 and IL-12 in human fibrocytes

doi: 10.4049/jimmunol.1900434

Figure Lengend Snippet: rhSlit2 attenuates bTSH-induced IL-23p19 while enhancing IL-12p35 induction in fibrocytes. Knocking-down Slit2 in GD-OF enhances IL-23p19 induction but attenuates the IL-12p35 response. (A and D) Fibrocytes and GD-OF were incubated with rhSlit2 (50 ng/ml) for 7–9 d, then received diluent or bTSH (5 mIU/mL) for 6 h. Cell layers were harvested, RNA extracted, reverse-transcribed and subjected to RT-PCR for the targets indicated. Values were normalized to their respective GAPDH signals. (B) Fibrocytes were treated as in A, media were harvested and subjected to IL-23 and IL-12 specific ELISAs. Values were normalized to respective cell layer protein content. (C) Fibrocytes were covered with GD-OF-conditioned medium that had been incubated for 48 h with uncoated beads or those coated with anti-Slit2 (100 μg) or isotype IgG (100μg), as described in “Methods”. Fibrocyte monolayers were processed as in (A). (D) Confluent GD-OF were transfected with scrambled (control) (3μg) siRNA or Slit2-targeting siRNA (3μg), were incubated for 3 d, and treated with diluent or bTSH for 6 h. They were then processed as in (A). (E) GD-OF were treated as in (D), media were collected and subjected to ELISAs for IL-23 and IL-12 as in (B). Data are expressed as the mean ± SD, *, p<0.05; **, p<0.01, ***, p<0.001 of three independent determinations.

Article Snippet: Human CD34 + nucleofection kit (cat # VPA-1003) was from Lonza, Allendale, NJ. siRNAs targeting Akt (cat #L-003000–00), tristetraprolin (cat # L-010789–01), Slit2 (cat #L-019853–00), JNK (cat #L-003514–00) and scramble siRNA (cat # D-001810–10) were from Dharmacon, Lafayette, CO. Anti-hIL-23p19 Ab was from Santa Cruz, Dallas, Tx (cat # sc-271279).

Techniques: Incubation, Reverse Transcription, Reverse Transcription Polymerase Chain Reaction, Transfection, Control

Divergent induction by bTSH of IL-23 and IL-12 in GD-fibrocytes versus GD-OF. (A,D) Expression levels of IL-23p19 and IL-12p35 mRNA under control (untreated) and bTSH-treated conditions in 5 strains of GD-fibrocytes and 3 strains of GD-OF, each from a different donor with GD. Medium covering confluent culture monolayers was replaced with DMEM supplemented with 1% FBS and containing nothing or bTSH (5 mIU/mL) for 6 h. Cell layers were harvested, cellular RNA was reverse transcribed, and subjected to quantitative real-time PCR for IL-23p19 and IL-12p35 mRNA. Values were normalized to their respective GAPDH levels and are expressed as the mean ± S.D of triplicate determinations from one representative experiment of three performed, **, p<0.01; ***, p<0.001 by ANOVA. (B and E) Fibrocyte cultures were treated with bTSH (5 mIU/mL) for the graded intervals indicated along the abscissa. IL-23p19 and IL-12p35 mRNA levels were quantified as in A and D and are expressed as mean ± SD. (C and F) Cultures were treated with bTSH for the graded intervals indicated. Media were collected and subjected to IL-23 and IL-12 ELISAs as described in “Methods”. Values were normalized to respective monolayer protein content. Data are expressed as mean ± SD of triplicate determinations. (Insets, C and F) Monolayer proteins from control and bTSH-treated cultures were subjected to Western blot analysis for IL-23p19 and IL-12p35 Blots were then re-probed with anti-β-actin.

Journal: Journal of immunology (Baltimore, Md. : 1950)

Article Title: Slit2 may underlie divergent induction by thyrotropin of IL-23 and IL-12 in human fibrocytes

doi: 10.4049/jimmunol.1900434

Figure Lengend Snippet: Divergent induction by bTSH of IL-23 and IL-12 in GD-fibrocytes versus GD-OF. (A,D) Expression levels of IL-23p19 and IL-12p35 mRNA under control (untreated) and bTSH-treated conditions in 5 strains of GD-fibrocytes and 3 strains of GD-OF, each from a different donor with GD. Medium covering confluent culture monolayers was replaced with DMEM supplemented with 1% FBS and containing nothing or bTSH (5 mIU/mL) for 6 h. Cell layers were harvested, cellular RNA was reverse transcribed, and subjected to quantitative real-time PCR for IL-23p19 and IL-12p35 mRNA. Values were normalized to their respective GAPDH levels and are expressed as the mean ± S.D of triplicate determinations from one representative experiment of three performed, **, p<0.01; ***, p<0.001 by ANOVA. (B and E) Fibrocyte cultures were treated with bTSH (5 mIU/mL) for the graded intervals indicated along the abscissa. IL-23p19 and IL-12p35 mRNA levels were quantified as in A and D and are expressed as mean ± SD. (C and F) Cultures were treated with bTSH for the graded intervals indicated. Media were collected and subjected to IL-23 and IL-12 ELISAs as described in “Methods”. Values were normalized to respective monolayer protein content. Data are expressed as mean ± SD of triplicate determinations. (Insets, C and F) Monolayer proteins from control and bTSH-treated cultures were subjected to Western blot analysis for IL-23p19 and IL-12p35 Blots were then re-probed with anti-β-actin.

Techniques: Expressing, Control, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot

bTSH up-regulates IL-23p19 gene transcription and enhances IL-23p19 mRNA stability in fibrocytes while enhancing IL-12p35 gene transcription and mRNA stability in GD-OF. (A and D) Confluent monolayers of fibrocytes and GD-OF remained untreated or received bTSH (5 mIU/mL) for 2 h. Cultures were harvested and subjected to Pol II Chip transcription assay as described in “Methods”. (B and E) Confluent cultures were pre-treated with bTSH for 2 h. At time “0” all culture wells received 5,6-dichlorobenzimidazole (20 μg/mL) without or in the continued presence of bTSH. Monolayers were harvested at the times indicated along the abscissas, mRNA was reversed transcribed and subjected to real-time PCR for IL-23p19 and IL-12p35. (C and F) Monolayers were transfected with scrambled (control) siRNA (3μg) or tristetraprolin (TTP)-targeting siRNA (3μg) for 2– 3 d. They were then treated with nothing or bTSH for 6 h. Monolayers were harvested, cellular RNA, extracted, reverse transcribed, and subjected to RT-PCR for IL-23p19 and IL-12p35. Values were normalized to their respective GAPDH levels and are expressed as the mean ± SD of three independent determinations. Experiments were repeated three times. *, P<0.05; **, p<0.01; ***. P<0.001.

Journal: Journal of immunology (Baltimore, Md. : 1950)

Article Title: Slit2 may underlie divergent induction by thyrotropin of IL-23 and IL-12 in human fibrocytes

doi: 10.4049/jimmunol.1900434

Figure Lengend Snippet: bTSH up-regulates IL-23p19 gene transcription and enhances IL-23p19 mRNA stability in fibrocytes while enhancing IL-12p35 gene transcription and mRNA stability in GD-OF. (A and D) Confluent monolayers of fibrocytes and GD-OF remained untreated or received bTSH (5 mIU/mL) for 2 h. Cultures were harvested and subjected to Pol II Chip transcription assay as described in “Methods”. (B and E) Confluent cultures were pre-treated with bTSH for 2 h. At time “0” all culture wells received 5,6-dichlorobenzimidazole (20 μg/mL) without or in the continued presence of bTSH. Monolayers were harvested at the times indicated along the abscissas, mRNA was reversed transcribed and subjected to real-time PCR for IL-23p19 and IL-12p35. (C and F) Monolayers were transfected with scrambled (control) siRNA (3μg) or tristetraprolin (TTP)-targeting siRNA (3μg) for 2– 3 d. They were then treated with nothing or bTSH for 6 h. Monolayers were harvested, cellular RNA, extracted, reverse transcribed, and subjected to RT-PCR for IL-23p19 and IL-12p35. Values were normalized to their respective GAPDH levels and are expressed as the mean ± SD of three independent determinations. Experiments were repeated three times. *, P<0.05; **, p<0.01; ***. P<0.001.

Techniques: Transcription Assay, Real-time Polymerase Chain Reaction, Transfection, Control, Reverse Transcription, Reverse Transcription Polymerase Chain Reaction

Induction by bTSH of IL-23p19 in fibrocytes and IL-12p35 in GD-OF is mediated through the Akt pathway. (A and C) Fibrocytes and GD-OFs were allowed to proliferate to confluence. They were pretreated with nothing or AKTi (1 μM) for 1 h, then treated without or with bTSH (5mIU/mL) for 6 h. (B, D) Cultures were transfected with control siRNA (3μg) or AKT-targeting siRNA (3μg), as described in “Methods”. Monolayers remained untreated or received bTSH for 6 h. Monolayers were harvested, RNA extracted, reverse transcribed, and subjected for real-time PCR for IL-23p19 or IL-12p35 as indicated. Values were normalized to their respective GAPDH levels and are expressed as mean ± SD, **, p<0.01 of three independent determinations.

Journal: Journal of immunology (Baltimore, Md. : 1950)

Article Title: Slit2 may underlie divergent induction by thyrotropin of IL-23 and IL-12 in human fibrocytes

doi: 10.4049/jimmunol.1900434

Figure Lengend Snippet: Induction by bTSH of IL-23p19 in fibrocytes and IL-12p35 in GD-OF is mediated through the Akt pathway. (A and C) Fibrocytes and GD-OFs were allowed to proliferate to confluence. They were pretreated with nothing or AKTi (1 μM) for 1 h, then treated without or with bTSH (5mIU/mL) for 6 h. (B, D) Cultures were transfected with control siRNA (3μg) or AKT-targeting siRNA (3μg), as described in “Methods”. Monolayers remained untreated or received bTSH for 6 h. Monolayers were harvested, RNA extracted, reverse transcribed, and subjected for real-time PCR for IL-23p19 or IL-12p35 as indicated. Values were normalized to their respective GAPDH levels and are expressed as mean ± SD, **, p<0.01 of three independent determinations.

Techniques: Transfection, Control, Reverse Transcription, Real-time Polymerase Chain Reaction

JNK pathway exerts divergent impact on the induction by bTSH of IL-23p19 and IL-12p35 in fibrocytes and GD-OF. (A and C) Confluent cultures were pretreated with nothing or JNKi (50μM) for 18 h, and then without or with bTSH (5mIU/mL) for 6 h. (B, D) Cultures were transfected with JNK-targeting siRNA (3μg) or control siRNA (3μg). Transfected cells (B, D, and F) were left untreated or were incubated with bTSH for 6 h, RNA extracted, reverse transcribed, and subjected for real-time PCR for IL-23p19 or IL-12p35. (E) Fibrocytes and GD-OF were treated with nothing or bTSH (5mIU/mL) for 30 m. Cell layers were collected, proteins subjected to Western blot analysis for pJNK and re-probed with anti-β-actin. Densitometry values: Fibrocyte control, 7.3 AU, Fibrocyte bTSH 51 AU, GD-OF control 12.4 AU, GD-OF bTSH 159.4 AU (F) Fibrocytes were transfected with a JNK expression plasmid (3μg) or its negative control (3μg) for 2–3 d. Cells were harvested and incubated without or with bTSH for 6 h. Extracted RNA was reversed transcribed and subjected to RT-PCR for IL-23p19 and or IL-12p35 levels. Results were normalized to their respective GAPDH signals. Data are expressed as mean ± SD, *, P<0.05; **, p<0.01 of three independent determinations.

Journal: Journal of immunology (Baltimore, Md. : 1950)

Article Title: Slit2 may underlie divergent induction by thyrotropin of IL-23 and IL-12 in human fibrocytes

doi: 10.4049/jimmunol.1900434

Figure Lengend Snippet: JNK pathway exerts divergent impact on the induction by bTSH of IL-23p19 and IL-12p35 in fibrocytes and GD-OF. (A and C) Confluent cultures were pretreated with nothing or JNKi (50μM) for 18 h, and then without or with bTSH (5mIU/mL) for 6 h. (B, D) Cultures were transfected with JNK-targeting siRNA (3μg) or control siRNA (3μg). Transfected cells (B, D, and F) were left untreated or were incubated with bTSH for 6 h, RNA extracted, reverse transcribed, and subjected for real-time PCR for IL-23p19 or IL-12p35. (E) Fibrocytes and GD-OF were treated with nothing or bTSH (5mIU/mL) for 30 m. Cell layers were collected, proteins subjected to Western blot analysis for pJNK and re-probed with anti-β-actin. Densitometry values: Fibrocyte control, 7.3 AU, Fibrocyte bTSH 51 AU, GD-OF control 12.4 AU, GD-OF bTSH 159.4 AU (F) Fibrocytes were transfected with a JNK expression plasmid (3μg) or its negative control (3μg) for 2–3 d. Cells were harvested and incubated without or with bTSH for 6 h. Extracted RNA was reversed transcribed and subjected to RT-PCR for IL-23p19 and or IL-12p35 levels. Results were normalized to their respective GAPDH signals. Data are expressed as mean ± SD, *, P<0.05; **, p<0.01 of three independent determinations.

Techniques: Transfection, Control, Incubation, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot, Expressing, Plasmid Preparation, Negative Control, Reverse Transcription Polymerase Chain Reaction

rhSlit2 attenuates bTSH induction of IL-23/p19 gene transcription while enhancing that of the IL-12p35 gene in fibrocytes. In contrast, knocking-down Slit2 in GD-OF enhances IL-23p19 gene transcription while attenuating that of the IL-12p35 gene. These effects are divergently affected by JNK inhibitor (JNKi). (A) Fibrocytes were incubated with nothing or rhSlit2 (50 ng/ml) for 7–9 d. (B) GD-OF monolayers were subjected to treatment with either control (3μg) siRNA or SLIT2-targeting siRNAs (3μg) for 3 d. (A, B), Cells were treated with nothing or bTSH (5 mIU/mL) for 2 h, harvested, and subjected to a Pol II Chip transcription assay as described in “Methods”. Values were normalized to respective monolayer protein content. (C) Confluent fibrocyte cultures treated without or with Slit2 for 7 d. were pre-treated with bTSH for 2 h. At time “0”, all cultures received 5,6-dichlorobenzimidazole (20 μg/mL) without or continued in the presence of bTSH. Monolayers were harvested at the times indicated along the abscissas, mRNA was reversed transcribed and subjected to real-time PCR for IL-23p19.. (D) Fibrocytes were pretreated without or with rhSlit2 (50 ng/ml) for 7 d, and were then incubated without or with bTSH (5mIU/mL) for 30 m. Cell layers were collected, proteins subjected to Western blot analysis for pJNK and then re-probed with anti-β-actin. Densitometric analysis: Control 5.4 AU, bTSH : 52.9 AU, rhSlit2 10.1 AU, bTSH plus rhSlit2 127.4 AU. rhSlit2 (50 ng/ml) treated fibrocyte cultures incubated with, nothing or JNKi (50μM) for 18 h, and then treated without or with bTSH (5mIU/mL) for 6 h. mRNA was reversed transcribed from the cell layers and subjected to real-time PCR for IL-23p19 and IL-12p35. Data are expressed as mean ± SD of triplicate determinations from a single experiment, representative of three studies performed. *, p<0.05; **, p<0.01

Journal: Journal of immunology (Baltimore, Md. : 1950)

Article Title: Slit2 may underlie divergent induction by thyrotropin of IL-23 and IL-12 in human fibrocytes

doi: 10.4049/jimmunol.1900434

Figure Lengend Snippet: rhSlit2 attenuates bTSH induction of IL-23/p19 gene transcription while enhancing that of the IL-12p35 gene in fibrocytes. In contrast, knocking-down Slit2 in GD-OF enhances IL-23p19 gene transcription while attenuating that of the IL-12p35 gene. These effects are divergently affected by JNK inhibitor (JNKi). (A) Fibrocytes were incubated with nothing or rhSlit2 (50 ng/ml) for 7–9 d. (B) GD-OF monolayers were subjected to treatment with either control (3μg) siRNA or SLIT2-targeting siRNAs (3μg) for 3 d. (A, B), Cells were treated with nothing or bTSH (5 mIU/mL) for 2 h, harvested, and subjected to a Pol II Chip transcription assay as described in “Methods”. Values were normalized to respective monolayer protein content. (C) Confluent fibrocyte cultures treated without or with Slit2 for 7 d. were pre-treated with bTSH for 2 h. At time “0”, all cultures received 5,6-dichlorobenzimidazole (20 μg/mL) without or continued in the presence of bTSH. Monolayers were harvested at the times indicated along the abscissas, mRNA was reversed transcribed and subjected to real-time PCR for IL-23p19.. (D) Fibrocytes were pretreated without or with rhSlit2 (50 ng/ml) for 7 d, and were then incubated without or with bTSH (5mIU/mL) for 30 m. Cell layers were collected, proteins subjected to Western blot analysis for pJNK and then re-probed with anti-β-actin. Densitometric analysis: Control 5.4 AU, bTSH : 52.9 AU, rhSlit2 10.1 AU, bTSH plus rhSlit2 127.4 AU. rhSlit2 (50 ng/ml) treated fibrocyte cultures incubated with, nothing or JNKi (50μM) for 18 h, and then treated without or with bTSH (5mIU/mL) for 6 h. mRNA was reversed transcribed from the cell layers and subjected to real-time PCR for IL-23p19 and IL-12p35. Data are expressed as mean ± SD of triplicate determinations from a single experiment, representative of three studies performed. *, p<0.05; **, p<0.01

Techniques: Incubation, Control, Transcription Assay, Real-time Polymerase Chain Reaction, Western Blot

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