Journal: bioRxiv

Article Title: The metabolic reprogramming of T cells controls airway remodeling in severe asthma

doi: 10.64898/2026.03.19.712985

Figure Lengend Snippet: To model EA or MGA respectively, Balb/c or Il4ra -/- mice were given five intranasal (i.n.) challenges with 100ug house dust mite (HDM) extract every week (followed by two days resting) for three consecutive weeks. A final i.n. HDM challenge was given 24 hours prior to harvest. ( A ) Lung sections were stained and representative Masson trichrome (collagen), α-smooth muscle actin (αSMA), and hematoxylin and eosin (H&E) sections and accompanying quantifications are shown. ( B ) Airway resistance to increasing doses of methacholine exposure (6-8 mice per group). (C) Expression of mRNA for IL13 and IL17, assessed by quantitative PCR analyses of lung samples. mRNA expression was calculated relative to GAPDH for 5 mice per group. ( D ) Number of neutrophils or eosinophils in the left lung lobe of EA or MGA induced mice, as assessed by flow cytometry. ( E ) MGA-induced animals were treated with 50ug dexamethasone intratracheally one hour prior to each allergen challenge, beginning on day 7. Lung sections were stained and representative Masson trichrome and αSMA sections and accompanying quantifications are shown. ( F ) Number of neutrophils or eosinophils in the left lung lobe of MGA induced mice treated with or without dexamethasone, as assessed by flow cytometry. ( G ) MGA-induced animals were treated with 100ug anti-IL17A or matching isotype control i.p. beginning on day 7 and continuing every other day until harvest. Lung sections were stained, and representative H&E sections and accompanying quantifications are shown. Trichrome data show area of interest values covering full lung section of 6 individual mice per condition. αSMA data show mean values of all bronchi scored from 6 mice per condition. Data are representative of 3 independent experiments. *P < 0.05, **P < 0.005, ***P < 0.0005, ****P < 0.00005; HPF, high-power field; ns, nonsignificant.

Article Snippet: To block IL-17 signaling, 100ug anti-IL17A (17F3; BioXCell) or matching isotype control (MOPC-21; BioXCell) were given intraperitoneally (i.p.) to HDM induced Ilr4a -/- mice beginning on day 7 and continuing every other day for a total of 7 injections.

Techniques: Staining, Expressing, Real-time Polymerase Chain Reaction, Flow Cytometry, Control

Journal: International Journal of Cardiology

Article Title: Enhanced IL-17 signalling following myocardial ischaemia/reperfusion injury

doi: 10.1016/j.ijcard.2011.08.849

Figure Lengend Snippet: Primers sequences used for qPCR analysis.

Article Snippet: In a different set of experiments rats were treated with 200 μg of anti-IL-17A polyclonal antibody intraperitoneally (R & D Systems, AF-421-NA) or PBS 2 h before undergoing in vivo ischemia/reperfusion injury.

Techniques:

Journal: International Journal of Cardiology

Article Title: Enhanced IL-17 signalling following myocardial ischaemia/reperfusion injury

doi: 10.1016/j.ijcard.2011.08.849

Figure Lengend Snippet: IL-17A, IL-17F, IL-17 receptor and IL-17 target genes are transcriptionally upregulated following in vivo I/R injury. RNA and protein was extracted from the left ventricles of rats undergoing sham operation or 25 min ischaemia and 2 h reperfusion (I/R). (A) IL-17RA, IL-17A and IL-17F expression was measured by qPCR. (B) IL-17A and IL-17RA protein levels were assessed by western blot, GAPDH was used as a loading control. (C) Expression of the IL-17 target genes IL-6, IL-1, iNOS and MMP-9 was measured by qPCR.

Article Snippet: In a different set of experiments rats were treated with 200 μg of anti-IL-17A polyclonal antibody intraperitoneally (R & D Systems, AF-421-NA) or PBS 2 h before undergoing in vivo ischemia/reperfusion injury.

Techniques: In Vivo, Expressing, Western Blot, Control

Journal: International Journal of Cardiology

Article Title: Enhanced IL-17 signalling following myocardial ischaemia/reperfusion injury

doi: 10.1016/j.ijcard.2011.08.849

Figure Lengend Snippet: IL-17 induces Cxcl1, IL-6 and Socs3 expression in cardiac myocytes. Neonatal rat ventricular myocytes were treated with 10 ng/ml IL-17 for the indicated times and the levels of (A) Cxcl1, (B) IL-6, (C) MCP-1 and (D) Socs3 were measured by qPCR. Experiments were repeated in duplicate, statistical analysis was carried out using a one-way ANOVA followed by Dunnett's post test, *p < 0.05, **p < 0.01, ***p < 0.001. (E) I/R injury and IL-17 have additive effects on Cxcl1 expression. NRVMs were subjected to 4 h ischaemia and 6 h reperfusion with or without 10 ng/ml IL-17 which was added at the time of reperfusion. The expression of Cxcl1 was analysed by qPCR. Statistical analysis was carried out using student's t -test. **p < 0.01, **p < 0.001.

Article Snippet: In a different set of experiments rats were treated with 200 μg of anti-IL-17A polyclonal antibody intraperitoneally (R & D Systems, AF-421-NA) or PBS 2 h before undergoing in vivo ischemia/reperfusion injury.

Techniques: Expressing

Journal: International Journal of Cardiology

Article Title: Enhanced IL-17 signalling following myocardial ischaemia/reperfusion injury

doi: 10.1016/j.ijcard.2011.08.849

Figure Lengend Snippet: IL-17 mediated upregulation of Cxcl1 and IL-6 in cardiac myocytes is MAPK dependent. (A) NRVMs were treated with 10 ng/ml IL-17 for the indicated times and cell lysates were analysed by Western blot using the indicated antibodies. (B) NRVMs were pre-treated for 30 min with the indicated inhibitors followed by IL-17 stimulation for 6 h. The expression of Cxcl1 and IL-6 was measured by qPCR. Statistical analysis was carried out using a student's t -test. *p < 0.05, **p < 0.01, **p < 0.001.

Article Snippet: In a different set of experiments rats were treated with 200 μg of anti-IL-17A polyclonal antibody intraperitoneally (R & D Systems, AF-421-NA) or PBS 2 h before undergoing in vivo ischemia/reperfusion injury.

Techniques: Western Blot, Expressing

Journal: International Journal of Cardiology

Article Title: Enhanced IL-17 signalling following myocardial ischaemia/reperfusion injury

doi: 10.1016/j.ijcard.2011.08.849

Figure Lengend Snippet: IL-17 receptor and IL-17F are transcriptionally upregulated in cardiac myocytes. (A) NRVM were subjected to 4 h in vitro ischaemia and up to 24 h reperfusion in normal media after which the levels of IL-17 receptor and IL-17F were assessed by qPCR. (B) H9c2 cells were subjected to in vitro I/R for the indicated times and the levels of IL-17F and Cxcl1 were measured by qPCR. (C) NRVMs were treated with 200 μM H 2 O 2 for 6 h and the expression of the indicated genes was measured by qPCR. (D) NRMVs were transduced with STAT3C adenovirus at MOI = 100. After 48 h, increased expression of STAT3 was confirmed by Western blot and IL-17F expression was measured by qPCR. *p < 0.05, **p < 0.01, ***p < 0.001, student's t -test, n = 3 per group, repeated in duplicate.

Article Snippet: In a different set of experiments rats were treated with 200 μg of anti-IL-17A polyclonal antibody intraperitoneally (R & D Systems, AF-421-NA) or PBS 2 h before undergoing in vivo ischemia/reperfusion injury.

Techniques: In Vitro, Expressing, Transduction, Western Blot

Journal: International Journal of Cardiology

Article Title: Enhanced IL-17 signalling following myocardial ischaemia/reperfusion injury

doi: 10.1016/j.ijcard.2011.08.849

Figure Lengend Snippet: Blocking IL-17 signalling with a specific anti-IL-17 neutralizing antibody reduced creatine phosphokinase and apoptotic cell death in the myocardium following in vivo I/R injury. Plasma concentration of CPK (A) and apoptosis assessed by the TUNEL assay (B) in sham-operated (control) or rats exposed to in vivo I/R injury (I/R) or I/R plus treatment with IL-17 neutralizing antibody (IL-17 Bo Ab). Immunofluorescence data (left panel) (Data are mean of ± 6 rats **P < 0.001). Anti-IL-17 neutralizing antibody also reduced the increase in cleaved/active caspase-3 expression following in vivo I/R injury (C). Western blot analysis was performed on tissue lysates prepared as in Fig. 3 A above and immunoblotted with a specific antibody against the cleaved and active form of caspase-3 and GAPDH.

Article Snippet: In a different set of experiments rats were treated with 200 μg of anti-IL-17A polyclonal antibody intraperitoneally (R & D Systems, AF-421-NA) or PBS 2 h before undergoing in vivo ischemia/reperfusion injury.

Techniques: Blocking Assay, In Vivo, Clinical Proteomics, Concentration Assay, TUNEL Assay, Control, Immunofluorescence, Expressing, Western Blot

Journal: Military Medical Research

Article Title: High-salt-driven gut microbiota dysfunction aggravates prostatitis by promoting AHR/SGK1/FOXO1 axis-mediated Th17 cell differentiation

doi: 10.1186/s40779-025-00607-1

Figure Lengend Snippet: HSD promoted Th17 cell development and worsened prostate inflammation in EAP mice. a Simple schematic diagram of the implementation plan of the experiment. b HE staining and inflammation scores of prostate tissues (scale bar = 100 μm, n = 4). c Tactile allodynia development in the 4 groups of mice ( n = 4). d The levels of IL-1β, TNF-α, IL-17A, and IFN-γ in the serum of the mice in the 4 groups ( n = 4). e Proportion of Th1 and Th17 cells of CD4 + T cells detected by flow cytometry in the splenic lymphocytes of vaccinated mice from those 4 groups ( n = 4). f The infiltration of Th17 cells in prostate tissues from mice was determined by immunofluorescence (white arrowheads, scale bar = 100 μm, n = 4). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001; ns non-significant. BF breeding feed, EAP experimental autoimmune prostatitis, HSD high-salt diet, NSD normal-salt diet, IL-1β interleukin-1β, TNF-α tumor necrosis factor-α, IFN-γ interferon-γ, IL-17A interleukin-17A, DAPI 4',6-diamidino-2-phenylindole, Th T helper

Article Snippet: The following reagents and antibodies were used: CFA (#F5881, Sigma, USA); commercial enzyme-linked immunosorbent assay (ELISA) kits for IFN-γ (#E-EL-M0048c), IL-1β (#E-EL-M0037), IL-17A (#E-EL-M0047c), tumor necrosis factor-α (TNF-α, #E-EL-M3063), and 5-HIAA (#E-EL-0075c) (Elabscience, China); anti-mouse CD4-fluorescein isothiocyanate (FITC, #553047), CD3e-allophycocyanin (APC, #561826), IFN-γ-phycoerythrin (PE, #562020), IL-17-PE (#559502), anti-human CD8-FITC (#555634), CD3-APC (#555342), IL-17-PE (#560436) (BD, USA); anti-CD3e (#BE0001-1), anti-CD28 (#BE0015-1), anti-IFN-γ (#BE0055), anti-IL-4 (#BE0045) (Bio X Cell, USA); IL-23 (#CS31), transforming growth factor-β1 (TGF-β1, #CA59), IL-6 (#CG39) (Novoprotein, China); anti-AHR (1:1000, #NB100-128, Novus, USA); anti-SGK1 (1:1000, #AF6789), anti-FOXO1 (1:1000, #AF6416), anti-p-FOXO1 (1:1000, #AF3417), anti-retinoic acid receptor-related orphan receptor gamma-t (RORγt; 1:1000, #DF3196), and anti-GAPDH (1:5000, #AF7021) (Affinity, USA).

Techniques: Staining, Flow Cytometry, Immunofluorescence

Journal: Military Medical Research

Article Title: High-salt-driven gut microbiota dysfunction aggravates prostatitis by promoting AHR/SGK1/FOXO1 axis-mediated Th17 cell differentiation

doi: 10.1186/s40779-025-00607-1

Figure Lengend Snippet: Transplantation of fecal microbiota from EAP mice with HSD elicited more severe prostate inflammation in psuedogerm-free mice. a Simple schematic diagram of the experimental workflow. b HE staining and inflammation scores of prostate tissues (scale bar = 100 μm, n = 4). c Development of tactile allodynia in mice belonging to the 4 groups ( n = 4). d The concentrations of IL-1β, TNF-α, IL-17A, and 5-HIAA in the serum of NOD mice in the 4 groups were measured ( n = 4). e Proportion of Th17 of CD4 + T cells, as determined by flow cytometry, among the splenic lymphocytes of immunized mice in the 4 groups ( n = 4). f The infiltration of Th17 cells in prostate tissues from mice was determined by immunofluorescence (white arrowheads, scale bar = 100 μm, n = 4). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001; ns non-significant. NOD nonobese male diabetic/LtJ, EAP experimental autoimmune prostatitis, HSD high-salt diet, NSD normal-salt diet, FMT fecal microbiota transplantation, HE hematoxylin–eosin, IL-1β interleukin-1β, TNF-α tumor necrosis factor-α, IL-17A interleukin-17A, 5-HIAA 5-hydroxyindole acetic acid, DAPI 4',6-diamidino-2-phenylindole

Article Snippet: The following reagents and antibodies were used: CFA (#F5881, Sigma, USA); commercial enzyme-linked immunosorbent assay (ELISA) kits for IFN-γ (#E-EL-M0048c), IL-1β (#E-EL-M0037), IL-17A (#E-EL-M0047c), tumor necrosis factor-α (TNF-α, #E-EL-M3063), and 5-HIAA (#E-EL-0075c) (Elabscience, China); anti-mouse CD4-fluorescein isothiocyanate (FITC, #553047), CD3e-allophycocyanin (APC, #561826), IFN-γ-phycoerythrin (PE, #562020), IL-17-PE (#559502), anti-human CD8-FITC (#555634), CD3-APC (#555342), IL-17-PE (#560436) (BD, USA); anti-CD3e (#BE0001-1), anti-CD28 (#BE0015-1), anti-IFN-γ (#BE0055), anti-IL-4 (#BE0045) (Bio X Cell, USA); IL-23 (#CS31), transforming growth factor-β1 (TGF-β1, #CA59), IL-6 (#CG39) (Novoprotein, China); anti-AHR (1:1000, #NB100-128, Novus, USA); anti-SGK1 (1:1000, #AF6789), anti-FOXO1 (1:1000, #AF6416), anti-p-FOXO1 (1:1000, #AF3417), anti-retinoic acid receptor-related orphan receptor gamma-t (RORγt; 1:1000, #DF3196), and anti-GAPDH (1:5000, #AF7021) (Affinity, USA).

Techniques: Transplantation Assay, Staining, Flow Cytometry, Immunofluorescence

Journal: Military Medical Research

Article Title: High-salt-driven gut microbiota dysfunction aggravates prostatitis by promoting AHR/SGK1/FOXO1 axis-mediated Th17 cell differentiation

doi: 10.1186/s40779-025-00607-1

Figure Lengend Snippet: 5-HIAA supplementation ameliorated the symptoms of EAP caused by HSD. a The levels of 5-HIAA secreted into the serum of the mice were measured in 4 groups: Ctrl + NSD, Ctrl + HSD, EAP + NSD, and EAP + HSD groups ( n = 4). b Simple schematic diagram of the experimental workflow. c HE staining and inflammation scores of prostate tissues (scale bar = 100 μm, n = 4). d Tactile allodynia development in NOD mice in the 4 groups ( n = 4). e Secretion levels of IL-1β, TNF-α, and IL-17A in the serum of mice in the 5 groups ( n = 4). f Flow cytometry was used to determine the proportion of Th17 of CD4 + T cells among the splenic lymphocytes of immunized mice in the 5 groups ( n = 4). g The infiltration of Th17 cells in prostate tissues from mice was determined by immunofluorescence (white arrowheads, scale bar = 100 μm, n = 4). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001; ns non-significant. NOD nonobese male diabetic/LtJ, BF breeding feed, EAP experimental autoimmune prostatitis, HSD high-salt diet, NSD normal-salt diet, HE hematoxylin–eosin, IL-1β interleukin-1β, TNF-α tumor necrosis factor-α, IL-17A interleukin-17A, 5-HIAA 5-hydroxyindole acetic acid, DAPI 4',6-diamidino-2-phenylindole

Article Snippet: The following reagents and antibodies were used: CFA (#F5881, Sigma, USA); commercial enzyme-linked immunosorbent assay (ELISA) kits for IFN-γ (#E-EL-M0048c), IL-1β (#E-EL-M0037), IL-17A (#E-EL-M0047c), tumor necrosis factor-α (TNF-α, #E-EL-M3063), and 5-HIAA (#E-EL-0075c) (Elabscience, China); anti-mouse CD4-fluorescein isothiocyanate (FITC, #553047), CD3e-allophycocyanin (APC, #561826), IFN-γ-phycoerythrin (PE, #562020), IL-17-PE (#559502), anti-human CD8-FITC (#555634), CD3-APC (#555342), IL-17-PE (#560436) (BD, USA); anti-CD3e (#BE0001-1), anti-CD28 (#BE0015-1), anti-IFN-γ (#BE0055), anti-IL-4 (#BE0045) (Bio X Cell, USA); IL-23 (#CS31), transforming growth factor-β1 (TGF-β1, #CA59), IL-6 (#CG39) (Novoprotein, China); anti-AHR (1:1000, #NB100-128, Novus, USA); anti-SGK1 (1:1000, #AF6789), anti-FOXO1 (1:1000, #AF6416), anti-p-FOXO1 (1:1000, #AF3417), anti-retinoic acid receptor-related orphan receptor gamma-t (RORγt; 1:1000, #DF3196), and anti-GAPDH (1:5000, #AF7021) (Affinity, USA).

Techniques: Staining, Flow Cytometry, Immunofluorescence

Journal: Military Medical Research

Article Title: High-salt-driven gut microbiota dysfunction aggravates prostatitis by promoting AHR/SGK1/FOXO1 axis-mediated Th17 cell differentiation

doi: 10.1186/s40779-025-00607-1

Figure Lengend Snippet: Inhibition of AHR abrogated the protective effects of 5-HIAA supplementation on EAP mice fed an HSD. a AHR levels in prostate tissues of mice among the Ctrl + NSD, Ctrl + HSD, EAP + NSD, EAP + HSD, and EAP + HSD + 5-HIAA groups ( n = 4). b A simple schematic diagram of the experimental workflow. c HE staining and inflammation scores of prostate tissues (scale bar = 100 μm, n = 4). d Tactile allodynia development in the mice from the Ctrl + NSD, Ctrl + HSD, EAP + NSD, EAP + HSD, EAP + HSD + 5-HIAA, and EAP + HSD + 5-HIAA + CH groups ( n = 4). e The levels of IL-1β, TNF-α, and IL-17A in the serum of the mice in the 6 groups ( n = 4). f Proportion of Th17 of CD4 + T cells, as determined by flow cytometry, among the splenic lymphocytes of immunized mice in the 6 groups (white arrowheads, n = 4). g The infiltration of Th17 cells in prostate tissues from mice was evaluated by immunofluorescence (scale bar = 100 μm, n = 4). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001; ns non-significant. NOD nonobese male diabetic/LtJ, BF breeding feed, EAP experimental autoimmune prostatitis, HSD high-salt diet, NSD normal-salt diet, CH CH223191 (an AHR inhibitor), HE hematoxylin–eosin, IL-1β interleukin-1β, TNF-α tumor necrosis factor-α, IL-17A interleukin-17A, 5-HIAA 5-hydroxyindole acetic acid, AHR aryl hydrocarbon receptor, DAPI 4',6-diamidino-2-phenylindole

Article Snippet: The following reagents and antibodies were used: CFA (#F5881, Sigma, USA); commercial enzyme-linked immunosorbent assay (ELISA) kits for IFN-γ (#E-EL-M0048c), IL-1β (#E-EL-M0037), IL-17A (#E-EL-M0047c), tumor necrosis factor-α (TNF-α, #E-EL-M3063), and 5-HIAA (#E-EL-0075c) (Elabscience, China); anti-mouse CD4-fluorescein isothiocyanate (FITC, #553047), CD3e-allophycocyanin (APC, #561826), IFN-γ-phycoerythrin (PE, #562020), IL-17-PE (#559502), anti-human CD8-FITC (#555634), CD3-APC (#555342), IL-17-PE (#560436) (BD, USA); anti-CD3e (#BE0001-1), anti-CD28 (#BE0015-1), anti-IFN-γ (#BE0055), anti-IL-4 (#BE0045) (Bio X Cell, USA); IL-23 (#CS31), transforming growth factor-β1 (TGF-β1, #CA59), IL-6 (#CG39) (Novoprotein, China); anti-AHR (1:1000, #NB100-128, Novus, USA); anti-SGK1 (1:1000, #AF6789), anti-FOXO1 (1:1000, #AF6416), anti-p-FOXO1 (1:1000, #AF3417), anti-retinoic acid receptor-related orphan receptor gamma-t (RORγt; 1:1000, #DF3196), and anti-GAPDH (1:5000, #AF7021) (Affinity, USA).

Techniques: Inhibition, Staining, Flow Cytometry, Immunofluorescence

Journal: Military Medical Research

Article Title: High-salt-driven gut microbiota dysfunction aggravates prostatitis by promoting AHR/SGK1/FOXO1 axis-mediated Th17 cell differentiation

doi: 10.1186/s40779-025-00607-1

Figure Lengend Snippet: HSD promoted the differentiation of Th17 cells by activating SGK1/FOXO1 signaling pathway. a The in vitro Th17 cell differentiation ratio was determined by flow cytometry ( n = 3). b Th17 cell differentiation ratio was determined in an in vitro differentiation experiment using immunofluorescence (scale bar = 100 μm, n = 3). c SGK1, p-FOXO1, and FOXO1 levels in prostate tissues from Ctrl + NSD, Ctrl + HSD, EAP + NSD, EAP + HSD, and EAP + HSD + 5-HIAA mice ( n = 4). d AHR, SGK1, p-FOXO1, and FOXO1 levels in prostate tissues of mice in the EAP + HSD + 5-HIAA and EAP + HSD + 5-HIAA + CH groups ( n = 4). e AHR, SGK1, p-FOXO1, and FOXO1 levels in naïve CD4 + T cells of Ctrl, Sti, Sti + HSD, Sti + HSD + 5-HIAA, Sti + HSD + 5-HIAA + CH groups ( n = 3). f Transcriptional levels of Sgk1 in naïve CD4 + T cells of Ctrl, Sti, Sti + HSD, Sti + HSD + 5-HIAA, Sti + HSD + 5-HIAA + CH groups (n = 3). g For the ChIP-qPCR assay, 3 potential enhancer segments of the mouse promoter region of Sgk1 were created. h qPCR was used to assess the immunoprecipitated DNA by a ChIP assay ( n = 3). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001; ns non-significant. EAP experimental autoimmune prostatitis, HSD high-salt diet, NSD normal-salt diet, IL-17A interleukin-17A, 5-HIAA 5-hydroxyindole acetic acid, AHR aryl hydrocarbon receptor, SGK1 serum and glucocorticoid-regulated kinase 1, FOXO1 forkhead box protein O1, CH CH223191 (an AHR inhibitor), ChIP chromatin immunoprecipitation, qPCR quantitative polymerase chain reaction, DAPI 4’,6-diamidino-2-phenylindole, Sti stimulation with IL-6, IL-23, TGF-β, anti-IFN-γ, and anti-IL-4

Article Snippet: The following reagents and antibodies were used: CFA (#F5881, Sigma, USA); commercial enzyme-linked immunosorbent assay (ELISA) kits for IFN-γ (#E-EL-M0048c), IL-1β (#E-EL-M0037), IL-17A (#E-EL-M0047c), tumor necrosis factor-α (TNF-α, #E-EL-M3063), and 5-HIAA (#E-EL-0075c) (Elabscience, China); anti-mouse CD4-fluorescein isothiocyanate (FITC, #553047), CD3e-allophycocyanin (APC, #561826), IFN-γ-phycoerythrin (PE, #562020), IL-17-PE (#559502), anti-human CD8-FITC (#555634), CD3-APC (#555342), IL-17-PE (#560436) (BD, USA); anti-CD3e (#BE0001-1), anti-CD28 (#BE0015-1), anti-IFN-γ (#BE0055), anti-IL-4 (#BE0045) (Bio X Cell, USA); IL-23 (#CS31), transforming growth factor-β1 (TGF-β1, #CA59), IL-6 (#CG39) (Novoprotein, China); anti-AHR (1:1000, #NB100-128, Novus, USA); anti-SGK1 (1:1000, #AF6789), anti-FOXO1 (1:1000, #AF6416), anti-p-FOXO1 (1:1000, #AF3417), anti-retinoic acid receptor-related orphan receptor gamma-t (RORγt; 1:1000, #DF3196), and anti-GAPDH (1:5000, #AF7021) (Affinity, USA).

Techniques: In Vitro, Cell Differentiation, Flow Cytometry, Immunofluorescence, ChIP-qPCR, Immunoprecipitation, Chromatin Immunoprecipitation, Real-time Polymerase Chain Reaction