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cxcl10  (R&D Systems)


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    R&D Systems cxcl10
    Cxcl10, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 21 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cxcl10+protein/pm41891183-606-80-81?v=R%26D+Systems
    Average 94 stars, based on 21 article reviews
    cxcl10 - by Bioz Stars, 2026-07
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    MMTs recruit a large number of MDSCs through <t>CXCL10</t> pathway. A Significantly upregulated genes in MMTs versus non-MMT fibroblasts from OSCC database (GSA-Human: HRA007439). B Differences in CXCL10 expression between non-MMT fibroblasts and MMTs were demonstrated in HNSCC (figure S1). C CXCL10 expression and release were detected by PCR and ELISA. D-H Exogenous CXCL10 was added to BMDMs, while the CXCL10 inhibitor AMG487 was administered to MMTs, followed by co-culturing with MDSCs. The migration of MDSCs was evaluated using transwell chambers and crystal violet staining ( D ). Flow cytometry was used to detect cell apoptosis ( E ), macrophage markers (F4/80 + CD11b + ) ( F ), as well as CFSE for assessing T cell proliferation inhibition ( G ). PCR and ELISA were employed to measure the expression of immunosuppressive factors IL10 and iNOS ( H ). I, J Tumor tissue photographs ( I ) and the tumor growth curve were taken and subjected to statistical analysis regarding volume and weight ( J ). K-M Flow cytometry was used to detect the proportion of MDSCs in the spleen ( K ) and tumors ( L ) of each group, while immunofluorescence staining ( M ) revealed the densest field of MDSCs within the tumor tissues across all groups. Data are expressed as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs experimental group. “ns” represents no statistical significance. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
    Cxcl10, supplied by Boster Bio, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    mouse interferon gamma induced protein 10 kda  (Elabscience Biotechnology)
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    MMTs recruit a large number of MDSCs through <t>CXCL10</t> pathway. A Significantly upregulated genes in MMTs versus non-MMT fibroblasts from OSCC database (GSA-Human: HRA007439). B Differences in CXCL10 expression between non-MMT fibroblasts and MMTs were demonstrated in HNSCC (figure S1). C CXCL10 expression and release were detected by PCR and ELISA. D-H Exogenous CXCL10 was added to BMDMs, while the CXCL10 inhibitor AMG487 was administered to MMTs, followed by co-culturing with MDSCs. The migration of MDSCs was evaluated using transwell chambers and crystal violet staining ( D ). Flow cytometry was used to detect cell apoptosis ( E ), macrophage markers (F4/80 + CD11b + ) ( F ), as well as CFSE for assessing T cell proliferation inhibition ( G ). PCR and ELISA were employed to measure the expression of immunosuppressive factors IL10 and iNOS ( H ). I, J Tumor tissue photographs ( I ) and the tumor growth curve were taken and subjected to statistical analysis regarding volume and weight ( J ). K-M Flow cytometry was used to detect the proportion of MDSCs in the spleen ( K ) and tumors ( L ) of each group, while immunofluorescence staining ( M ) revealed the densest field of MDSCs within the tumor tissues across all groups. Data are expressed as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs experimental group. “ns” represents no statistical significance. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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    cxcl10  (Elabscience Biotechnology)
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    MMTs recruit a large number of MDSCs through <t>CXCL10</t> pathway. A Significantly upregulated genes in MMTs versus non-MMT fibroblasts from OSCC database (GSA-Human: HRA007439). B Differences in CXCL10 expression between non-MMT fibroblasts and MMTs were demonstrated in HNSCC (figure S1). C CXCL10 expression and release were detected by PCR and ELISA. D-H Exogenous CXCL10 was added to BMDMs, while the CXCL10 inhibitor AMG487 was administered to MMTs, followed by co-culturing with MDSCs. The migration of MDSCs was evaluated using transwell chambers and crystal violet staining ( D ). Flow cytometry was used to detect cell apoptosis ( E ), macrophage markers (F4/80 + CD11b + ) ( F ), as well as CFSE for assessing T cell proliferation inhibition ( G ). PCR and ELISA were employed to measure the expression of immunosuppressive factors IL10 and iNOS ( H ). I, J Tumor tissue photographs ( I ) and the tumor growth curve were taken and subjected to statistical analysis regarding volume and weight ( J ). K-M Flow cytometry was used to detect the proportion of MDSCs in the spleen ( K ) and tumors ( L ) of each group, while immunofluorescence staining ( M ) revealed the densest field of MDSCs within the tumor tissues across all groups. Data are expressed as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs experimental group. “ns” represents no statistical significance. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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    mouse ip  (Elabscience Biotechnology)
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    MMTs recruit a large number of MDSCs through <t>CXCL10</t> pathway. A Significantly upregulated genes in MMTs versus non-MMT fibroblasts from OSCC database (GSA-Human: HRA007439). B Differences in CXCL10 expression between non-MMT fibroblasts and MMTs were demonstrated in HNSCC (figure S1). C CXCL10 expression and release were detected by PCR and ELISA. D-H Exogenous CXCL10 was added to BMDMs, while the CXCL10 inhibitor AMG487 was administered to MMTs, followed by co-culturing with MDSCs. The migration of MDSCs was evaluated using transwell chambers and crystal violet staining ( D ). Flow cytometry was used to detect cell apoptosis ( E ), macrophage markers (F4/80 + CD11b + ) ( F ), as well as CFSE for assessing T cell proliferation inhibition ( G ). PCR and ELISA were employed to measure the expression of immunosuppressive factors IL10 and iNOS ( H ). I, J Tumor tissue photographs ( I ) and the tumor growth curve were taken and subjected to statistical analysis regarding volume and weight ( J ). K-M Flow cytometry was used to detect the proportion of MDSCs in the spleen ( K ) and tumors ( L ) of each group, while immunofluorescence staining ( M ) revealed the densest field of MDSCs within the tumor tissues across all groups. Data are expressed as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs experimental group. “ns” represents no statistical significance. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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    MMTs recruit a large number of MDSCs through <t>CXCL10</t> pathway. A Significantly upregulated genes in MMTs versus non-MMT fibroblasts from OSCC database (GSA-Human: HRA007439). B Differences in CXCL10 expression between non-MMT fibroblasts and MMTs were demonstrated in HNSCC (figure S1). C CXCL10 expression and release were detected by PCR and ELISA. D-H Exogenous CXCL10 was added to BMDMs, while the CXCL10 inhibitor AMG487 was administered to MMTs, followed by co-culturing with MDSCs. The migration of MDSCs was evaluated using transwell chambers and crystal violet staining ( D ). Flow cytometry was used to detect cell apoptosis ( E ), macrophage markers (F4/80 + CD11b + ) ( F ), as well as CFSE for assessing T cell proliferation inhibition ( G ). PCR and ELISA were employed to measure the expression of immunosuppressive factors IL10 and iNOS ( H ). I, J Tumor tissue photographs ( I ) and the tumor growth curve were taken and subjected to statistical analysis regarding volume and weight ( J ). K-M Flow cytometry was used to detect the proportion of MDSCs in the spleen ( K ) and tumors ( L ) of each group, while immunofluorescence staining ( M ) revealed the densest field of MDSCs within the tumor tissues across all groups. Data are expressed as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs experimental group. “ns” represents no statistical significance. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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    MMTs recruit a large number of MDSCs through <t>CXCL10</t> pathway. A Significantly upregulated genes in MMTs versus non-MMT fibroblasts from OSCC database (GSA-Human: HRA007439). B Differences in CXCL10 expression between non-MMT fibroblasts and MMTs were demonstrated in HNSCC (figure S1). C CXCL10 expression and release were detected by PCR and ELISA. D-H Exogenous CXCL10 was added to BMDMs, while the CXCL10 inhibitor AMG487 was administered to MMTs, followed by co-culturing with MDSCs. The migration of MDSCs was evaluated using transwell chambers and crystal violet staining ( D ). Flow cytometry was used to detect cell apoptosis ( E ), macrophage markers (F4/80 + CD11b + ) ( F ), as well as CFSE for assessing T cell proliferation inhibition ( G ). PCR and ELISA were employed to measure the expression of immunosuppressive factors IL10 and iNOS ( H ). I, J Tumor tissue photographs ( I ) and the tumor growth curve were taken and subjected to statistical analysis regarding volume and weight ( J ). K-M Flow cytometry was used to detect the proportion of MDSCs in the spleen ( K ) and tumors ( L ) of each group, while immunofluorescence staining ( M ) revealed the densest field of MDSCs within the tumor tissues across all groups. Data are expressed as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs experimental group. “ns” represents no statistical significance. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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    human cxcl10 elisa kit  (Elabscience Biotechnology)
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    MMTs recruit a large number of MDSCs through <t>CXCL10</t> pathway. A Significantly upregulated genes in MMTs versus non-MMT fibroblasts from OSCC database (GSA-Human: HRA007439). B Differences in CXCL10 expression between non-MMT fibroblasts and MMTs were demonstrated in HNSCC (figure S1). C CXCL10 expression and release were detected by PCR and ELISA. D-H Exogenous CXCL10 was added to BMDMs, while the CXCL10 inhibitor AMG487 was administered to MMTs, followed by co-culturing with MDSCs. The migration of MDSCs was evaluated using transwell chambers and crystal violet staining ( D ). Flow cytometry was used to detect cell apoptosis ( E ), macrophage markers (F4/80 + CD11b + ) ( F ), as well as CFSE for assessing T cell proliferation inhibition ( G ). PCR and ELISA were employed to measure the expression of immunosuppressive factors IL10 and iNOS ( H ). I, J Tumor tissue photographs ( I ) and the tumor growth curve were taken and subjected to statistical analysis regarding volume and weight ( J ). K-M Flow cytometry was used to detect the proportion of MDSCs in the spleen ( K ) and tumors ( L ) of each group, while immunofluorescence staining ( M ) revealed the densest field of MDSCs within the tumor tissues across all groups. Data are expressed as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs experimental group. “ns” represents no statistical significance. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
    Human Cxcl10 Elisa Kit, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ( A and B ) Flow cytometry and statistical analysis of CD8 + CD45 + T cells in the mouse tail epidermis and dermis of vehicle, 6-OHDA, and 6-OHDA + NE groups ( n =3 per group). ( C and D ) Flow cytometry and statistical analysis of IFN-γ + CD8 + T cells in the mouse tail epidermis and dermis of vehicle, 6-OHDA, and 6-OHDA + NE groups ( n =3 per group). ( E and F ) Flow cytometry and statistical analysis of Granzyme B + CD8 + T cells in the mouse tail epidermis and dermis of vehicle, 6-OHDA, and 6-OHDA + NE groups ( n =3 per group). ( G ) The secretion levels of CXCL9, <t>CXCL10,</t> IL-6, and IL-15 in the tail skin of mice in the vehicle, 6-OHDA, and 6-OHDA + NE groups were detected by ELISA ( n =4 per group). All vehicle mice were only treated with 0.1% ascorbic acid in 0.9% sterile NaCl. Error bars represent mean ± SD from three independent experiments. * P < 0.05, ** P < 0.01, and *** P < 0.001.
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    respective enzyme linked immunosorbent assay elisa kits  (Elabscience Biotechnology)
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    ( A and B ) Flow cytometry and statistical analysis of CD8 + CD45 + T cells in the mouse tail epidermis and dermis of vehicle, 6-OHDA, and 6-OHDA + NE groups ( n =3 per group). ( C and D ) Flow cytometry and statistical analysis of IFN-γ + CD8 + T cells in the mouse tail epidermis and dermis of vehicle, 6-OHDA, and 6-OHDA + NE groups ( n =3 per group). ( E and F ) Flow cytometry and statistical analysis of Granzyme B + CD8 + T cells in the mouse tail epidermis and dermis of vehicle, 6-OHDA, and 6-OHDA + NE groups ( n =3 per group). ( G ) The secretion levels of CXCL9, <t>CXCL10,</t> IL-6, and IL-15 in the tail skin of mice in the vehicle, 6-OHDA, and 6-OHDA + NE groups were detected by ELISA ( n =4 per group). All vehicle mice were only treated with 0.1% ascorbic acid in 0.9% sterile NaCl. Error bars represent mean ± SD from three independent experiments. * P < 0.05, ** P < 0.01, and *** P < 0.001.
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    MMTs recruit a large number of MDSCs through CXCL10 pathway. A Significantly upregulated genes in MMTs versus non-MMT fibroblasts from OSCC database (GSA-Human: HRA007439). B Differences in CXCL10 expression between non-MMT fibroblasts and MMTs were demonstrated in HNSCC (figure S1). C CXCL10 expression and release were detected by PCR and ELISA. D-H Exogenous CXCL10 was added to BMDMs, while the CXCL10 inhibitor AMG487 was administered to MMTs, followed by co-culturing with MDSCs. The migration of MDSCs was evaluated using transwell chambers and crystal violet staining ( D ). Flow cytometry was used to detect cell apoptosis ( E ), macrophage markers (F4/80 + CD11b + ) ( F ), as well as CFSE for assessing T cell proliferation inhibition ( G ). PCR and ELISA were employed to measure the expression of immunosuppressive factors IL10 and iNOS ( H ). I, J Tumor tissue photographs ( I ) and the tumor growth curve were taken and subjected to statistical analysis regarding volume and weight ( J ). K-M Flow cytometry was used to detect the proportion of MDSCs in the spleen ( K ) and tumors ( L ) of each group, while immunofluorescence staining ( M ) revealed the densest field of MDSCs within the tumor tissues across all groups. Data are expressed as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs experimental group. “ns” represents no statistical significance. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

    Journal: Journal of Advanced Research

    Article Title: The pro-cancer and immunosuppressive activity of macrophage-transformed cancer-associated fibroblasts in oral squamous cell carcinoma

    doi: 10.1016/j.jare.2025.07.027

    Figure Lengend Snippet: MMTs recruit a large number of MDSCs through CXCL10 pathway. A Significantly upregulated genes in MMTs versus non-MMT fibroblasts from OSCC database (GSA-Human: HRA007439). B Differences in CXCL10 expression between non-MMT fibroblasts and MMTs were demonstrated in HNSCC (figure S1). C CXCL10 expression and release were detected by PCR and ELISA. D-H Exogenous CXCL10 was added to BMDMs, while the CXCL10 inhibitor AMG487 was administered to MMTs, followed by co-culturing with MDSCs. The migration of MDSCs was evaluated using transwell chambers and crystal violet staining ( D ). Flow cytometry was used to detect cell apoptosis ( E ), macrophage markers (F4/80 + CD11b + ) ( F ), as well as CFSE for assessing T cell proliferation inhibition ( G ). PCR and ELISA were employed to measure the expression of immunosuppressive factors IL10 and iNOS ( H ). I, J Tumor tissue photographs ( I ) and the tumor growth curve were taken and subjected to statistical analysis regarding volume and weight ( J ). K-M Flow cytometry was used to detect the proportion of MDSCs in the spleen ( K ) and tumors ( L ) of each group, while immunofluorescence staining ( M ) revealed the densest field of MDSCs within the tumor tissues across all groups. Data are expressed as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs experimental group. “ns” represents no statistical significance. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

    Article Snippet: According to the manufacturer's instructions, the cytokine concentrations of TGFβ1, iNOS, IL-10, and CXCL10 in the supernatant were determined using ELISA kits (Boster, California, USA).

    Techniques: Expressing, Enzyme-linked Immunosorbent Assay, Migration, Staining, Flow Cytometry, Inhibition, Immunofluorescence

    ( A and B ) Flow cytometry and statistical analysis of CD8 + CD45 + T cells in the mouse tail epidermis and dermis of vehicle, 6-OHDA, and 6-OHDA + NE groups ( n =3 per group). ( C and D ) Flow cytometry and statistical analysis of IFN-γ + CD8 + T cells in the mouse tail epidermis and dermis of vehicle, 6-OHDA, and 6-OHDA + NE groups ( n =3 per group). ( E and F ) Flow cytometry and statistical analysis of Granzyme B + CD8 + T cells in the mouse tail epidermis and dermis of vehicle, 6-OHDA, and 6-OHDA + NE groups ( n =3 per group). ( G ) The secretion levels of CXCL9, CXCL10, IL-6, and IL-15 in the tail skin of mice in the vehicle, 6-OHDA, and 6-OHDA + NE groups were detected by ELISA ( n =4 per group). All vehicle mice were only treated with 0.1% ascorbic acid in 0.9% sterile NaCl. Error bars represent mean ± SD from three independent experiments. * P < 0.05, ** P < 0.01, and *** P < 0.001.

    Journal: Science Advances

    Article Title: Sympathetic nerve aggravates autoimmune skin disease via NE–adrenergic receptor axis: Neuroimmune cross-talk insights from vitiligo

    doi: 10.1126/sciadv.aea7017

    Figure Lengend Snippet: ( A and B ) Flow cytometry and statistical analysis of CD8 + CD45 + T cells in the mouse tail epidermis and dermis of vehicle, 6-OHDA, and 6-OHDA + NE groups ( n =3 per group). ( C and D ) Flow cytometry and statistical analysis of IFN-γ + CD8 + T cells in the mouse tail epidermis and dermis of vehicle, 6-OHDA, and 6-OHDA + NE groups ( n =3 per group). ( E and F ) Flow cytometry and statistical analysis of Granzyme B + CD8 + T cells in the mouse tail epidermis and dermis of vehicle, 6-OHDA, and 6-OHDA + NE groups ( n =3 per group). ( G ) The secretion levels of CXCL9, CXCL10, IL-6, and IL-15 in the tail skin of mice in the vehicle, 6-OHDA, and 6-OHDA + NE groups were detected by ELISA ( n =4 per group). All vehicle mice were only treated with 0.1% ascorbic acid in 0.9% sterile NaCl. Error bars represent mean ± SD from three independent experiments. * P < 0.05, ** P < 0.01, and *** P < 0.001.

    Article Snippet: ELISA analysis on serum samples, skin samples, and cell culture supernatants were performed using the NE ELISA Kit (E-EL-0047c, Elabscience, Wuhan, China), Human CXCL9 ELISA Kit (EHC114.96, Neobioscience Technology Co, Ltd., China), Human CXCL10 ELISA Kit (EHC157.96, Neobioscience Technology Co, Ltd., China), Human IL-6 ELISA Kit (EHC007.96, Neobioscience Technology Co, Ltd., China), Human IL-15 ELISA Kit (EHC013.96, Neobioscience Technology Co, Ltd., China), Mouse CXCL9 ELISA Kit (E-EL-M3077, Elabscience, Wuhan, China), Mouse CXCL10 ELISA Kit (E-EL-M0021, Elabscience, Wuhan, China), Mouse IL-6 ELISA Kit (EMC004.96, Neobioscience Technology Co, Ltd., China), and Mouse IL-15 ELISA Kit (EMC126.96, Neobioscience Technology Co, Ltd., China) following the manufacturer’s instructions.

    Techniques: Flow Cytometry, Enzyme-linked Immunosorbent Assay, Sterility

    ( A ) Volcano plots illustrated the expression of adrenergic receptors on fibroblasts in human skin, including ADRA1A, ADRA1B, ADRA1D, ADRA2A, ADRA2B, ADRA2C, ADRB1, ADRB2, and ADRB3. ( B ) Bubble map illustrated the up-regulation of ADRA2A expression on fibroblasts in the lesional skin of patients with vitiligo and the normal skin of healthy controls. ( C ) Representative immunofluorescence images of fibroblasts, ADRA2A, CXCL9, CXCL10, and CD8 + T cells from the normal skin of the healthy control and the lesional skin of the patient with vitiligo ( n =3 per group). Nuclei were counterstained with DAPI (blue). Scale bars, 50 μm. ( D ) Immunofluorescence analysis of ADRA2A (red) expression in BJ cells after treatment with 5 μM NE for 48 hours. Cell nuclei were stained with DAPI (blue). Scale bar, 50 μm. ( E ) Secretion levels of CXCL9, CXCL10, IL-6, and IL-15 in BJ cells were detected by ELISA with treatment with aposcopolamine (Apos) or NE ( n =3 per group). ( F ) Secretion levels of CXCL9, CXCL10, IL-6, and IL-15 in BJ cells with ADRA2A siRNA or control siRNA were detected by ELISA ( n =3 per group). Error bars represent mean ± SD from three independent experiments. * P < 0.05, ** P < 0.01, and *** P < 0.001; ns, not significant.

    Journal: Science Advances

    Article Title: Sympathetic nerve aggravates autoimmune skin disease via NE–adrenergic receptor axis: Neuroimmune cross-talk insights from vitiligo

    doi: 10.1126/sciadv.aea7017

    Figure Lengend Snippet: ( A ) Volcano plots illustrated the expression of adrenergic receptors on fibroblasts in human skin, including ADRA1A, ADRA1B, ADRA1D, ADRA2A, ADRA2B, ADRA2C, ADRB1, ADRB2, and ADRB3. ( B ) Bubble map illustrated the up-regulation of ADRA2A expression on fibroblasts in the lesional skin of patients with vitiligo and the normal skin of healthy controls. ( C ) Representative immunofluorescence images of fibroblasts, ADRA2A, CXCL9, CXCL10, and CD8 + T cells from the normal skin of the healthy control and the lesional skin of the patient with vitiligo ( n =3 per group). Nuclei were counterstained with DAPI (blue). Scale bars, 50 μm. ( D ) Immunofluorescence analysis of ADRA2A (red) expression in BJ cells after treatment with 5 μM NE for 48 hours. Cell nuclei were stained with DAPI (blue). Scale bar, 50 μm. ( E ) Secretion levels of CXCL9, CXCL10, IL-6, and IL-15 in BJ cells were detected by ELISA with treatment with aposcopolamine (Apos) or NE ( n =3 per group). ( F ) Secretion levels of CXCL9, CXCL10, IL-6, and IL-15 in BJ cells with ADRA2A siRNA or control siRNA were detected by ELISA ( n =3 per group). Error bars represent mean ± SD from three independent experiments. * P < 0.05, ** P < 0.01, and *** P < 0.001; ns, not significant.

    Article Snippet: ELISA analysis on serum samples, skin samples, and cell culture supernatants were performed using the NE ELISA Kit (E-EL-0047c, Elabscience, Wuhan, China), Human CXCL9 ELISA Kit (EHC114.96, Neobioscience Technology Co, Ltd., China), Human CXCL10 ELISA Kit (EHC157.96, Neobioscience Technology Co, Ltd., China), Human IL-6 ELISA Kit (EHC007.96, Neobioscience Technology Co, Ltd., China), Human IL-15 ELISA Kit (EHC013.96, Neobioscience Technology Co, Ltd., China), Mouse CXCL9 ELISA Kit (E-EL-M3077, Elabscience, Wuhan, China), Mouse CXCL10 ELISA Kit (E-EL-M0021, Elabscience, Wuhan, China), Mouse IL-6 ELISA Kit (EMC004.96, Neobioscience Technology Co, Ltd., China), and Mouse IL-15 ELISA Kit (EMC126.96, Neobioscience Technology Co, Ltd., China) following the manufacturer’s instructions.

    Techniques: Expressing, Immunofluorescence, Control, Staining, Enzyme-linked Immunosorbent Assay

    ( A ) Volcano plots illustrated the expression of adrenergic receptors on keratinocytes in human skin, including ADRA1A, ADRA1B, ADRA1D, ADRA2A, ADRA2B, ADRA2C, ADRB1, ADRB2, and ADRB3. ( B ) Bubble map illustrated the up-regulation of ADRB2 expression on keratinocytes in the lesional skin of patients with vitiligo and the normal skin of healthy controls. ( C ) Representative immunofluorescence images of keratinocytes, ADRB2, CXCL9, CXCL10, and CD8 + T cells from the normal skin of the healthy control and the lesional skin of the patient with vitiligo ( n =3 per group). Nuclei were counterstained with DAPI (blue). Scale bars, 50 μm. ( D ) Immunofluorescence analysis of ADRB2 (red) expression in keratinocytes after treatment with 5 μM NE for 48 hours. Cell nuclei were stained with DAPI (blue). Scale bar, 50 μm. ( E ) Secretion levels of CXCL9, CXCL10, IL-6, and IL-15 in keratinocytes were detected by ELISA with treatment with NE or ICI ( n =3 per group). ( F ) Secretion levels of CXCL9, CXCL10, IL-6, and IL-15 in keratinocytes with ADRB2 siRNA or control siRNA were detected by ELISA ( n =3 per group). Error bars represent mean ± SD from three independent experiments. * P < 0.05, ** P < 0.01, and *** P < 0.001; ns, not significant.

    Journal: Science Advances

    Article Title: Sympathetic nerve aggravates autoimmune skin disease via NE–adrenergic receptor axis: Neuroimmune cross-talk insights from vitiligo

    doi: 10.1126/sciadv.aea7017

    Figure Lengend Snippet: ( A ) Volcano plots illustrated the expression of adrenergic receptors on keratinocytes in human skin, including ADRA1A, ADRA1B, ADRA1D, ADRA2A, ADRA2B, ADRA2C, ADRB1, ADRB2, and ADRB3. ( B ) Bubble map illustrated the up-regulation of ADRB2 expression on keratinocytes in the lesional skin of patients with vitiligo and the normal skin of healthy controls. ( C ) Representative immunofluorescence images of keratinocytes, ADRB2, CXCL9, CXCL10, and CD8 + T cells from the normal skin of the healthy control and the lesional skin of the patient with vitiligo ( n =3 per group). Nuclei were counterstained with DAPI (blue). Scale bars, 50 μm. ( D ) Immunofluorescence analysis of ADRB2 (red) expression in keratinocytes after treatment with 5 μM NE for 48 hours. Cell nuclei were stained with DAPI (blue). Scale bar, 50 μm. ( E ) Secretion levels of CXCL9, CXCL10, IL-6, and IL-15 in keratinocytes were detected by ELISA with treatment with NE or ICI ( n =3 per group). ( F ) Secretion levels of CXCL9, CXCL10, IL-6, and IL-15 in keratinocytes with ADRB2 siRNA or control siRNA were detected by ELISA ( n =3 per group). Error bars represent mean ± SD from three independent experiments. * P < 0.05, ** P < 0.01, and *** P < 0.001; ns, not significant.

    Article Snippet: ELISA analysis on serum samples, skin samples, and cell culture supernatants were performed using the NE ELISA Kit (E-EL-0047c, Elabscience, Wuhan, China), Human CXCL9 ELISA Kit (EHC114.96, Neobioscience Technology Co, Ltd., China), Human CXCL10 ELISA Kit (EHC157.96, Neobioscience Technology Co, Ltd., China), Human IL-6 ELISA Kit (EHC007.96, Neobioscience Technology Co, Ltd., China), Human IL-15 ELISA Kit (EHC013.96, Neobioscience Technology Co, Ltd., China), Mouse CXCL9 ELISA Kit (E-EL-M3077, Elabscience, Wuhan, China), Mouse CXCL10 ELISA Kit (E-EL-M0021, Elabscience, Wuhan, China), Mouse IL-6 ELISA Kit (EMC004.96, Neobioscience Technology Co, Ltd., China), and Mouse IL-15 ELISA Kit (EMC126.96, Neobioscience Technology Co, Ltd., China) following the manufacturer’s instructions.

    Techniques: Expressing, Immunofluorescence, Control, Staining, Enzyme-linked Immunosorbent Assay