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rabbit anti human il 22r antibody  (R&D Systems)


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    R&D Systems rabbit anti human il 22r antibody
    (A) To block <t>IL-22R-mediated</t> signaling, pre-treatment of HaCaT cells with 50 μg/ml of anti-IL-22R blocking antibody for 2 h prior to IL-22 stimulation resulted in reduced NLRP3 and caspase-1 expression (B) as well as a consequent reduction in IL-1β secretion as measured by ELISA. (C) To reduce NLRP3 expression in HaCaT cells, we transfected NLRP3 siRNA or control siRNA into HaCaT cells. The level of protein was quantified to evaluate the knockdown efficiency of the endogenous NLRP3 protein in HaCaT cells. Data from three independent experiments for protein expression are shown. (D) The active form of IL-1β in culture supernatants was quantitated by ELISA. (E) NLRP3 knockdown in HaCaT cells resulted in a reduction in the levels of caspase-1 and the active form of IL-1β in IL-22-treated cells. Representative blots of three independent experiments are shown. Results were normalized against β-actin expression. The data are expressed as means ± SD (i.e. n=3) ( ** P < 0.05). Ab, anti-IL-22R blocking antibody; IgG, isotype antibody for the negative control of IL-22R antibody.
    Rabbit Anti Human Il 22r Antibody, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 12 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rabbit+anti+human+il+22r+antibody/pmc05752511-181-6-11?v=R%26D+Systems
    Average 93 stars, based on 12 article reviews
    rabbit anti human il 22r antibody - by Bioz Stars, 2026-07
    93/100 stars

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    1) Product Images from "Interleukin-22 participates in the inflammatory process of vitiligo"

    Article Title: Interleukin-22 participates in the inflammatory process of vitiligo

    Journal: Oncotarget

    doi: 10.18632/oncotarget.22644

    (A) To block IL-22R-mediated signaling, pre-treatment of HaCaT cells with 50 μg/ml of anti-IL-22R blocking antibody for 2 h prior to IL-22 stimulation resulted in reduced NLRP3 and caspase-1 expression (B) as well as a consequent reduction in IL-1β secretion as measured by ELISA. (C) To reduce NLRP3 expression in HaCaT cells, we transfected NLRP3 siRNA or control siRNA into HaCaT cells. The level of protein was quantified to evaluate the knockdown efficiency of the endogenous NLRP3 protein in HaCaT cells. Data from three independent experiments for protein expression are shown. (D) The active form of IL-1β in culture supernatants was quantitated by ELISA. (E) NLRP3 knockdown in HaCaT cells resulted in a reduction in the levels of caspase-1 and the active form of IL-1β in IL-22-treated cells. Representative blots of three independent experiments are shown. Results were normalized against β-actin expression. The data are expressed as means ± SD (i.e. n=3) ( ** P < 0.05). Ab, anti-IL-22R blocking antibody; IgG, isotype antibody for the negative control of IL-22R antibody.
    Figure Legend Snippet: (A) To block IL-22R-mediated signaling, pre-treatment of HaCaT cells with 50 μg/ml of anti-IL-22R blocking antibody for 2 h prior to IL-22 stimulation resulted in reduced NLRP3 and caspase-1 expression (B) as well as a consequent reduction in IL-1β secretion as measured by ELISA. (C) To reduce NLRP3 expression in HaCaT cells, we transfected NLRP3 siRNA or control siRNA into HaCaT cells. The level of protein was quantified to evaluate the knockdown efficiency of the endogenous NLRP3 protein in HaCaT cells. Data from three independent experiments for protein expression are shown. (D) The active form of IL-1β in culture supernatants was quantitated by ELISA. (E) NLRP3 knockdown in HaCaT cells resulted in a reduction in the levels of caspase-1 and the active form of IL-1β in IL-22-treated cells. Representative blots of three independent experiments are shown. Results were normalized against β-actin expression. The data are expressed as means ± SD (i.e. n=3) ( ** P < 0.05). Ab, anti-IL-22R blocking antibody; IgG, isotype antibody for the negative control of IL-22R antibody.

    Techniques Used: Blocking Assay, Expressing, Enzyme-linked Immunosorbent Assay, Transfection, Control, Knockdown, Negative Control



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    rabbit anti human il 22r antibody  (R&D Systems)
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    R&D Systems rabbit anti human il 22r antibody
    (A) To block <t>IL-22R-mediated</t> signaling, pre-treatment of HaCaT cells with 50 μg/ml of anti-IL-22R blocking antibody for 2 h prior to IL-22 stimulation resulted in reduced NLRP3 and caspase-1 expression (B) as well as a consequent reduction in IL-1β secretion as measured by ELISA. (C) To reduce NLRP3 expression in HaCaT cells, we transfected NLRP3 siRNA or control siRNA into HaCaT cells. The level of protein was quantified to evaluate the knockdown efficiency of the endogenous NLRP3 protein in HaCaT cells. Data from three independent experiments for protein expression are shown. (D) The active form of IL-1β in culture supernatants was quantitated by ELISA. (E) NLRP3 knockdown in HaCaT cells resulted in a reduction in the levels of caspase-1 and the active form of IL-1β in IL-22-treated cells. Representative blots of three independent experiments are shown. Results were normalized against β-actin expression. The data are expressed as means ± SD (i.e. n=3) ( ** P < 0.05). Ab, anti-IL-22R blocking antibody; IgG, isotype antibody for the negative control of IL-22R antibody.
    Rabbit Anti Human Il 22r Antibody, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rabbit+anti+human+il+22r+antibody/pmc05752511-181-6-11?v=R%26D+Systems
    Average 93 stars, based on 1 article reviews
    rabbit anti human il 22r antibody - by Bioz Stars, 2026-07
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    rabbit anti human il 22r  (ProSci Incorporated)
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    ProSci Incorporated rabbit anti human il 22r
    (A) To block <t>IL-22R-mediated</t> signaling, pre-treatment of HaCaT cells with 50 μg/ml of anti-IL-22R blocking antibody for 2 h prior to IL-22 stimulation resulted in reduced NLRP3 and caspase-1 expression (B) as well as a consequent reduction in IL-1β secretion as measured by ELISA. (C) To reduce NLRP3 expression in HaCaT cells, we transfected NLRP3 siRNA or control siRNA into HaCaT cells. The level of protein was quantified to evaluate the knockdown efficiency of the endogenous NLRP3 protein in HaCaT cells. Data from three independent experiments for protein expression are shown. (D) The active form of IL-1β in culture supernatants was quantitated by ELISA. (E) NLRP3 knockdown in HaCaT cells resulted in a reduction in the levels of caspase-1 and the active form of IL-1β in IL-22-treated cells. Representative blots of three independent experiments are shown. Results were normalized against β-actin expression. The data are expressed as means ± SD (i.e. n=3) ( ** P < 0.05). Ab, anti-IL-22R blocking antibody; IgG, isotype antibody for the negative control of IL-22R antibody.
    Rabbit Anti Human Il 22r, supplied by ProSci Incorporated, 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/rabbit+anti+human+il+22r+antibody/pm24056519-91-12-16?v=ProSci+Incorporated
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    Image Search Results


    (A) To block IL-22R-mediated signaling, pre-treatment of HaCaT cells with 50 μg/ml of anti-IL-22R blocking antibody for 2 h prior to IL-22 stimulation resulted in reduced NLRP3 and caspase-1 expression (B) as well as a consequent reduction in IL-1β secretion as measured by ELISA. (C) To reduce NLRP3 expression in HaCaT cells, we transfected NLRP3 siRNA or control siRNA into HaCaT cells. The level of protein was quantified to evaluate the knockdown efficiency of the endogenous NLRP3 protein in HaCaT cells. Data from three independent experiments for protein expression are shown. (D) The active form of IL-1β in culture supernatants was quantitated by ELISA. (E) NLRP3 knockdown in HaCaT cells resulted in a reduction in the levels of caspase-1 and the active form of IL-1β in IL-22-treated cells. Representative blots of three independent experiments are shown. Results were normalized against β-actin expression. The data are expressed as means ± SD (i.e. n=3) ( ** P < 0.05). Ab, anti-IL-22R blocking antibody; IgG, isotype antibody for the negative control of IL-22R antibody.

    Journal: Oncotarget

    Article Title: Interleukin-22 participates in the inflammatory process of vitiligo

    doi: 10.18632/oncotarget.22644

    Figure Lengend Snippet: (A) To block IL-22R-mediated signaling, pre-treatment of HaCaT cells with 50 μg/ml of anti-IL-22R blocking antibody for 2 h prior to IL-22 stimulation resulted in reduced NLRP3 and caspase-1 expression (B) as well as a consequent reduction in IL-1β secretion as measured by ELISA. (C) To reduce NLRP3 expression in HaCaT cells, we transfected NLRP3 siRNA or control siRNA into HaCaT cells. The level of protein was quantified to evaluate the knockdown efficiency of the endogenous NLRP3 protein in HaCaT cells. Data from three independent experiments for protein expression are shown. (D) The active form of IL-1β in culture supernatants was quantitated by ELISA. (E) NLRP3 knockdown in HaCaT cells resulted in a reduction in the levels of caspase-1 and the active form of IL-1β in IL-22-treated cells. Representative blots of three independent experiments are shown. Results were normalized against β-actin expression. The data are expressed as means ± SD (i.e. n=3) ( ** P < 0.05). Ab, anti-IL-22R blocking antibody; IgG, isotype antibody for the negative control of IL-22R antibody.

    Article Snippet: The cells were pretreated with either rabbit anti-human IL-22R antibody (AF2770; R&D systems) or with the isotype control (AB-108-C; R&D systems) at a concentration of 50 μg/ml for 2 h to block IL-22R in HaCaT cells.

    Techniques: Blocking Assay, Expressing, Enzyme-linked Immunosorbent Assay, Transfection, Control, Knockdown, Negative Control