IRBP (1-20), human
目录号 : GC30558
IRBP (1-20)，人类是光学受体视黄醇结合蛋白 (IRBP) 的 1-20 个氨基酸片段。
Cas No.:298202-25-2
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >98.00%
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- Datasheet
| Animal experiment [1]: | |
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Animal models |
Female C57BL/6J mice (6-8 weeks of age) |
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Preparation Method |
Each C57BL/6J mouse was immunized subcutaneously in one rear footpad and the tail head, and rump (total of 200 μl) with an emulsion containing 300 μg of IRBP (1-20), human in phosphate-buffered saline (PBS) and 300 μg of Mycobacterium tuberculosis H37Ra in complete Freund s adjuvant. |
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Dosage form |
300 μg IRBP (1-20), human |
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Applications |
Female C57BL/6J mice induced by IRBP (1-20), human successfully showed eau phenotype. |
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References: [1]. Meng X, Fang S, et,al. Preventive effect of chrysin on experimental autoimmune uveitis triggered by injection of human IRBP peptide 1-20 in mice. Cell Mol Immunol. 2017 Aug;14(8):702-711. doi: 10.1038/cmi.2015.107. Epub 2016 Mar 21. PMID: 26996065; PMCID: PMC5549600. |
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IRBP (1-20), human is the 1-20 amino acid fragment of the optical interreceptor retinoid binding protein (IRBP). IRBP is a 140 kda glycoprotein found in the photoreceptor matrix between the neural retina and the retinal pigment epithelium. Human IRBP peptides 1-20 contain a major epitope of the H-2b haplotype. IRBP(1-20) immunity induces t cell-mediated experimental autoimmune uveoretinitis (EAU) disease[1,2].
Female C57BL/6J mice induced by IRBP (1-20), human successfully showed eau phenotype[3,5]. The consequences of IRBP deficiency on the T-cell repertoire were also investigated. IRBP+/+, IRBP+/- and IRBP-/- mice on the C57BL/6 background were immunized with IRBP or with a pathogenic epitope, IRBP (1-20), human peptide in adjuvant, and were evaluated for disease severity and immunological responses. C57BL/6 IRBP-/- mice were completely resistant to EAU and EAP, and had enhanced immunological responses to IRBP and to its pathogenic peptide 1-20, as compared to their IRBP+/+ counterparts. IRBP-/- mice exhibited an altered IRBP epitope recognition[4].
References:
[1]. Avichezer D, Chan CC,et,al. Residues 1-20 of IRBP and whole IRBP elicit different uveitogenic and immunological responses in interferon gamma deficient mice. Exp Eye Res. 2000 Aug;71(2):111-8. doi: 10.1006/exer.2000.0860. PMID: 10930316.
[2]. Avichezer D, Silver PB,et,al. Identification of a new epitope of human IRBP that induces autoimmune uveoretinitis in mice of the H-2b haplotype. Invest Ophthalmol Vis Sci. 2000 Jan;41(1):127-31. PMID: 10634611.
[3]. Meng X, Fang S, et,al. Preventive effect of chrysin on experimental autoimmune uveitis triggered by injection of human IRBP peptide 1-20 in mice. Cell Mol Immunol. 2017 Aug;14(8):702-711. doi: 10.1038/cmi.2015.107. Epub 2016 Mar 21. PMID: 26996065; PMCID: PMC5549600.
[4]. Avichezer D, Liou GI, et,al. Interphotoreceptor retinoid-binding protein (IRBP)-deficient C57BL/6 mice have enhanced immunological and immunopathogenic responses to IRBP and an altered recognition of IRBP epitopes. J Autoimmun. 2003 Nov;21(3):185-94. doi: 10.1016/j.jaut.2003.08.004. PMID: 14599843.
[5]. Tajiri N, Kato T, et,al. The protective function of invariant natural killer T cells in the relapse of experimental autoimmune uveoretinitis. Exp Eye Res. 2021 Feb;203:108406. doi: 10.1016/j.exer.2020.108406. Epub 2020 Dec 19. PMID: 33347870.
IRBP (1-20),人类是光学受体视黄醇结合蛋白 (IRBP) 的 1-20 个氨基酸片段。 IRBP 是一种 140 kda 的糖蛋白,存在于神经视网膜和视网膜色素上皮细胞之间的光感受器基质中。人类 IRBP 肽 1-20 包含 H-2b 单倍型的主要表位。 IRBP(1-20)免疫诱导t细胞介导的实验性自身免疫性葡萄膜视网膜炎(EAU)疾病[1,2]。
IRBP(1-20)诱导的雌性C57BL/6J小鼠,人类成功显示出eau表型 [3,5]。还研究了 IRBP 缺乏对 T 细胞库的影响。 IRBP+/+、IRBP+/- 和 IRBP-/- 小鼠在 C57BL/6 背景下用 IRBP 或致病性表位、IRBP (1-20)、佐剂中的人肽免疫,并评估疾病严重程度和免疫反应.与其 IRBP+/+ 对应物相比,C57BL/6 IRBP-/- 小鼠对 EAU 和 EAP 具有完全抗性,并且对 IRBP 及其致病肽 1-20 具有增强的免疫反应。 IRBP-/- 小鼠表现出改变的 IRBP 表位识别[4]。
| Cas No. | 298202-25-2 | SDF | |
| Canonical SMILES | Gly-Pro-Thr-His-Leu-Phe-Gln-Pro-Ser-Leu-Val-Leu-Asp-Met-Ala-Lys-Val-Leu-Leu-Asp | ||
| 分子式 | C101H164N24O28S | 分子量 | 2194.59 |
| 溶解度 | Soluble in Water | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 0.4557 mL | 2.2783 mL | 4.5567 mL |
| 5 mM | 0.0911 mL | 0.4557 mL | 0.9113 mL |
| 10 mM | 0.0456 mL | 0.2278 mL | 0.4557 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Residues 1-20 of IRBP and whole IRBP elicit different uveitogenic and immunological responses in interferon gamma deficient mice
Exp Eye Res2000 Aug;71(2):111-8.PMID: 10930316DOI: 10.1006/exer.2000.0860
Experimental autoimmune uveoretinitis (EAU) is a T-cell-mediated autoimmune disease induced by immunization with uveitogenic retinal antigens, or by the adoptive transfer of uveitogenic T-cells of the Th-1-like phenotype. We have previously shown that IFN-gamma-deficient mice (GKO) on the C57BL/6 background are equally susceptible to interphotoreceptor retinoid binding protein (IRBP)-induced EAU as the wild type (WT). In the present study, we evaluated EAU induction in GKO mice by the newly described H-2(b)epitope contained in residues 1-20 of human IRBP, and compared it to the response to the whole IRBP molecule. Similarly to previous observations with IRBP-induced EAU, delayed type hypersensitivity (DTH) and lymphocyte proliferation responses were elevated in GKO mice, as was production of IL-5 and TNF-alpha. However, unlike the responses induced by whole IRBP, there was no detectable IL-10 production to the peptide. Histopathology on day 21 after immunization, revealed that both GKO and WT mice developed retinal lesions, including damage to the photoreceptor cell layer, vasculitis and inflammatory cellular infiltration, but disease scores were significantly higher in GKO, and retinal detachment was observed only in GKO mice. In contrast to the wild type, the cellular infiltrate in eyes of GKO mice contained a prominent component of eosinophils, although of lower proportion in peptide-induced than in IRBP-induced EAU. We conclude that the cytokine and inflammatory responses to human peptide 1-20 differ perceptibly from the responses to whole bovine IRBP, and may explain the elevated EAU scores of GKO mice compared to wild type.
Preventive effect of chrysin on experimental autoimmune uveitis triggered by injection of human IRBP peptide 1-20 in mice
Cell Mol Immunol2017 Aug;14(8):702-711.PMID: 26996065DOI: 10.1038/cmi.2015.107
Uveitis is a common cause of blindness worldwide. Experimental autoimmune uveitis (EAU) is an animal model of noninfectious uveitis. Chrysin (5,7-dihydroxyflavone) is a member of the flavonoid family and has anti-inflammatory effects. We immunized C57BL/6J mice with human interphotoreceptor retinoid-binding protein peptide 1-20 to induce EAU. Chrysin was administered intragastrically at 25 mg/kg daily to the chrysin-treated mice from 3 days before immunization to 21 days after immunization. Vehicle was administered to the mice in the control group according to the same protocol. Lower clinical and histopathological scores, increased integrity of the blood-retinal barrier (BRB) and higher expression of tight junction proteins were observed in the chrysin-treated mice. Chrysin significantly decreased the proportions of Th1, Th17 and CD4+CD3+CD62L+ Th0 cells, and increased the proportion of Treg cells. Both macrophage infiltration and the expression of inducible nitric oxide synthase in the retina were efficiently inhibited by chrysin treatment. In chrysin-treated mice, the expression of interferon-¦ì interleukin (IL)-17A, IL-6, IL-1¦ and tumor necrosis factor-¦Á was reduced in the retina, whereas higher levels of transforming growth factor-¦ were detected. Furthermore, NF-¦ʂp65 was downregulated after chrysin treatment. In conclusion, as an anti-inflammatory molecule, chrysin exerts a preventive effect on EAU by modulating the balance among helper T-cell subsets and suppressing ocular inflammation, thereby maintaining the integrity of the BRB.
Melatonin, an endogenous hormone, modulates Th17 cells via the reactive-oxygen species/TXNIP/HIF-1¦Á axis to alleviate autoimmune uveitis
J Neuroinflammation2022 May 27;19(1):124.PMID: 35624485DOI: 10.1186/s12974-022-02477-z
Background: Melatonin, an indoleamine produced by the pineal gland, plays a pivotal role in maintaining circadian rhythm homeostasis. Recently, the strong antioxidant and anti-inflammatory properties of melatonin have attracted attention of researchers. We evaluated the therapeutic efficacy of melatonin in experimental autoimmune uveitis (EAU), which is a representative animal model of human autoimmune uveitis.
Methods: EAU was induced in mice via immunization with the peptide interphotoreceptor retinoid binding protein 1-20 (IRBP1-20). Melatonin was then administered via intraperitoneal injection to induce protection against EAU. With EAU induction for 14 days, clinical and histopathological scores were graded to evaluate the disease progression. T lymphocytes accumulation and the expression of inflammatory cytokines in the retinas were assessed via flow cytometry and RT-PCR, respectively. T helper 1 (Th1), T helper 17 (Th17), and regulatory T (Treg) cells were detected via flow cytometry for both in vivo and in vitro experiments. Reactive-oxygen species (ROS) from CD4 + T cells was tested via flow cytometry. The expression of thioredoxin-interacting protein (TXNIP) and hypoxia-inducible factor 1 alpha (HIF-1¦Á) proteins were quantified via western blot.
Results: Melatonin treatment resulted in notable attenuation of ocular inflammation in EAU mice, evidenced by decreasing optic disc edema, few signs of retinal vasculitis, and minimal retinal and choroidal infiltrates. Mechanistic studies revealed that melatonin restricted the proliferation of peripheral Th1 and Th17 cells by suppressing their transcription factors and potentiated Treg cells. In vitro studies corroborated that melatonin restrained the polarization of retina-specific T cells towards Th17 and Th1 cells in addition to enhancing the proportion of Treg cells. Pretreatment of retina-specific T cells with melatonin failed to induce EAU in na?ve recipients. Furthermore, the ROS/ TXNIP/ HIF-1¦Á pathway was shown to mediate the therapeutic effect of melatonin in EAU.
Conclusions: Melatonin regulates autoimmune T cells by restraining effector T cells and facilitating Treg generation, indicating that melatonin could be a hopeful treatment alternative for autoimmune uveitis.
Identification of a new epitope of human IRBP that induces autoimmune uveoretinitis in mice of the H-2b haplotype
Invest Ophthalmol Vis Sci2000 Jan;41(1):127-31.PMID: 10634611DOI: 10.1136/bjo.2006.099192
Purpose: Experimental autoimmune uveoretinitis (EAU) is a T-cell-mediated disease induced by immunization with interphotoreceptor retinoid binding protein (IRBP). Major uveitogenic sites have been identified for mice of the H-2r and H-2k haplotypes but not for the H-2b haplotype. The present communication describes the characterization of an epitope contained in residues 1 to 20 of human IRBP that induces EAU in H-2b mice.
Methods: H-2b (C57BL/6, 129/J) and H-2r (BIO.RIII) mice were immunized with peptide 1-20 or with whole (bovine) IRBP. EAU (histopathology) and immunologic responses (delayed-type hypersensitivity [DTH], lymphocyte proliferation, and cytokine production) were assessed after 21 days.
Results: C57BL/6 mice, 129/J and (129/JxC57BL/6)F1 mice, immunized with 200 to 300 microg of peptide, developed DTH and EAU with scores comparable to those induced by 100 microg IRBP. Their lymphocytes proliferated to the peptide and produced interferon-gamma (but not interleukin-4) and transferred EAU to syngeneic recipients. Lymphocytes of IRBP-immunized mice also responded to the peptide. Peptide 1-20-immunized B1O.RIII mice failed to develop either disease or immunologic responses. CONCLUSIONS. Human IRBP peptide 1-20 contains a major epitope for the H-2b haplotype, which is apparently not presented by the H-2r haplotype.
Supplementation of CD4+CD25+ regulatory T cells suppresses experimental autoimmune uveoretinitis
Br J Ophthalmol2007 Jan;91(1):105-10.PMID: 16943228DOI: 10.1136/bjo.2006.099192
Aims: To investigate whether supplementation of natural CD4+CD25+ regulatory T cells ameliorates mouse experimental autoimmune uveoretinitis (EAU) induced by CD4+ T cell-dependent interphotoreceptor retinoid-binding protein (IRBP).
Methods: C57BL/6 mice were immunised with human interphotoreceptor retinoid-binding protein peptide 1-20 (IRBP(1-20)), and IRBP(1-20)-sensitised T cells were obtained. CD4+CD25+ T cells derived from naive mice were cocultured with IRBP(1-20)-sensitised T cells, and their proliferation responses and cytokine production were measured. In addition, CD4+CD25+ T cells were transferred intravenously into mice 7 or 15 days after immunisation with IRBP(1-20), and the severity of EAU and T cell proliferation responses were evaluated.
Results: CD4+CD25+ regulatory T cells effectively inhibited both the proliferation of, and interleukin (IL)2, IL5 and interferon (IFN)gamma production by, IRBP(1-20)-sensitised T cells. Adoptive transfer of CD4+CD25+ regulatory T cells to IRBP(1-20)-immunised mice conferred considerable protection from EAU development and inhibition of T cell proliferation responses to IRBP(1-20).
Conclusion: These findings show that natural CD4+CD25+ regulatory T cells possess the ability to inhibit activation of IRBP-reactive T cells that have been already sensitised in vivo, and adoptive transfer of these cells ameliorates EAU even in the effector phase. Supplementation of natural CD4+CD25+ regulatory T cells may have therapeutic potential for effective treatment of uveitis.