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Broad applicability of the Goldspire™ platform for the treatment of solid tumors Goldspire™ 平台广泛适用于实体瘤的治疗。
IF 4.5 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-09-28 DOI: 10.1016/j.clim.2024.110373
Jenny Zilberberg , Christopher Uhl , Charles B. Scott , David W. Andrews , Mark A. Exley
Goldspire™ is a personalized immunotherapy platform that combines whole tumor-derived cells with antisense oligonucleotide (IMV-001) against Insulin-Like Growth Factor-1 Receptor (IGF-1R) in biodiffusion chambers (BDCs; 0.1 μm pore). BDCs are exposed to 5–6 Gy and implanted at abdominal sites for ∼48 h to deliver an antigenic payload and immunostimulatory factors to train the immune system. Lead product IGV-001 was evaluated in newly diagnosed glioblastoma (ndGBM) patients in Phase 1a and 1b trials (NCT02507583). A Phase 2b study (NCT04485949) recently completed enrollment.
Preventative treatment with tumor-specific products manufactured with Goldspire limited tumor progression and extended overall survival in mice challenged with bladder, pancreatic, ovarian, colorectal, or renal carcinomas. The benefit of this immunotherapy was enhanced with anti-PD-1; combination treatment was superior to either monotherapy in orthotopic GBM and melanoma models. Lastly, Goldspire elicited immune T cell activation and memory phenotypes against patient-derived endometrial tumor-derived products in co-cultures with matching immune cells.
Goldspire™ 是一种个性化免疫疗法平台,它将整个肿瘤衍生细胞与生物扩散室(BDC;孔径 0.1 μm)中针对胰岛素样生长因子-1 受体(IGF-1R)的反义寡核苷酸(IMV-001)结合在一起。BDCs暴露于5-6Gy,并在腹部部位植入约48小时,以传递抗原载荷和免疫刺激因子来训练免疫系统。主导产品IGV-001在新诊断胶质母细胞瘤(ndGBM)患者中进行了1a和1b期试验评估(NCT02507583)。一项 2b 期研究(NCT04485949)最近完成了入组。在膀胱癌、胰腺癌、卵巢癌、结肠直肠癌或肾癌小鼠中,使用 Goldspire 生产的肿瘤特异性产品进行预防性治疗可限制肿瘤进展并延长总生存期。抗-PD-1可增强这种免疫疗法的疗效;在原位癌和黑色素瘤模型中,联合疗法优于单一疗法。最后,Goldspire 在与匹配的免疫细胞共同培养的过程中,激发了针对患者子宫内膜肿瘤衍生产物的免疫 T 细胞活化和记忆表型。
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引用次数: 0
Bisphenol A triggers activation of ocular immune system and aggravates allergic airway inflammation 双酚 A 会引发眼部免疫系统激活,加重过敏性气道炎症。
IF 4.5 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-09-28 DOI: 10.1016/j.clim.2024.110370
Tatsuo Ueda , Takumi Adachi , Tomoya Hayashi , Koubun Yasuda , Kazufumi Matsushita , Eiko Koike , Rie Yanagisawa , Takahiro Nagatake , Jun Kunisawa , Ken J. Ishii , Kenzo Tsuzuki , Etsushi Kuroda
Bisphenol A (BPA) is widely used in manufacturing plastic products, and it has been reported that exposure through the airway or orally aggravates allergic airway inflammation. Because BPA is detected in the atmosphere and indoor environments, the eyes can also be exposed to BPA. After ocular exposure to BPA and antigen via eye drops, we observed enhanced antigen uptake of antigen-presenting cells (APCs) in tear duct-associated lymphoid tissue (TALT). Additionally, we observed the formation of germinal center (GC) B cells in TALT and induction of allergic airway inflammation in mice sensitized with BPA and antigen via eye drops, followed by airway antigen exposure. We also found that DNAX-activating protein of 12 kDa (DAP12)-deficient mice displayed impaired activation of APCs enhanced by ocular exposure to BPA. These results indicate that ocular sensitization to BPA and allergen triggers allergic inflammation via TALT activation, and that DAP12 might be a key molecule for modulating the ocular immune system.
双酚 A(BPA)被广泛用于制造塑料产品,据报道,通过呼吸道或口服接触双酚 A 会加重过敏性气道炎症。由于大气和室内环境中都能检测到双酚 A,因此眼睛也可能接触到双酚 A。通过滴眼液将双酚 A 和抗原暴露于眼部后,我们观察到泪管相关淋巴组织(TALT)中的抗原呈递细胞(APC)对抗原的吸收增强。此外,我们还观察到泪管相关淋巴组织(TALT)中形成了生殖中心(GC)B 细胞,并通过滴眼液诱导了对双酚 A 和抗原过敏的小鼠的过敏性气道炎症。我们还发现,DNAX-活化蛋白 12 kDa(DAP12)缺陷小鼠在眼部暴露于双酚 A 的情况下,APCs 的活化能力受损。这些结果表明,眼部对双酚 A 和过敏原的致敏会通过 TALT 激活引发过敏性炎症,而 DAP12 可能是调节眼部免疫系统的关键分子。
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引用次数: 0
Immune response in vaccinated healthcare workers with frequent COVID-19 infections is characterised by blunted IFNγ and IL-2 responses to SARS-CoV-2 variants 频繁感染 COVID-19 的接种过疫苗的医护人员对 SARS-CoV-2 变体的免疫反应特点是 IFNγ 和 IL-2 反应减弱。
IF 4.5 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-09-27 DOI: 10.1016/j.clim.2024.110371
Liam Townsend , Jean Dunne , Jacklyn Sui , Carla Sanchez Perez , Matt McElheron , Cian Reid , William McCormack , Colm Bergin , Catherine Fleming , Cliona O'Farrelly , Gareth Brady , PRECISE Steering group, Niall Conlon
Healthcare workers (HCWs) are at increased risk of SARS-CoV-2 infection. Despite widespread vaccination, some HCWs develop frequent symptomatic infection. We hypothesised that HCWs with frequent symptomatic COVID-19 have impaired T and B cell mediated immunity to SARS-CoV-2.
Vaccinated HCWs with no prior COVID infection (n = 9), asymptomatic recent infection (n = 10), and frequent recent infection (n = 15) were recruited from a longitudinal HCW cohort study. Whole blood stimulation with SARS-CoV-2 variants (Wuhan, B.1.617, BA.2, BA.2.75, BA.4/5, XBB.1.5, BQ.1.1) was performed, with IFNγ and IL-2 responses, total IgG produced, and anti-Spike antibody neutralising capacity measured.
Frequent infections had similar IFNγ and IL-2 responses to the never infected group, with significantly higher responses in the asymptomatic group. The frequent cohort had higher IgG responses to Delta and BA.4/5 and higher neutralising capacity against Omicron variants. An immune signature of blunted IL-2 and IFNγ in frequent infections may identify HCWs at increased risk of further infection.
医护人员(HCWs)感染 SARS-CoV-2 的风险增加。尽管广泛接种了疫苗,但一些医护人员仍经常出现无症状感染。我们假设,频繁出现 COVID-19 症状的医护人员的 T 细胞和 B 细胞介导的 SARS-CoV-2 免疫力受损。我们从一项纵向HCW队列研究中招募了既往未感染COVID(9人)、近期无症状感染(10人)和近期频繁感染(15人)的已接种疫苗的HCW。用 SARS-CoV-2 变体(武汉、B.1.617、BA.2、BA.2.75、BA.4/5、XBB.1.5、BQ.1.1)进行全血刺激,测量 IFNγ 和 IL-2 反应、产生的总 IgG 和抗史派克抗体中和能力。频繁感染组的 IFNγ 和 IL-2 反应与从未感染组相似,而无症状组的反应明显更高。频繁感染组对Delta和BA.4/5的IgG反应较高,对Omicron变体的中和能力也较高。在频繁感染的人群中,IL-2和IFNγ反应减弱的免疫特征可能会识别出进一步感染风险增加的高危工人。
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引用次数: 0
CXCL5 inhibition improves kidney function by protecting renal tubular epithelial cells in diabetic kidney disease 抑制 CXCL5 可保护糖尿病肾病患者的肾小管上皮细胞,从而改善肾功能。
IF 4.5 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-09-24 DOI: 10.1016/j.clim.2024.110369
Ching Chen , Liang-Yu Lin , Yen-Wen Wu , Jaw-Wen Chen , Ting-Ting Chang
Inflammation is one of exacerbating factors of diabetic kidney disease (DKD). Upregulated CXCL5 is found in clinical and experimental diabetes studies. This study aimed to investigate the impact and mechanism of CXCL5 on DKD. DKD patients with different levels of urine albumin-to-creatinine ratio were enrolled. Leprdb/db mice and CXCL5-knockout diabetic mice were used as mouse models for DKD. Human renal tubular epithelial cells were used for in vitro experiments. Circulating CXCL5 were increased in DKD patients compared to the non-DKD subjects. CXCL5 inhibition through CXCL5-neutralizing antibodies or genetic knockout improved kidney function and ameliorated tubular injury and renal fibrosis. In high-glucose-stimulated tubular epithelial cells, administration of CXCL5-neutralizing antibodies or siRNA resulted in reduced phospho-JNK/c-JUN/p65 and the downstream inflammatory, fibrotic, and apoptotic protein expressions. Administration of CXCR2 and JNK inhibitors impeded the CXCL5-induced tubular epithelial cell damages. In conclusion, these findings indicated that anti-CXCL5 strategies may be potential treatments for DKD.
炎症是糖尿病肾病(DKD)的恶化因素之一。在临床和实验性糖尿病研究中都发现了 CXCL5 的上调。本研究旨在探讨CXCL5对DKD的影响和机制。研究人员招募了不同尿白蛋白与肌酐比值水平的 DKD 患者。以 Leprdb/db 小鼠和 CXCL5 基因剔除糖尿病小鼠为 DKD 小鼠模型。体外实验使用人肾小管上皮细胞。与非 DKD 患者相比,DKD 患者循环中的 CXCL5 增加。通过 CXCL5 中和抗体或基因敲除抑制 CXCL5 可改善肾功能,减轻肾小管损伤和肾脏纤维化。在高葡萄糖刺激的肾小管上皮细胞中,给予 CXCL5 中和抗体或 siRNA 可减少磷酸-JNK/c-JUN/p65 以及下游炎症、纤维化和凋亡蛋白的表达。服用 CXCR2 和 JNK 抑制剂可抑制 CXCL5 诱导的肾小管上皮细胞损伤。总之,这些研究结果表明,抗CXCL5策略可能是治疗DKD的潜在方法。
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引用次数: 0
Insights into the multifaceted role of interleukin-37 on human immune cell regulation 洞察白细胞介素-37 对人类免疫细胞调节的多方面作用。
IF 4.5 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-09-20 DOI: 10.1016/j.clim.2024.110368
Lisa U. Teufel , Vasiliki Matzaraki , Lukas Folkman , Rob ter Horst , Simone J.C.F.M. Moorlag , Catharina M. Mulders-Manders , Mihai G. Netea , Thomas Krausgruber , Leo A.B. Joosten , Rob J.W. Arts
Autoinflammatory diseases, while having a variety of underlying causes, are mediated by dysfunctional innate immune responses. Therefore, standard treatments target innate cytokines or block their receptors. Despite excellent responses in some patients, first-line treatments fail in others, for reasons which remain to be understood.
We studied the effects of IL-37, an anti-inflammatory cytokine, on immune cells using multi-omics profiling of 325 healthy adults. Our findings show that IL-37 is associated with inflammation control and generally reduced immune cell activity. Further, genetic variants in IL37 are associated with impaired trained immunity, a memory phenotype of innate immune cells contributing to autoinflammation. To underpin the medical potential of IL-37, an explorative cohort of seven autoinflammatory disorders was built. In vitro stimulation experiments argue for recombinant IL-37 as a potential therapy in IL-6-, and IL-22-driven conditions.
Concluding, IL-37 is highlighted as a cytokine with broad anti-inflammatory functions, implicating its potential as therapeutic intervention.
自身炎症性疾病的根本原因多种多样,但都是由功能失调的先天性免疫反应介导的。因此,标准治疗以先天性细胞因子或阻断其受体为目标。尽管一线治疗在一些患者中取得了很好的疗效,但在另一些患者中却失败了,其原因尚不清楚。我们通过对 325 名健康成年人进行多组学分析,研究了抗炎细胞因子 IL-37 对免疫细胞的影响。我们的研究结果表明,IL-37 与炎症控制和免疫细胞活性普遍降低有关。此外,IL37 的遗传变异与训练有素的免疫力受损有关,而训练有素的免疫力是先天性免疫细胞的一种记忆表型,会导致自身炎症。为了证实 IL-37 的医疗潜力,我们建立了一个由七种自身炎症疾病组成的探索性队列。体外刺激实验证明,重组 IL-37 有可能治疗 IL-6 和 IL-22 驱动的疾病。总之,IL-37 是一种具有广泛抗炎功能的细胞因子,具有治疗干预的潜力。
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引用次数: 0
Transcriptomic studies unravel the molecular and cellular complexity of systemic lupus erythematosus: A review 转录组研究揭示了系统性红斑狼疮分子和细胞的复杂性:综述
IF 4.5 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-09-16 DOI: 10.1016/j.clim.2024.110367
Frank Qingyun Wang, Xiao Dang, Wanling Yang

Transcriptomic analysis plays a vital role in investigating Systemic Lupus Erythematosus (SLE), a complex autoimmune disease characterized by diverse clinical manifestations. This approach has yielded valuable insights into gene expression patterns and molecular regulatory mechanisms involved in SLE pathogenesis. Notably, interferon-stimulated gene (ISG) signatures are significantly upregulated in immune cells, skin, and kidney. Although a correlation with serological parameters and clinical symptoms has been proposed, the association with global disease activities remains controversial. Key findings in the field include an upregulated plasmablast signature, which positively correlates with disease activity; a neutrophil signature associated with lupus nephritis; and a decreased lymphocyte signature, reflecting lymphopenia. Tissue-level studies highlight the critical role of infiltrating immune cells in organ damage. Future research should leverage advanced technologies and integrate multi-omics data to deepen our understanding of SLE's molecular underpinnings, facilitating the development of targeted therapies.

系统性红斑狼疮(SLE)是一种复杂的自身免疫性疾病,临床表现多种多样。这种方法为了解系统性红斑狼疮发病机制中的基因表达模式和分子调控机制提供了宝贵的信息。值得注意的是,干扰素刺激基因(ISG)特征在免疫细胞、皮肤和肾脏中明显上调。虽然有人提出了与血清学参数和临床症状的相关性,但与整体疾病活动的关联仍存在争议。该领域的主要发现包括与疾病活动呈正相关的浆细胞特征上调;与狼疮肾炎相关的中性粒细胞特征;以及反映淋巴细胞减少的淋巴细胞特征下降。组织层面的研究强调了浸润免疫细胞在器官损伤中的关键作用。未来的研究应利用先进技术并整合多组学数据,以加深我们对系统性红斑狼疮分子基础的了解,从而促进靶向疗法的开发。
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引用次数: 0
High symptom burden in female X-linked chronic granulomatous disease carriers 女性X连锁慢性肉芽肿病携带者的高症状负担
IF 4.5 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-09-13 DOI: 10.1016/j.clim.2024.110364
Mary Ann Miranda , Athanasios Tsalatsanis , Jessica R. Trotter , Danielle E. Arnold , Jacqueline D. Squire , Sharon Kidd , Suhag Parikh , Rebecca A. Marsh , Linda M. Griffith , Kanwaldeep Mallhi , Deepak Chellapandian , Stephanie Si Lim , Eyal Grunebaum , Kathleen E. Sullivan , Peter E. Newburger , Mary C. Dinauer , Morton J. Cowan , Christopher C. Dvorak , Elie Haddad , Donald B. Kohn , Jennifer W. Leiding
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引用次数: 0
Enhanced fatty acid oxidation by selective activation of PPARα alleviates autoimmunity through metabolic transformation in T-cells 选择性激活 PPARα 可增强脂肪酸氧化,通过 T 细胞的新陈代谢转变缓解自身免疫。
IF 4.5 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-09-05 DOI: 10.1016/j.clim.2024.110357
Satoshi Masuyama , Masayuki Mizui , Masashi Morita , Takatomo Shigeki , Hisakazu Kato , Takeshi Yamamoto , Yusuke Sakaguchi , Kazunori Inoue , Tomoko Namba-Hamano , Isao Matsui , Tatsusada Okuno , Ryohei Yamamoto , Seiji Takashima , Yoshitaka Isaka

While fatty acid oxidation (FAO) in mitochondria is a primary energy source for quiescent lymphocytes, the impact of promoting FAO in activated lymphocytes undergoing metabolic reprogramming remains unclear. Here, we demonstrate that pemafibrate, a selective PPARα modulator used clinically for the treatment of hypertriglyceridemia, transforms metabolic system of T-cells and alleviates several autoimmune diseases. Pemafibrate suppresses Th17 cells but not Th1 cells, through the inhibition of glutaminolysis and glycolysis initiated by enhanced FAO. In contrast, a conventional PPARα agonist fenofibrate significantly inhibits cell growth by restraining overall metabolisms even at a dose insufficient to induce fatty acid oxidation. Clinically, patients receiving pemafibrate showed a significant decrease of Th17/Treg ratio in peripheral blood. Our results suggest that augmented FAO by pemafibrate-mediated selective activation of PPARα restrains metabolic programs of Th17 cells and could be a viable option for the treatment of autoimmune diseases.

线粒体中的脂肪酸氧化(FAO)是静止淋巴细胞的主要能量来源,而促进线粒体中的脂肪酸氧化对正在进行代谢重编程的活化淋巴细胞的影响尚不清楚。在这里,我们证明了培马贝特--一种在临床上用于治疗高甘油三酯血症的选择性 PPARα 调节剂--能改变 T 细胞的代谢系统并缓解多种自身免疫性疾病。培马贝特通过抑制由 FAO 增强引发的谷氨酰胺酵解和糖酵解,抑制 Th17 细胞,但不抑制 Th1 细胞。与此相反,传统的 PPARα 激动剂非诺贝特通过抑制整体代谢显著抑制细胞生长,即使剂量不足以诱导脂肪酸氧化。在临床上,接受非诺贝特治疗的患者外周血中Th17/Treg比率明显下降。我们的研究结果表明,通过培马贝特介导的 PPARα 选择性激活,增强了脂肪酸氧化,从而抑制了 Th17 细胞的代谢程序,这可能是治疗自身免疫性疾病的一种可行方案。
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引用次数: 0
Leveraging pleiotropy identifies common-variant associations with selective IgA deficiency 利用多态性确定选择性 IgA 缺乏症的共变体关联。
IF 4.5 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-09-04 DOI: 10.1016/j.clim.2024.110356
Thomas W. Willis , Effrossyni Gkrania-Klotsas , Nicholas J. Wareham , Eoin F. McKinney , Paul A. Lyons , Kenneth G.C. Smith , Chris Wallace

Selective IgA deficiency (SIgAD) is the most common inborn error of immunity (IEI). Unlike many IEIs, evidence of a role for highly penetrant rare variants in SIgAD is lacking. Previous SIgAD studies have had limited power to identify common variants due to their small sample size. We overcame this problem first through meta-analysis of two existing GWAS. This identified four novel common-variant associations and enrichment of SIgAD-associated variants in genes linked to Mendelian IEIs. SIgAD showed evidence of shared genetic architecture with serum IgA and a number of immune-mediated diseases. We leveraged this pleiotropy through the conditional false discovery rate procedure, conditioning our SIgAD meta-analysis on large GWAS of asthma and rheumatoid arthritis, and our own meta-analysis of serum IgA. This identified an additional 18 variants, increasing the number of known SIgAD-associated variants to 27 and strengthening the evidence for a polygenic, common-variant aetiology for SIgAD.

选择性 IgA 缺乏症(SIgAD)是最常见的先天性免疫错误(IEI)。与许多先天性免疫缺陷(IEI)不同,目前还没有证据表明高渗透性罕见变异在 SIgAD 中起作用。以往的 SIgAD 研究由于样本量小,识别常见变异的能力有限。我们首先通过对现有的两项全球基因组研究进行荟萃分析,克服了这一问题。这发现了四个新的共同变异关联,并在与孟德尔IEIs相关的基因中富集了SIgAD相关变异。有证据表明,SIgAD 与血清 IgA 和一些免疫介导疾病具有共同的遗传结构。我们通过条件假发现率程序利用了这一多向性,将哮喘和类风湿性关节炎的大型 GWAS 以及我们自己对血清 IgA 的荟萃分析作为 SIgAD 荟萃分析的条件。这又发现了 18 个变体,使已知的 SIgAD 相关变体增加到 27 个,从而加强了 SIgAD 多基因、共变体病因学的证据。
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引用次数: 0
The anti-mCRP199–206 antibodies aggravate tubulointerstitial lesions in lupus nephritis 抗mCRP199-206抗体会加重狼疮肾炎的肾小管间质病变。
IF 4.5 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-09-03 DOI: 10.1016/j.clim.2024.110353
Mo Yuan , Ming-hui Zhao , Ying Tan

Tubulointerstitial lesions could also be prominent in lupus nephritis, and the pathogenesis of tubulointerstitial lesions may be different from glomerular lesions. Previous studies have showed that plasma antibodies against modified /monomeric C-reactive protein (mCRP) are associated with renal tubulointerstitial lesions in patients with lupus nephritis, and amino acid (aa) 199–206 was one of the major epitopes of mCRP. However, the role of anti-mCRP199–206 antibodies in the pathogenesis of tubulointerstitial lesions in lupus nephritis is unknown. A total of 95 patients with renal biopsy-proven lupus nephritis were enrolled in this study. Plasma levels of anti-mCRP199–206 antibodies were screened by enzyme-linked immunosorbent assay (ELISA). A lupus prone mouse model was immunized using peptides mCRP199–206 to explore the potential role of anti-mCRP199–206 antibodies in tubulointerstitial lesions. The mechanism of anti-mCRP199–206 antibodies damage to renal tubular epithelial cells was investigated in vitro. Plasma antibodies against mCRP199–206 were associated with renal tubulointerstitial lesions and prognosis in patients with lupus nephritis. Immunization with peptides mCRP199–206 in lupus prone mice could aggravate tubulointerstitial lesions and drive tubulointerstitial inflammation and fibrosis. Anti-mCRP 199–206 antibodies could activate the TGF-β1/Smad3 signal pathway and induce tubular damage by binding with CRP. Circulating antibodies against mCRP199–206 could be a biomarker to reveal tubulointerstitial lesion, and participate in the pathogenesis of tubulointerstitial lesions, which might provide a potential therapeutic target for lupus nephritis.

狼疮肾炎的肾小管间质病变也可能很突出,而肾小管间质病变的发病机制可能与肾小球病变不同。先前的研究表明,狼疮肾炎患者血浆中的修饰/单体C反应蛋白(mCRP)抗体与肾小管间质病变有关,而氨基酸(aa)199-206是mCRP的主要表位之一。然而,抗 mCRP199-206 抗体在狼疮肾炎肾小管间质病变发病机制中的作用尚不清楚。本研究共招募了95名经肾活检证实的狼疮性肾炎患者。通过酶联免疫吸附试验(ELISA)检测了血浆中抗 mCRP199-206 抗体的水平。使用多肽 mCRP199-206 免疫狼疮易感小鼠模型,以探讨抗 mCRP199-206 抗体在肾小管间质病变中的潜在作用。体外研究了抗 mCRP199-206 抗体对肾小管上皮细胞的损伤机制。血浆中的mCRP199-206抗体与狼疮性肾炎患者的肾小管间质病变和预后有关。对狼疮易感小鼠进行多肽 mCRP199-206 免疫可加重肾小管间质病变,促使肾小管间质炎症和纤维化。抗 mCRP 199-206 抗体可激活 TGF-β1/Smad3 信号通路,并通过与 CRP 结合诱发肾小管损伤。循环中的mCRP199-206抗体可作为揭示肾小管间质病变的生物标志物,并参与肾小管间质病变的发病机制,从而为狼疮性肾炎提供潜在的治疗靶点。
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引用次数: 0
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Clinical immunology
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