Ask about this productRelated genes to: IL11 antibody
- Gene:
- IL11 NIH gene
- Name:
- interleukin 11
- Previous symbol:
- -
- Synonyms:
- IL-11, AGIF
- Chromosome:
- 19q13.42
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-06
- Date modifiied:
- 2016-10-11
Related products to: IL11 antibody
Related articles to: IL11 antibody
- Systemic sclerosis (SSc) is a multi-organ autoimmune disease characterized by fibrosis of the skin and internal organs. Interstitial lung disease (ILD) is a major complication and leading cause of mortality in SSc. Transforming growth factor-β (TGF-β) has been implicated as a central mediator of fibrosis; however, while TGF-β1 has been extensively studied, the roles of TGF-β2 and TGF-β3 remain incompletely defined. Here, we systematically compared the effects of TGF-β1, TGF-β2, and TGF-β3 in dermal and lung fibroblasts, evaluating extracellular matrix synthesis and contraction, cytokine secretion, proliferation, and myofibroblast differentiation. TGF-β2 and TGF-β3 induced greater profibrotic cytokine release of Interleukin (IL)-6 and IL-11 and increased collagen-I and fibronectin synthesis compared with TGF-β1 in dermal and lung fibroblasts (all < 0.05). TGF-β2 and TGF-β3 stimulated greater collagen-I contraction in dermal fibroblasts ( < 0.05), but greater myofibroblast differentiation in lung fibroblasts ( < 0.05). The TGF-β isoforms did not affect proliferation. All TGF-β isoforms activated SMAD2/3 signalling; however, TGF-β2 and TGF-β3 reduced expression of TGF-β Receptor II and the inhibitory regulator, SMAD7. In summary, TGF-β2 and TGF-β3 have a more pronounced profibrotic effect than TGF-β1 on dermal and lung fibroblast functions, making them potential targets for treatment for skin and lung fibrosis in diseases such as SSc. - Source: PubMed
Publication date: 2026/04/10
Badyal RaveenKohlen BrandonKeen Kevin JDunne James VHackett Tillie-Louise - Lung adenocarcinoma (LUAD) is the main histologic subtype of lung cancer, and its incidence is on the rise. However, since the vast majority of patients are already in advanced stages at the time of diagnosis, their 5-year survival rate is only 15%, so it is urgent to explore the mechanism of the development of LUAD and improve the survival time of patients. Interleukin-11 (IL-11), a member of the IL-6 cytokine family, has an influential role in the development and progression of a variety of tumors, but the specific molecular mechanisms that promote the malignant progression of LUAD are unknown. Here, we found that the IL-11-induced activation of Akt, Erk, and STAT3 could be inhibited by knocking out the expression of Gαi1/3. In contrast, overexpression of Gαi1/3 could enhance IL-11-induced signaling. The binding of Gαi1/3 to GP130 mediates IL-11-induced downstream activation of Akt-mTOR, Erk, and STAT3, which requires recruitment of Grb2-associated binding protein 1 (Gab1). In LUAD cells, shGαi1/3 inhibited cell growth, proliferation, and migration as well as blocked the tumor-promoting ability of IL-11. However, overexpression of Gαi1/3 enhanced the IL-11-induced cell growth, proliferation, and migration. ShGαi1/3 also inhibited the proliferation of LUAD cells in vivo. Overall, the findings of this study demonstrate the Gαi1 and Gαi3 are critical for IL-11 signal transduction. Moreover, we reveal that Gαi1 and Gαi3 are highly expressed and associated with poor overall survival in lung adenocarcinoma and may thus act as potential therapeutic targets in LUAD. These results provide a novel therapeutic strategy for LUAD patients with upregulated IL-11 expression. - Source: PubMed
Publication date: 2026/04/25
Luo GaomengHu WenxuanYang JianLu ZhengCui YuanZeng WeibiaoDing HaoLi QifanChen ZhikeTong XinDing ChengXu ChunZhao Jun - Inflammatory bowel disease (IBD) is frequently accompanied by intestinal fibrosis, with non-response (NR) to long-term anti-tumor necrosis factor α (anti-TNFα) therapy occurring in approximately 23-46% of patients. Integrated analysis of single-cell and bulk RNA sequencing datasets revealed an expansion of IL11⁺ fibroblasts in inflamed intestine and their significant enrichment in non-responders. We further identified IL11⁺ fibroblasts as a central communication hub that engaged in extensive crosstalk with monocytes and may contribute to inflammatory amplification and fibrotic remodeling. Additionally, we employed machine learning approaches including least absolute shrinkage and selection operator (LASSO), support vector machines (SVM), and random forest (RF) to derive an IL11⁺ fibroblast-related gene signature effectively predicting NR to anti-TNFα in validation and test cohorts. IHC further confirmed the overexpression of IL-11 in non-responders. The signature genes we found are not only associated with immune and inflammatory responses but also with fibrosis, indicating a robust association between fibrosis and anti-TNFα treatment failure. In summary, this study highlights the important role of IL11⁺ fibroblasts in orchestrating both inflammation and fibrosis and provides an applicable model for predicting NR to anti-TNFα in IBD, thereby laying the foundation for precision medicine and targeted therapeutic strategies. - Source: PubMed
Publication date: 2026/04/23
Li WangyueHuang WeiWang JiaxinTu YiwenYang QidiZhou YaoZhang ZileZhuang HaimingGu YubeiZou DuowuZhang Yao - Graves' orbitopathy (GO), a complex autoimmune disorder, remains the most common extrathyroidal manifestation of Graves' disease. Its pathogenesis is characterized by a progressive transition from inflammation to fibrosis, leading to debilitating ocular complications. While high-dose intravenous glucocorticoids have been the standard treatment for active moderate-to-severe GO, their lack of specificity to GO pathogenesis and limited efficacy in the fibrotic phase underscore the need for targeted therapies. This review explores emerging therapeutic targets in GO, focusing on pathways implicated in both inflammatory and fibrotic mechanisms. Teprotumumab, an insulin-like growth factor 1 receptor (IGF-1R) inhibitor, has revolutionized GO treatment, demonstrating clinical efficacy in reducing proptosis and inflammation. Interleukin-6 (IL-6) inhibitors including satralizumab are undergoing clinical trials. New studies on molecular pathways have been conducted regarding inflammation and fibrosis of GO, including platelet-derived growth factor/fibroblast growth factor signaling, yes-associated protein 1/transcriptional coactivator with PDZ-binding motif mechanotransduction, sphingosine-1-phosphate (S1P)/S1P receptor axis, bone morphogenic protein 7, IL-11, IL-17 and microRNAs as well as, IGF-1R/thyroid-stimulating hormone receptor crosstalk, and IL-6 trans-signaling. Most studies focus on exploring the potential of therapeutic agents through preclinical investigations but represent promising therapeutic avenues. Therapies targeting these pathways may offer a promising potential efficacy across the entire disease spectrum, from inflammation to fibrosis, thus overcome the limitations of conventional glucocorticoid therapy and expand therapeutic options in GO. Advances in GO models may bring forward a new era of GO treatment. - Source: PubMed
Publication date: 2025/08/14
Kang Young JaeYoon Jin Sook - This study aims to elucidate the role of Enterococcusin the progression from inflammatory bowel disease to colorectal cancer (CRC), with a focus on identifying key metabolites and host genes regulated by Enterococcusand their influence on CRC development. - Source: PubMed
Publication date: 2026/03/30
Huang GangLiu JianiCheng ZhipengChen YixinChen KexinLiu WanLiu HancongXia XinhaoLu ManCui WenxiZhang QingqingYuan YiZhong FeiLiao Yiwen