Human IL13RA1 _CD213A1 Protein Vector: HEK293
- Known as:
- Human IL13RA1 _CD213A1 Protein Vector: HEK293
- Catalog number:
- 10081-H01H
- Product Quantity:
- 100μg
- Category:
- -
- Supplier:
- Provo
- Gene target:
- Human IL13RA1 _CD213A1 Protein Vector: HEK293
Related genes to: Human IL13RA1 _CD213A1 Protein Vector: HEK293
- Gene:
- IL13RA1 NIH gene
- Name:
- interleukin 13 receptor subunit alpha 1
- Previous symbol:
- -
- Synonyms:
- IL-13Ra, NR4, CD213a1
- Chromosome:
- Xq24
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-26
- Date modifiied:
- 2015-12-11
Related products to: Human IL13RA1 _CD213A1 Protein Vector: HEK293
Related articles to: Human IL13RA1 _CD213A1 Protein Vector: HEK293
- Pancreatitis is a life-threatening inflammatory disease of the pancreas. The cytokine interleukin-1α has been demonstrated to act as an alarmin released by necrotic cells. In the present study, we investigated the influence of IL-1α on the immune response during acute and chronic pancreatitis. Following tissue injury, pancreatic acinar cells released IL-1α, which activates tissue-resident fibroblasts to differentiate toward a pro-inflammatory phenotype. By secreting chemokines and cytokines such as CXCL5, CCL2, and IL-6, these fibroblasts recruit immune cells to the pancreas. The absence of IL-1α reduces disease severity in acute pancreatitis and chemokine release. Furthermore, IL-1α primes fibroblasts to enhance the production of extracellular matrix-components by the up-regulation of pro-fibrotic receptors such as Il4ra, Il13ra1, and Tgfbr3. Therefore, the deletion of IL-1α significantly reduced the development of tissue fibrosis. A therapeutic blockade of the IL1R1-signaling by i.p. administration of the IL-1-receptor antagonist Anakinra showed the same effect; the severity of acute pancreatitis and fibrogenesis during chronic pancreatitis were reduced. In conclusion, the crosstalk between necrotic acinar cells and fibroblasts mediated by IL-1α plays a crucial role in acute inflammation of the pancreas and fibrogenic signaling. Blockade of IL1R1-signaling by Anakinra is therefore a promising therapeutic intervention for both acute and chronic pancreatitis. - Source: PubMed
Publication date: 2026/09/03
Mazloum HalaBuchholz ShenjaSchifter HannaAmeling SabineSteil LeifBecker Ben LewinHammer ElkeHomuth GeorgVölker UweBröker Barbara MZierke LukasWeiss Frank UlrichGlaubitz JulianeSendler Matthias - Chronic rhinosinusitis with nasal polyps (CRSwNP) features marked infiltration of diverse inflammatory cells. Cadherin-26 (CDH26) is an adhesion molecule associated with eosinophilic inflammation, but its role in CRSwNP remains undefined. - Source: PubMed
Publication date: 2026/09/03
Zhang QinqinWang XiangdongHe TingZhang YuanZhuang MengyanSu JunMingYu XiaoruLi YingBachert ClausZhang LuoJiao Jian - Intradermal injections of anti-canine immunoglobulin E (IgE) in healthy dogs have been utilized in preclinical drug testing to evaluate the efficacy of anti-allergic drugs used to treat canine atopic dermatitis (AD). However, the molecular effects of established canine anti-allergic drugs on this acute canine IgE-mediated atopic model remain largely uninvestigated. The objective of this study was to characterize the effect of proactive oclacitinib and prednisolone treatments on the immune and skin barrier transcriptome of IgE-mediated late-phase reactions (LPRs) in an acute model of canine AD. Sixteen healthy adult research-bred beagles were randomized to receive either oclacitinib or prednisolone orally for six days, followed by an intradermal anti-canine IgE injection. Biopsies were collected 24 h post-injection for RNA isolation and sequencing; previously analyzed transcriptomes (healthy skin, saline-injected skin, IgE lesions without drug modulation) from the same colony of dogs served as controls. Administration of prednisolone and oclacitinib prior to intradermal anti-IgE injections reduced the number of differentially expressed genes (DEGs) in 24 h samples to 1251 and 1471, respectively. Both treatments resulted in a decrease in expression of several significantly upregulated T helper-(Th)1 (e.g., , , ), Th2 (e.g., , , , , , ), chemokine and receptor (e.g., , , , , ) genes in comparison to the untreated IgE-mediated lesions. Interestingly, only prednisolone treatment significantly reduced upregulation, an important gene in the Th2 immune response. In conclusion, both prednisolone and oclacitinib reduced the transcriptomic changes observed in the acute lesions of the canine IgE-induced atopic dermatitis model, with prednisolone inducing a broader inhibitory immune response. - Source: PubMed
Publication date: 2026/07/13
Leon RenatoBlubaugh AmandaStarr HaleyBanovic Frane - Atopic dermatitis (AD) is characterized by peripheral inflammation and intense pruritus. While itch-induced brain activation in AD is documented, our previous work revealed aberrant resting-state activation in the left superior frontal gyrus (LSFG). However, whether this central dysfunction is linked to peripheral immune status remains unclear. - Source: PubMed
Publication date: 2026/06/26
Dai WenyuXue ShengjieHuang XinLong XuanLou LouWang BolunWu HaishanLiao Jieyue - Cutaneous allergen sensitization (CAS) is a primary driver of atopic dermatitis (AD) and a key initiator of the "atopic march", which can lead to systemic conditions such as food allergy and anaphylaxis. The type 2 cytokine interleukin-13 (IL-13) is an important regulator of high-affinity IgE antibodies, yet the precise cellular targets and mechanisms by which it orchestrates systemic allergic responses remain incompletely understood. Here, we evaluated the role of IL-13 in a murine CAS model that links skin inflammation to systemic anaphylaxis. Using cell-specific deletions of the IL-13 receptor α1 subunit (), we identify conventional dendritic cells (cDCs), and not T or B cells, as the essential targets of IL-13 for generating high-affinity IgE. Single-cell transcriptomics reveal that IL-13 signaling acts specifically in a cDC2 subset characterized by high expression of CX3CR1, Clec10a (CD301a), and CD301b (Mgl2). Licensing by IL-13 endows these cDC2 with superior antigen-presenting capacity, characterized by the upregulation of MHC class II and costimulatory molecules, including CD301a, CD301b, and ICOSL. These mature cDC2s are mobilized from the periphery to the spleen by a CX3CR1-dependent mechanism, where they are uniquely equipped to induce the differentiation of IL-13-producing T follicular helper (T13) cells. This cascade results in robust germinal center reactions and production of pathogenic, high-affinity IgE. Our findings define an IL-13-cDC2 axis that functions as a critical regulator of the atopic march, providing a mechanistic rationale for the clinical efficacy of IL-13-targeted therapies in allergic diseases. - Source: PubMed
Publication date: 2026/07/09
Harada YasuyoSasaki TakanoriObata-Ninomiya KazushigeMatsuyama TakahiroUeha SatoshiShichino ShigeyukiWatanabe TakashiOgawa ShuheiKi SewonSuzuki YoshieIto NaotoMotomura YasutakaUeno HidekiZiegler Steven FInoue HiromasaBurrows PeterKim Brian SMurphy Kenneth MKubo Masato