IFI44L

Last update 08 May 2025

Basic Info

Synonyms

C1orf29, GS3686, IFI44L

+ [3]

Introduction

Type I interferon-stimulated gene (ISG) that plays a critical role in antiviral and antibacterial activity (PubMed:34722780). During bacterial infection, promotes macrophage differentiation and facilitates inflammatory cytokine secretion (PubMed:34722780). Plays a role in the control of respiratory syncytial virus/RSV infection, reducing the ability of the virus to replicate (PubMed:32611756). Exhibits a low antiviral activity against hepatitis C virus (PubMed:21478870). Acts also as a feedback regulator of IFN responses by negatively regulating IKBKB and IKBKE kinase activities through interaction with FKBP5 (PubMed:31434731).

100 Clinical Results associated with IFI44L

100 Translational Medicine associated with IFI44L

0 Patents (Medical) associated with IFI44L

227

Literatures (Medical) associated with IFI44L

01 May 2025·Journal of Allergy and Clinical Immunology: Global

Profiling type I and II interferon responses reveals distinct subgroups of pediatric patients with autoinflammatory disorders

Article

Author: Belot, Alexandre ; Trouillet-Assant, Sophie ; Pescarmona, Remi ; Khaldi-Plassart, Samira ; Garnier, Lorna ; Perret, Magali ; Walzer, Thierry ; Viel, Sébastien ; Villard, Marine ; Nombel, Anaïs ; Foray, Anne-Perrine ; Benezech, Sarah ; Lombard, Christine

BackgroundElevation of type I interferon (IFN-I) is characteristic of a group of diseases known as type I interferonopathies. Several technologies are available to monitor IFN-I, but there is no consensus on their routine use in medical laboratories.ObjectiveWe aimed to compare the performance of two technologies for this purpose: NanoString, which monitors messenger RNA expression of interferon-stimulated genes (ISGs), and Simoa, which quantifies IFN-α2 protein in an ultrasensitive way. We also designed a NanoString assay to monitor type II ISGs and tested its value to discriminate clinical conditions.MethodsA total of 196 samples from patients with diseases associated or not with IFN-I pathway activation were analyzed by NanoString and Simoa.ResultsThe comparison between NanoString IFN-I score and IFN-α2 Simoa revealed a r ² coefficient of 0.55. We identified IFI27, IFI44L, and SIGLEC1 as the ISGs most closely related to IFN-α2 concentration. Nineteen samples had a positive IFN-I score but undetectable IFN-α2. These samples were also positive according to IFN-II score, pointing to IFN-II as the primary ISG inducer in corresponding patients. By measuring IFN-I and IFN-II scores in a subset of patients with systemic lupus erythematosus and systemic juvenile idiopathic arthritis, we identified two subgroups of patients in whom IFN-I and IFN-II were dominant.ConclusionBoth IFN-α2 quantification and NanoString reliably distinguish type I interferonopathies from other diseases. Type I and II interferons induce different transcriptomic signatures in vitro and in vivo, and our results highlight the value of monitoring both IFN-I and IFN-II in interferon-related diseases.

01 Mar 2025·Genomics

GnRHR inhibits the malignant progression of triple-negative breast cancer by upregulating FOS and IFI44L

Article

Author: Lu, Ning ; Xue, Li ; Chen, Caiping ; Han, Chao ; Wu, Wanxin ; Lu, Xiang

Gonadotropin-releasing hormone receptor (GnRHR) has been identified as a factor that hinders the malignant advancement of triple-negative breast cancer (TNBC). Nevertheless, the specific molecular mechanism responsible for this impact remains unclear. This study demonstrates that GnRHR exhibits low expression levels in TNBC, which correlates with an unfavorable prognosis for patients. GnRHR promotes the expression of FOS, subsequently enhancing IFI44L transcription and expression, thereby inhibiting TNBC cell proliferation, migration, and invasion. Goserelin reduced the growth rate of TNBC tumors in nude mice, resulting in elevated levels of GnRHR, FOS, and IFI44L in tumor tissues, while the expression of Ki67, vimentin, and N-cadherin decreased. Overall, our results reveal that GnRHR suppresses the malignant progression of TNBC by upregulating FOS and IFI44L. Goserelin slows down the proliferation of TNBC tumors in vivo through the GnRHR/FOS/IFI44L pathway, which may present a new therapeutic approach for the management of TNBC.

31 Jan 2025·Journal of Clinical Microbiology

Two-transcript signature for differentiation and clinical outcomes in severe fever with thrombocytopenia syndrome (SFTS) patients: a double-blind, multicenter, validation study

Article

Author: Wang, Gang ; Xu, Nannan ; He, Yishan ; Guan, Yanyan ; Wen, Sai ; Yang, Lulu ; Yang, Hui ; Zhao, Lianhui ; Yao, Yongyuan

ABSTRACTSevere fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease with a high mortality rate that is often underdiagnosed due to the limitations of current laboratory testing. Timely diagnosis and early identification of severe cases are crucial to improving patient outcomes and overall survival rates. This study aimed to evaluate the efficacy of two transcripts, IFI44L and PI3, in the early differentiation between SFTS virus (SFTSV) infection and bacterial sepsis, as well as in the prompt identification of severe cases during epidemic seasons. In a prospective study conducted between 1 May 2021 and 30 September 2022, we enrolled 225 patients who presented with acute fever and thrombocytopenia at four hospitals in Shandong Province, China. The two-transcript signature provided a clear distinction between SFTS and bacterial infection, achieving an area under the receiver operating characteristic curve of 0.961 (95% confidence interval [95% CI] 0.916–0.986), outperforming C-reactive protein (0.810 [95% CI 0.738–0.870]) and procalcitonin (0.764 [95% CI 0.687–0.830]). Importantly, the relative expression of the IFI44L gene was significantly elevated in fatal SFTS cases, with an area under the curve (AUC) of 0.820 (95% CI 0.727–0.914), indicating its potential as an early prognostic marker. Additionally, IFI44L and PI3 were identified as potential biomarkers for distinguishing SFTS patients with and without invasive pulmonary aspergillosis, with AUC values of 0.817 and 0.753, respectively. Our findings demonstrate that the two-transcript signature effectively distinguishes SFTSV infection from bacterial sepsis and helps identify high-risk individuals, guiding appropriate treatment during SFTS outbreak.

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IFI44L

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