ArticleJournal of clinical immunology2023
IL4Rα and IL17A Blockade Rescue Autoinflammation in SOCS1 Haploinsufficiency.
Article in Journal of clinical immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The trial behind it
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Neurological Phenotypes of SOCS1 Haploinsufficiency: Insights from Functional and Histological Investigations.Journal of clinical immunology · 2025Article
- A multimorphic variant in ThPOK causes an inborn error of immunity with T cell defects and fibrosis.The Journal of experimental medicine · 2025Article
- Research progress of SOCS in autoimmune diseases: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- The Correlation Between the Expression Levels of Serum miR-19b and SOCS-1 mRNA and Clinical Symptoms in Patients with Allergic Rhinitis.Journal of asthma and allergy · 2025Article
- Mendelian Causes of Autoimmunity: the Lupus Phenotype.Journal of clinical immunology · 2024Review
- One gene to rule them all - clinical perspectives of a potent suppressor of cytokine signaling - SOCS1.Frontiers in immunology · 2024Review
- SOCS1 deficiency-crossroads of autoimmunity and autoinflammation-two case reports.Frontiers in pediatrics · 2024Article
- SOCS1 is a critical checkpoint in immune homeostasis, inflammation and tumor immunity.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
By inhibition of JAK-STAT signaling, SOCS1 acts as a master regulator of the cytokine response across numerous tissue types and cytokine pathways. Haploinsufficiency of SOCS1 has recently emerged as a monogenic immunodysregulatory disease with marked clinical variability. Here, we describe a patient with severe dermatitis, recurrent skin infections, and psoriatic arthritis that harbors a novel heterozygous mutation in SOCS1. The variant, c.202_203delAC, generates a frameshift in SOCS1, p.Thr68fsAla*49, which leads to complete loss of protein expression. Unlike WT SOCS1, Thr68fs SOCS1 fails to inhibit JAK-STAT signaling when expressed in vitro. The peripheral immune signature from this patient was marked by a redistribution of monocyte sub-populations and hyper-responsiveness to multiple cytokines. Despite this broad hyper-response across multiple cytokine pathways in SOCS1 haploinsufficiency, the patient's clinical disease was markedly responsive to targeted IL4Rα- and IL17-blocking therapy. In accordance, the mutant allele was unable to regulate IL4Rα signaling. Further, patient cells were unresponsive to IL4/IL13 while on monoclonal antibody therapy. Together, this study reports a novel SOCS1 mutation and suggests that IL4Rα blockade may serve as an unexpected, but fruitful therapeutic target for some patients with SOCS1 haploinsufficiency.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.