ArticleThe Journal of experimental medicine2021
High Th2 cytokine levels and upper airway inflammation in human inherited T-bet deficiency.
Article in The Journal of experimental medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- Human inherited RORγT deficiency encompasses genetic heterogeneity, T cell deficiency, and clinical homogeneity.medRxiv : the preprint server for health sciences · 2026Article
- Mendelian susceptibility to mycobacterial disease: IFN-γ-driven immunity collapse underlies heterogeneous infections.Frontiers in immunology · 2026Review
- Article
- Dendritic Cells: Origin, Classification, Development, Biological Functions, and Therapeutic Potential.MedComm · 2025Review
- Pathological IgE Production in Inborn Errors of Immunity and Beyond.Immunological reviews · 2025Review
- TThe Journal of allergy and clinical immunology · 2024Review
- Cang-ai volatile oil alleviates nasal inflammation via Th1/Th2 cell imbalance regulation in a rat model of ovalbumin-induced allergic rhinitis.Frontiers in pharmacology · 2024Article
- Rapid identification of primary atopic disorders (PAD) by a clinical landmark-guided, upfront use of genomic sequencing.Allergologie select · 2024Article
- A model of Th2 differentiation based on polarizing cytokine repression.Trends in immunology · 2023Review
- IL-6 prevents Th2 cell polarization by promoting SOCS3-dependent suppression of IL-2 signaling.Cellular & molecular immunology · 2023Article
- The ins and outs of innate and adaptive type 2 immunity.Immunity · 2023Review
- Inborn errors of human transcription factors governing IFN-γ antimycobacterial immunity.Current opinion in immunology · 2023Review
- Transcription factor defects in inborn errors of immunity with atopy.Frontiers in allergy · 2023Review
- Sensing of protease activity as a triggering mechanism of Th2 cell immunity and allergic disease.Frontiers in allergy · 2023Review
- Impaired IL-23-dependent induction of IFN-γ underlies mycobacterial disease in patients with inherited TYK2 deficiency.The Journal of experimental medicine · 2022Article
- Human Inborn Errors of Immunity: 2022 Update on the Classification from the International Union of Immunological Societies Expert Committee.Journal of clinical immunology · 2022Article
- Human T-bet governs the generation of a distinct subset of CD11cScience immunology · 2022Article
- Tissue-based IL-10 signalling in helminth infection limits IFNγ expression and promotes the intestinal Th2 response.Mucosal immunology · 2022Article
- Differential regulation of transcription factor T-bet induction during NK cell development and T helper-1 cell differentiation.Immunity · 2022Article
- ILC2s - development, divergence, dispersal.Current opinion in immunology · 2022Review
Corrections and comments
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Authors and funding
22 authors at 10 institutions in 5 countries.
Funding
Abstract
We have described a child suffering from Mendelian susceptibility to mycobacterial disease (MSMD) due to autosomal recessive, complete T-bet deficiency, which impairs IFN-γ production by innate and innate-like adaptive, but not mycobacterial-reactive purely adaptive, lymphocytes. Here, we explore the persistent upper airway inflammation (UAI) and blood eosinophilia of this patient. Unlike wild-type (WT) T-bet, the mutant form of T-bet from this patient did not inhibit the production of Th2 cytokines, including IL-4, IL-5, IL-9, and IL-13, when overexpressed in T helper 2 (Th2) cells. Moreover, Herpesvirus saimiri-immortalized T cells from the patient produced abnormally large amounts of Th2 cytokines, and the patient had markedly high plasma IL-5 and IL-13 concentrations. Finally, the patient's CD4+ αβ T cells produced most of the Th2 cytokines in response to chronic stimulation, regardless of their antigen specificities, a phenotype reversed by the expression of WT T-bet. T-bet deficiency thus underlies the excessive production of Th2 cytokines, particularly IL-5 and IL-13, by CD4+ αβ T cells, causing blood eosinophilia and UAI. The MSMD of this patient results from defective IFN-γ production by innate and innate-like adaptive lymphocytes, whereas the UAI and eosinophilia result from excessive Th2 cytokine production by adaptive CD4+ αβ T lymphocytes.
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