ArticlePloS one2018
LatY136F knock-in mouse model for human IgG4-related disease.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 31 citations in OpenAlex.
- Effects of anti-CD19 CAR-T cells in a murine model of IgG4-related disease.Arthritis research & therapy · 2026Article
- IgG4-related Disease: Recent Topics on Immunological Aspects of This Disorder and Their Application in New Treatment Strategies.Internal medicine (Tokyo, Japan) · 2025Review
- Effects of Corticosteroid Treatment on Olfactory Dysfunction in LATY136F Knock-In Mice.Cureus · 2024Article
- Expression of USP25 associates with fibrosis, inflammation and metabolism changes in IgG4-related disease.Nature communications · 2024Article
- Defective LAT signalosome pathology in mice mimics human IgG4-related disease at single-cell level.The Journal of experimental medicine · 2023Article
- Article
- TSLP promoting B cell proliferation and polarizing follicular helper T cell as a therapeutic target in IgG4-related disease.Journal of translational medicine · 2022Article
- ZAP70, too little, too much can lead to autoimmunity.Immunological reviews · 2022Review
- Potential roles of non-lymphocytic cells in the pathogenesis of IgG4-related disease.Frontiers in immunology · 2022Review
- Pathogenic roles and therapeutic potential of the CCL8-CCR8 axis in a murine model of IgG4-related sialadenitis.Arthritis research & therapy · 2021Article
- The Clinical Aspect of Adaptor Molecules in T Cell Signaling: Lessons Learnt From Inborn Errors of Immunity.Frontiers in immunology · 2021Review
- The pronounced lung lesions developing in LATY136F knock-in mice mimic human IgG4-related lung disease.PloS one · 2021Article
- Animal Models of Autoimmune Liver Diseases: a Comprehensive Review.Clinical reviews in allergy & immunology · 2020Review
- A novel model for treatment of hypertrophic pachymeningitis.Annals of clinical and translational neurology · 2019Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe adaptor protein Linker for activation of T cell (LAT) is a key signaling hub used by the T cell antigen receptor. Mutant mice expressing loss-of-function mutations affecting LAT and including a mutation in which tyrosine 136 is replaced by a phenylalanine (LatY136F) develop lymphoproliferative disorder involving T helper type 2 effector cells capable of triggering a massive polyclonal B cell activation that leads to hypergammaglobulinemia G1 and E and to non-resolving inflammation and autoimmunity. The purpose of this study was to evaluate whether the phenotypes of LatY136F knock-in mice resemble the immunohistopathological features of immunoglobulin G4-related disease (IgG4-RD).
methodsLatY136F knock-in mice were sacrificed at 4-20 weeks of age, and pancreas, kidney, salivary gland and lung were obtained. All organs were stained with hematoxylin-eosin and with Azan for estimation of collagen in fibrosis, and the severity scores of inflammation and fibrosis were evaluated. Immunostainings were performed to analyze the types of infiltrating cells. In addition, the effects of corticosteroid treatment on the development of tissue lesions and serum levels of IgG1 were assessed.
resultsTissue lesions characterized by inflammatory mononuclear cell infiltration and fibrosis were detected in pancreas, kidney, and salivary gland starting from 6 weeks of age. Immunostainings showed pronounced infiltration of plasma cells, CD4-positive T cells, and macrophages. Infiltrating plasma cells predominantly expressed IgG1. The extent of inflammation in pancreas and salivary glands was markedly reduced by corticosteroid treatment.
conclusionsLatY136F knock-in mice displayed increased production of Th2-type IgG1 (a homologue of human IgG4) and developed multiple organ tissue lesions reminiscent of those seen in patients with IgG4-RD. Moreover, the development of these tissue lesions was highly sensitive to corticosteroid treatment like in IgG4-RD. For these reasons we consider the LatY136F knock-in mouse strain to represent a promising model for human IgG4-RD.
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