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Single-Cell RNA sequencing reveals clonally-expanded CD4+ tissue-resident memory T cells in Histidyl-tRNA Synthetase-induced myositis

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE335842 | GEO | 2026/07/17

REPOSITORIES: GEO

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Single-Cell RNA sequencing reveals clonally-expanded CD4+ tissue-resident memory T cells in Histidyl-tRNA Synthetase-induced myositis [2]

Project description:The precise mechanisms underlying the pathogenesis of idiopathic inflammatory myopathy (IIM) remain undefined. However, there has been increasing recognition that tissue-resident memory cells (TRMs) play an important role in the pathogenesis of systemic autoimmune disease. In IIM, TRM-associated transcriptional signatures have been reported, but on a very limited basis. By using multimodal single-cell RNA sequencing analysis in our established murine model of histidyl-tRNA synthetase (HRS)-induced myositis, we identified a prominent population of CD4+ TRMs in inflamed skeletal muscle. Muscle CD4+ TRMs exhibited high expression of genes encoding Cd69, Cxcr6, Runx3, and Prdm1, alongside low expression of Klf2, Ccr7, Sell, S1pr1, and Tcf7—a profile that is generally consistent with previous reports of TRM gene signature and that we validate through comparison to transcriptomic profiles of human muscle tissue. Detailed pathway analysis in our model indicates that muscle CD4+ TRMs contribute to innate immune regulatory pathways enriched for TNF and IFN-γ signaling. Furthermore, analysis of TCR clonotype distribution and CDR3 sequence similarity revealed pronounced clonal expansion of CD4⁺ TRMs relative to other T-cell subsets—a pattern that remained stable from 2 to 6 weeks post-immunization. Collectively, these results suggest a potential role for CD4+ TRMs in the pathogenesis of autoimmune myositis.

2026-07-17 | GSE335841 | GEO

Single-Cell RNA sequencing reveals clonally-expanded CD4+ tissue-resident memory T cells in Histidyl-tRNA Synthetase-induced myositis [1]

2026-07-17 | GSE335819 | GEO

Single-Cell RNA sequencing reveals clonally-expanded CD4+ tissue-resident memory T cells in Histidyl-tRNA Synthetase-induced myositis [RNA-seq]

2026-07-17 | GSE336063 | GEO

Single-Cell RNA sequencing reveals clonally-expanded CD4+ tissue-resident memory T cells in Histidyl-tRNA Synthetase-induced myositis

Project description:Single-Cell RNA sequencing reveals clonally-expanded CD4+ tissue-resident memory T cells in Histidyl-tRNA Synthetase-induced myositis

| PRJNA1479671 | ENA

Single-Cell RNA sequencing reveals clonally-expanded CD4+ tissue-resident memory T cells in Histidyl-tRNA Synthetase-induced myositis [1]

Project description:Single-Cell RNA sequencing reveals clonally-expanded CD4+ tissue-resident memory T cells in Histidyl-tRNA Synthetase-induced myositis [1]

| PRJNA1479637 | ENA

Single-Cell RNA sequencing reveals clonally-expanded CD4+ tissue-resident memory T cells in Histidyl-tRNA Synthetase-induced myositis [2]

Project description:Single-Cell RNA sequencing reveals clonally-expanded CD4+ tissue-resident memory T cells in Histidyl-tRNA Synthetase-induced myositis [2]

| PRJNA1479675 | ENA

Single-Cell RNA sequencing reveals clonally-expanded CD4+ tissue-resident memory T cells in Histidyl-tRNA Synthetase-induced myositis [RNA-seq]

Project description:Single-Cell RNA sequencing reveals clonally-expanded CD4+ tissue-resident memory T cells in Histidyl-tRNA Synthetase-induced myositis [RNA-seq]

| PRJNA1480651 | ENA

Secreted histidyl-tRNA synthetase splice variants elaborate major epitopes for autoantibodies in inflammatory myositis.

Project description: Not available

| S-EPMC4094037 | biostudies-literature

Antigen-driven T cell-macrophage interactions mediate the interface between innate and adaptive immunity in histidyl-tRNA synthetase-induced myositis.

Project description: Not available

| S-EPMC10556668 | biostudies-literature

T cell-Macrophage Interactions Mediate Innate and Adaptive Immune Responses in Histidyl-tRNA Synthetase-Induced Myositis

Project description:The relative contribution of innate and adaptive immunity to idiopathic inflammatory myopathy is poorly defined. We therefore sought to clarify these components of disease pathogenesis using our novel murine model of histidyl-tRNA synthetase (HRS)-induced myositis. Myositis was induced in WT and various congenic strains of C57BL/6 mice through intramuscular immunization with recombinant HRS. Histopathological, immunohistochemical, flow cytometric, and transcriptomic assessments were used to characterize muscle-infiltrating cell populations in these congenic strains. RAG1 KO mice developed markedly reduced muscle inflammation relative to WT mice, demonstrating a key requirement for T cells in driving HRS-induced myositis. Diminished cellular infiltration in CD4-Cre.MyD88fl/fl conditional knockout and OT-II TCR transgenic mice highlighted roles for innate and TCR-mediated/adaptive immune signaling in T cells. Transcriptionally-based pathway analyses showed that disruption of T cell signaling alters the function of macrophages, fibroblasts, and other non-lymphoid cell populations. Overall, these findings demonstrate that HRS-induced myositis reflects complex cellular interactions requiring the activation of both innate and adaptive T cell-mediated signaling pathways.

2023-10-18 | GSE229059 | GEO

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