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Type I IFN impedes early bacterial control in TB-resistant and -susceptible mice and activates neutrophils to restrict lung macrophage-T cell interactions [scRNA-seq]

ABSTRACT: Type I IFN impedes early bacterial control in TB-resistant and -susceptible mice and activates neutrophils to restrict lung macrophage-T cell interactions [scRNA-seq]

PROVIDER: PRJNA1271107 | ENA |

REPOSITORIES: ENA

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Type I IFN impedes early bacterial control in TB-resistant and -susceptible mice and activates neutrophils to restrict lung macrophage-T cell interactions

Project description:Type I IFN impedes early bacterial control in TB-resistant and -susceptible mice and activates neutrophils to restrict lung macrophage-T cell interactions

| PRJNA1287792 | ENA

Type I IFN impedes early bacterial control in TB-resistant and -susceptible mice and activates neutrophils to restrict lung macrophage-T cell interactions [RNA-seq]

Project description:Type I IFN impedes early bacterial control in TB-resistant and -susceptible mice and activates neutrophils to restrict lung macrophage-T cell interactions [RNA-seq]

| PRJNA1271108 | ENA

Type I IFN impedes early bacterial control in TB-resistant and -susceptible mice and activates neutrophils to restrict lung macrophage-T cell interactions [scRNA-seq]

Project description:Only a minority of M. tuberculosis-infected individuals progress to tuberculosis, however the early immune mechanisms determining outcome are unclear. C3HeB/FeJ mice display high, partially type I IFN-dependent, tuberculosis susceptibility, compared to relatively tuberculosis-resistant C57BL/6 mice. Using bulk and scRNA-seq over the first weeks of M. tuberculosis infection, we describe an unexpected, higher early pulmonary type I IFN response in C57BL/6 than C3HeB/FeJ mice, accompanying more pronounced early monocyte-derived macrophage (MDM) accumulation and lesion formation. The C57BL/6 type I IFN response plateaued with formation of extensive CD4+ T cell-MDM interactions in lesions, accompanied by high expression of T cell-attractant chemokines by MDMs. Conversely, delayed immune initiation in C3HeB/FeJ mice preceded rapid domination of lesions by inflammatory neutrophils, depletion of which enhanced CD4+ T cell-MDM interactions. Type I IFNs unexpectedly promoted early bacterial replication and limited lesion CD4+ T cell numbers in both C57BL/6 and C3HeB/FeJ mice, while pronounced later effects on inflammatory neutrophil activation were observed in C3HeB/FeJ, suggestive of context-dependent effects of type I IFNs during M. tuberculosis infection.

2025-09-12 | GSE298787 | GEO

Type I IFN impedes early bacterial control in TB-resistant and -susceptible mice and activates neutrophils to restrict lung macrophage-T cell interactions [RNA-seq]

2025-09-12 | GSE298786 | GEO

CD177+ neutrophils restrict neuroinflammation following CNS injury

Project description:CD177+ neutrophils restrict neuroinflammation following CNS injury

| PRJNA1242790 | ENA

Type I IFN impedes early bacterial control in TB-resistant and -susceptible mice and activates neutrophils to restrict lung macrophage-T cell interactions

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-09-09 | GSE301965 | GEO

CD177+ neutrophils restrict neuroinflammation following CNS injury

Project description:Neutrophils are the most abundant circulating leukocyte population that play critical roles in neuroinflammation after ischemic stroke. CD177, a glycoprotein on neutrophils, is emerging as an important immune regulator which fundamentally affects multiple inflammatory diseases. However, the role and regulatory mechanism of CD177 protein of neutrophils in neuroinflammation remains elusive. Using single-cell RNA sequencing (scRNA-Seq), we characterized CD177high neutrophils as a novel anti-inflammatory subset in response to ischemic stroke.

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Transcriptome analysis of lung neutrophils from mice infected with Mycobacterium tuberculosis

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HSF1 Activation Can Restrict HIV Replication

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Replisomes restrict SMC translocation in vivo

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