ArticleCell reports2024
CpsA mediates infection of recruited lung myeloid cells by Mycobacterium tuberculosis.
Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- An intrinsically disordered domain of transcription terminator Rho governs genome-wide Rho utilization (Rut) site selection in Mycobacterium tuberculosis.Nucleic acids research · 2026Article
- Membrane atg8ylation and autophagy in protection against Mycobacterium tuberculosis.Journal of immunology (Baltimore, Md. : 1950) · 2026Review
- Genes required forbioRxiv : the preprint server for biology · 2025Article
- Macrophage-T cell interactions promote SLAMF1 expression for enhanced TB defense.Nature communications · 2025Article
- Antigen-specific CD4+ T cells promote monocyte recruitment and differentiation into glycolytic lung macrophages to control Mycobacterium tuberculosis.PLoS pathogens · 2025Article
- Mycobacterium tuberculosis virulence lipid PDIM inhibits autophagy in mice.Nature microbiology · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Mycobacterium tuberculosis (Mtb) possesses an arsenal of virulence factors to evade host immunity. Previously, we showed that the Mtb protein CpsA, which protects Mtb against the host NADPH oxidase, is required in mice during the first 3 weeks of infection but is thereafter dispensable for full virulence. Using flow cytometry, we find that ΔcpsA Mtb is retained in alveolar macrophages, impaired in recruiting and disseminating into monocyte-derived cells, and more likely to be localized in airway cells than wild-type Mtb. The lungs of ΔcpsA-infected mice also have markedly fewer antigen-specific T cells, indicating a delay in adaptive immunity. Thus, we conclude that CpsA promotes dissemination of Mtb from alveolar macrophages and the airways and generation of an adaptive immune response. Our studies of ΔcpsA Mtb show that a more effective innate immune response against Mtb can be undermined by a corresponding delay in the adaptive immune response.
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Registered trials
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