ArticleJournal of immunology research2016
Group B Streptococcus Induces a Robust IFN-γ Response by CD4(+) T Cells in an In Vitro and In Vivo Model.
Article in Journal of immunology research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Surface protein distribution in Group B Streptococcus isolates from South Africa and identifying vaccine targets through in silico analysis.Scientific reports · 2024Article
- Gamma-Irradiated Non-Capsule Group B Streptococcus Promotes T-Cell Dependent Immunity and Provides a Cross-Protective Reaction.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Article
- Bacterial and Host Determinants of Group B Streptococcal Infection of the Neonate and Infant.Frontiers in microbiology · 2022Review
- Secretion of IFN-γ by Transgenic Mammary Epithelial CellsFrontiers in veterinary science · 2022Article
- Protective role of IL-18 in host defenses against group B Streptococcus.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2021Article
- IL-17A Secreted by Th17 Cells Is Essential for the Host againstJournal of microbiology and biotechnology · 2021Article
- TRIM32 Drives Pathogenesis in Streptococcal Toxic Shock-Like Syndrome and Streptococcus suis Meningitis by Regulating Innate Immune Responses.Infection and immunity · 2020Article
- Lipid analogs reveal features critical for hemolysis and diminish granadaene mediated Group B Streptococcus infection.Nature communications · 2020Article
- Differential outcomes of TLR2 engagement in inflammation-induced preterm birth.Journal of leukocyte biology · 2018Article
- Neonatal neutrophils stimulated by group B Streptococcus induce a proinflammatory T-helper cell bias.Pediatric research · 2018Article
- Article
- Group B Streptococcal Maternal Colonization and Neonatal Disease: Molecular Mechanisms and Preventative Approaches.Frontiers in pediatrics · 2018Review
- Natural Killer Cell Functions during the Innate Immune Response to Pathogenic Streptococci.Frontiers in microbiology · 2017Article
- Immune-responsiveness of CD4Scientific reports · 2016Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Group B Streptococcus (GBS) serotype III causes life-threatening infections. Cytokines have emerged as important players for the control of disease, particularly IFN-γ. Although potential sources of this cytokine have been proposed, no specific cell line has ever been described as a leading contributor. In this study, CD4(+) T cell activation profiles in response to GBS were evaluated through in vivo, ex vivo, and in vitro approaches. Total splenocytes readily produce a type 1 proinflammatory response by releasing IFN-γ, TNF-α, and IL-6 and actively recruit T cells via chemokines like CXCL9, CXCL10, and CCL3. Responding CD4(+) T cells differentiate into Th1 cells producing large amounts of IFN-γ, TNF-α, and IL-2. In vitro studies using dendritic cell and CD4(+) T cell cocultures infected with wild-type GBS or a nonencapsulated mutant suggested that GBS capsular polysaccharide, one of the major bacterial virulence factors, differentially modulates surface expression of CD69 and IFN-γ production. Overall, CD4(+) T cells are important producers of IFN-γ and might thus influence the course of GBS infection through the expression balance of this cytokine.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.