ArticleThe Journal of experimental medicine2015
ICOS and Bcl6-dependent pathways maintain a CD4 T cell population with memory-like properties during tuberculosis.
Article in The Journal of experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
86 citing papers in PubMed, 143 citations in OpenAlex.
- Antigen Availability Shapes T Cell Differentiation and Function during Tuberculosis.Cell host & microbe · 2017Trial
- Interleukin 27R regulates CD4+ T cell phenotype and impacts protective immunity during Mycobacterium tuberculosis infection.The Journal of experimental medicine · 2015Trial
- Lymphocyte-mediated immune responses to Leishmania infection.Nature reviews. Immunology · 2026Review
- Monocytic niches escape T cell surveillance and promote Mycobacterium tuberculosis persistence in lymph nodes.Immunity · 2026Article
- The study of immunological markers in tuberculosis across animal models and its translation to human research.Lab animal · 2026Review
- Nasal CD4+ tissue-resident memory T cells provide cross-protective immunity to influenza.The Journal of experimental medicine · 2026Article
- Expression of CD103 facilitates localization and activation of CD4Mucosal immunology · 2026Article
- Peptide nanofibers and PAMP agonist combinations enhance pulmonary CD4Journal of nanobiotechnology · 2026Article
- T cell-macrophage interactions in tuberculosis: What we've got here is failure to communicate.Journal of internal medicine · 2026Review
- Article
- Viral control is required for intravenous BCG-mediated protection against tuberculosis in simian immunodeficiency virus-infected macaques.Research square · 2025Article
- Beyond T-cell subsets: stemness and adaptation redefining immunity and immunotherapy.Cellular & molecular immunology · 2025Review
- Tertiary Lymphoid Structures in Tuberculosis: Persistence, Protection, and Pathology.Immunological reviews · 2025Review
- Adjunctive beneficial effect of c-di-GMP, a STING agonist, in enhancing protective efficacy of TLR4-adjuvanted tuberculosis subunit vaccine formulations.Journal of biomedical science · 2025Article
- Protein Kinase C δ: a critical hub regulating macrophage immunomodulatory functions duringbioRxiv : the preprint server for biology · 2025Article
- Heterologous prime-boost immunization combining parenteral and mucosal routes with different adjuvants mounts long-lived CD4+ T cell responses in lungs.Frontiers in immunology · 2025Article
- Article
- Reappraising the Role of T Cell-Derived IFN-γ in Restriction of Mycobacterium tuberculosis in the Murine Lung.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Re-appraising the role of T-cell derived interferon gamma in restriction ofbioRxiv : the preprint server for biology · 2024Article
- TOLLIP inhibits lipid accumulation and the integrated stress response in alveolar macrophages to control Mycobacterium tuberculosis infection.Nature microbiology · 2024Article
26 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Immune control of persistent infection with Mycobacterium tuberculosis (Mtb) requires a sustained pathogen-specific CD4 T cell response; however, the molecular pathways governing the generation and maintenance of Mtb protective CD4 T cells are poorly understood. Using MHCII tetramers, we show that Mtb-specific CD4 T cells are subject to ongoing antigenic stimulation. Despite this chronic stimulation, a subset of PD-1(+) cells is maintained within the lung parenchyma during tuberculosis (TB). When transferred into uninfected animals, these cells persist, mount a robust recall response, and provide superior protection to Mtb rechallenge when compared to terminally differentiated Th1 cells that reside preferentially in the lung-associated vasculature. The PD-1(+) cells share features with memory CD4 T cells in that their generation and maintenance requires intrinsic Bcl6 and intrinsic ICOS expression. Thus, the molecular pathways required to maintain Mtb-specific CD4 T cells during ongoing infection are similar to those that maintain memory CD4 T cells in scenarios of antigen deprivation. These results suggest that vaccination strategies targeting the ICOS and Bcl6 pathways in CD4 T cells may provide new avenues to prevent TB.
Indexed as
Identifiers
What OpenQuestion holds
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.