Evidence map›Paper›PMID 29506153›Full record

ArticleThe Journal of infectious diseases2018

Interleukin-7 Unveils Pathogen-Specific T Cells by Enhancing Antigen-Recall Responses.

Nadia Terrazzini, Paola Mantegani, Florian Kern, Claudio Fortis, Anna Mondino, Stefano Caserta

Open access · hybridAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.5field-weighted citation impact, top 39% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 12 citations in OpenAlex.

  1. Persistent lymphopaenia in critically ill patients with and without sepsis: An Australian and New Zealand point prevalence study.Critical care and resuscitation : journal of the Australasian Academy of Critical Care Medicine · 2026
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  11. Involvement of TNF-Producing CD8The American journal of tropical medicine and hygiene · 2019
    Article
  12. Recombinant interleukin-7 treatment of refractoryTherapeutic advances in infectious disease
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 2 countries.

Nadia TerrazziniSchool of Pharmacy and Biomolecular Sciences, University of Brighton, United Kingdom.
Paola ManteganiLaboratory of Clinical Immunology, Clinic of Infectious Diseases, San Raffaele Scientific Institute, Milan, Italy.
Florian KernBrighton and Sussex Medical School, The University of Sussex, Falmer, East Sussex, United Kingdom.
Claudio FortisLaboratory of Clinical Immunology, Clinic of Infectious Diseases, San Raffaele Scientific Institute, Milan, Italy.
Anna MondinoDivision of Immunology, Transplantation and Infectious Diseases, San Raffaele Scientific Institute, Milan, Italy.
Stefano CasertaBrighton and Sussex Medical School, The University of Sussex, Falmer, East Sussex, United Kingdom.
Vita-Salute San Raffaele University · ITUniversity of Brighton · GBUniversity of Hull · GBUniversity of Sussex · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Interleukin (IL)-7 promotes the generation, expansion, and survival of memory T cells. Previous mouse and human studies showed that IL-7 can support immune cell reconstitution in lymphopenic conditions, expand tumor-reactive T cells for adoptive immunotherapy, and enhance effector cytokine expression by autoreactive T cells. Whether pathogen-reactive T cells also benefit from IL-7 exposure remains unknown. Methods: In this study, we investigated this issue in cultures of peripheral blood mononuclear cells (PBMCs) derived from patients infected with various endemic pathogens. After short-term exposure to IL-7, we measured PBMC responses to antigens derived from pathogens, such as Mycobacterium tuberculosis, Candida albicans, and cytomegalovirus, and to the superantigen Staphylococcus aureus enterotoxin B. Results: We found that IL-7 favored the expansion and, in some instances, the uncovering of pathogen-reactive CD4 T cells, by promoting pathogen-specific interferon-γ, IL-2, and tumor necrosis factor recall responses. Conclusions: Our findings indicate that IL-7 unveils and supports reactivation of pathogen-specific T cells with possible diagnostic, prognostic, and therapeutic significance of clinical value, especially in conditions of pathogen persistence and chronic infection.

Indexed as

AgedAntigensCandida albicansCandidiasisCD4-Positive T-LymphocytesCytomegalovirusCytomegalovirus InfectionsFemaleHumansImmunotherapy, AdoptiveInterferon-gammaInterleukin-2Interleukin-7Leukocytes, MononuclearLymphocyte ActivationMaleAntigensIL7 protein, humanInterferon-gammaInterleukin-2Interleukin-7Tumor Necrosis Factor-alpha

Identifiers

PMID29506153
PMCPMC5972594
OpenAlexW2791850006

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.