Evidence map›Paper›PMID 33383959›Full record

ArticleInternational journal of molecular sciences2020

The Proteomic Landscape of Resting and Activated CD4+ T Cells Reveal Insights into Cell Differentiation and Function.

Yashwanth Subbannayya, Markus Haug, Sneha M Pinto, Varshasnata Mohanty, Hany Zakaria Meås, Trude Helen Flo, T S Keshava Prasad, Richard K Kandasamy

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Signature Proteins in Small Extracellular Vesicles of Granulocytes and CD4International journal of molecular sciences · 2024
    Article
  6. Article
  7. Targeting NAD+ Metabolism to Modulate Autoimmunity and Inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2024
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
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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

8 authors at 2 institutions in 2 countries.

Yashwanth SubbannayyaCentre of Molecular Inflammation Research (CEMIR),Department of Clinical and Molecular Medicine (IKOM), Norwegian University of Science and Technology, 7491 Trondheim, Norway.
Markus HaugCentre of Molecular Inflammation Research (CEMIR),Department of Clinical and Molecular Medicine (IKOM), Norwegian University of Science and Technology, 7491 Trondheim, Norway.
Sneha M PintoCentre of Molecular Inflammation Research (CEMIR),Department of Clinical and Molecular Medicine (IKOM), Norwegian University of Science and Technology, 7491 Trondheim, Norway.
Varshasnata MohantyCenter for Systems Biology and Molecular Medicine, Yenepoya (Deemed to be University), Mangalore 575018, India.
Hany Zakaria MeåsCentre of Molecular Inflammation Research (CEMIR),Department of Clinical and Molecular Medicine (IKOM), Norwegian University of Science and Technology, 7491 Trondheim, Norway.
Trude Helen FloCentre of Molecular Inflammation Research (CEMIR),Department of Clinical and Molecular Medicine (IKOM), Norwegian University of Science and Technology, 7491 Trondheim, Norway.
T S Keshava PrasadCenter for Systems Biology and Molecular Medicine, Yenepoya (Deemed to be University), Mangalore 575018, India.
Richard K KandasamyCentre of Molecular Inflammation Research (CEMIR),Department of Clinical and Molecular Medicine (IKOM), Norwegian University of Science and Technology, 7491 Trondheim, Norway.ORCID 0000-0002-0894-1222
Norwegian University of Science and Technology · NOYenepoya University · IN

Funding

Research Council of Norway 223255/F50Research Council of Norway 263168
6 · The paper itself

Abstract

CD4+ T cells (T helper cells) are cytokine-producing adaptive immune cells that activate or regulate the responses of various immune cells. The activation and functional status of CD4+ T cells is important for adequate responses to pathogen infections but has also been associated with auto-immune disorders and survival in several cancers. In the current study, we carried out a label-free high-resolution FTMS-based proteomic profiling of resting and T cell receptor-activated (72 h) primary human CD4+ T cells from peripheral blood of healthy donors as well as SUP-T1 cells. We identified 5237 proteins, of which significant alterations in the levels of 1119 proteins were observed between resting and activated CD4+ T cells. In addition to identifying several known T-cell activation-related processes altered expression of several stimulatory/inhibitory immune checkpoint markers between resting and activated CD4+ T cells were observed. Network analysis further revealed several known and novel regulatory hubs of CD4+ T cell activation, including IFNG, IRF1, FOXP3, AURKA, and RIOK2. Comparison of primary CD4+ T cell proteomic profiles with human lymphoblastic cell lines revealed a substantial overlap, while comparison with mouse CD+ T cell data suggested interspecies proteomic differences. The current dataset will serve as a valuable resource to the scientific community to compare and analyze the CD4+ proteome.

Indexed as

Cell DifferentiationLymphocyte ActivationProteomeProteomicsAdaptive ImmunityAnimalsCD4-Positive T-LymphocytesCell LineHumansImmune Checkpoint ProteinsMass SpectrometryMiceSignal TransductionImmune Checkpoint ProteinsProteomeadaptive immunityCD4+ T helper cellslabel-free quantitationmass spectrometryproteomicssystems biologyT-lymphocytes

Identifiers

PMID33383959
PMCPMC7795831
OpenAlexW3116200015

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.