Evidence map›Paper›PMID 34503523›Full record

ReviewCell communication and signaling : CCS2021

Mechanisms and functions of endocytosis in T cells.

John C Charpentier, Philip D King

Open access · goldAbstract readReview
In one paragraph

Review in Cell communication and signaling : CCS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. BLOC1S1 regulates autolysosomal and exosomal dynamics during CD4bioRxiv : the preprint server for biology · 2026
    Article
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  12. Macropinosomes are a site of HIV-1 entry into primary CD4Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  13. Converting TCR-based chimeric antigen receptor STAR into dual-specific targeting receptor for cancer immunotherapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  14. 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

2 authors at 1 institution in 1 country.

John C CharpentierDepartment of Microbiology and Immunology, University of Michigan Medical School, 6606 Med Sci II, 1150 West Medical Center Drive, Ann Arbor, MI, 48109-5620, USA.
Philip D KingDepartment of Microbiology and Immunology, University of Michigan Medical School, 6606 Med Sci II, 1150 West Medical Center Drive, Ann Arbor, MI, 48109-5620, USA. kingp@umich.edu.ORCID 0000-0002-5598-2748
University of Michigan · US

Funding

NIH HHS AI T32007413
6 · The paper itself

Abstract

Once thought of primarily as a means to neutralize pathogens or to facilitate feeding, endocytosis is now known to regulate a wide range of eukaryotic cell processes. Among these are regulation of signal transduction, mitosis, lipid homeostasis, and directed migration, among others. Less well-appreciated are the roles various forms of endocytosis plays in regulating αβ and, especially, γδ T cell functions, such as T cell receptor signaling, antigen discovery by trogocytosis, and activated cell growth. Herein we examine the contribution of both clathrin-mediated and clathrin-independent mechanisms of endocytosis to T cell biology. Video Abstract.

Indexed as

EndocytosisHumansIntraepithelial LymphocytesReceptors, Antigen, T-CellReceptors, Antigen, T-Cell, alpha-betaSignal TransductionT-LymphocytesReceptors, Antigen, T-CellReceptors, Antigen, T-Cell, alpha-betaCell growthEndocytosisMacropinocytosisTCR signalingT lymphocytes

Identifiers

PMID34503523
PMCPMC8427877
OpenAlexW3198507431

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.