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Study · In vitro (cells) · 2009

1 result

Thymosin beta 4 enhances NK cell cytotoxicity mediated by ICAM-1.

Lee HR, Yoon SY, Kang HB, Park S, Kim KE, Cho YH, Kim S, Kim CW, Cho BJ, Lee WJ, Bang SI, Park H, Cho D

Immunology letters1 Mar 2009Cited by 15 (Europe PMC)

PMID19369144 (opens in a new tab)DOI10.1016/j.imlet.2009.02.008 (opens in a new tab)PepBankPUB-19369144
Publisher pagePubMedAsk about this study
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Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study1

1 result from studies that gave the peptide. No result from this study comes from people.

  1. 01LabIn vitro (cells)Activity measurement

    In NK cells, synthetic thymosin beta‑4 peptide increased ICAM-1-mediated cytotoxicity through secretion of cytolytic granules to target cells.

    In plain wordsIn cells, synthetic thymosin beta‑4 made natural killer cells kill target cells more, through release of cytolytic granules.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseNK cell cytotoxicity mediated by ICAM-1
    Study

    n: not reported in source

    NK cells
    Outcome group
    Immune response · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In this study, we show that synthetic T beta 4 peptide increases NK cell cytotoxicity mediated by intercellular adhesion molecule-1 (ICAM-1) through the secretion of cytolytic granules to target cells.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    13 Oct 2026, 01:52 UTC

    Study results updated

  2. Version 1

    12 Oct 2026, 18:17 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

Publication types

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