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Study · Animal study (in vivo) · 2015

7 results

Thymosin alpha1 enhanced cytotoxicity of iNKT cells against colon cancer via upregulating CD1d expression.

Ni C, Wu P, Wu X, Zhang T, Zhang T, Wang Z, Zhang S, Qiu F, Huang J

Cancer letters7 Oct 2014Cited by 26 (Europe PMC)

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 study7

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In vivo, thymosin alpha‑1 enhanced mutual recognition between colorectal cancer cells and iNKT cells, giving stronger killing efficiency.

    In plain wordsIn animals, thymosin alpha‑1 helped immune iNKT cells attack colon cancer more strongly.

    Outcome
    IncreaseiNKT cell killing of CRC cells in vivo
    Study

    n: not reported in source

    Colorectal cancer model with iNKT cells
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    the mutual recognition between CRC and iNKT cells could be greatly enhanced by Thymosinα1 (TA), which resulted in stronger killing efficiency both in vitro and in vivo.
  2. 02LabIn vitro (cells)Efficacy outcome

    In vitro, thymosin alpha‑1 enhanced mutual recognition between colorectal cancer cells and iNKT cells, giving stronger killing of the cancer cells.

    In plain wordsIn lab tests, thymosin alpha‑1 helped immune iNKT cells kill colon cancer cells more strongly.

    Outcome
    IncreaseiNKT cell killing of CRC cells in vitro
    Study

    n: not reported in source

    Colorectal cancer (CRC) cells with iNKT cells and α-Galcer
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    the mutual recognition between CRC and iNKT cells could be greatly enhanced by Thymosinα1 (TA), which resulted in stronger killing efficiency both in vitro and in vivo.
  3. 03LabIn vitro (cells)Mechanism

    Thymosin alpha‑1 upregulated CD80 expression on colorectal cancer cells.

    In plain wordsIn lab tests, thymosin alpha‑1 raised CD80 on colon cancer cells.

    Outcome
    IncreaseCD80 expression on CRC cells
    Study

    n: not reported in source

    Colorectal cancer (CRC) cells
    Outcome group
    Immune response · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We found TA could upregulate CD80, B7H2 and CD1d expression on CRC cells.
  4. 04LabIn vitro (cells)Mechanism

    Thymosin alpha‑1 upregulated B7H2 expression on colorectal cancer cells.

    In plain wordsIn lab tests, thymosin alpha‑1 raised B7H2 on colon cancer cells.

    Outcome
    IncreaseB7H2 expression on CRC cells
    Study

    n: not reported in source

    Colorectal cancer (CRC) cells
    Outcome group
    Immune response · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We found TA could upregulate CD80, B7H2 and CD1d expression on CRC cells.
  5. 05LabIn vitro (cells)Mechanism

    Thymosin alpha‑1 upregulated CD1d expression on colorectal cancer cells.

    In plain wordsIn lab tests, thymosin alpha‑1 raised CD1d on colon cancer cells.

    Outcome
    IncreaseCD1d expression on CRC cells
    Study

    n: not reported in source

    Colorectal cancer (CRC) cells
    Outcome group
    Immune response · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We found TA could upregulate CD80, B7H2 and CD1d expression on CRC cells.
  6. 06LabIn vitro (cells)Mechanism

    In a neutralization assay, iNKT cell activation after thymosin alpha‑1 treatment depended on CD1d expression rather than on CD80 or B7H2.

    In plain wordsIn lab tests, iNKT cell activation after thymosin alpha‑1 depended on CD1d, not on CD80 or B7H2.

    Outcome
    Not applicableDependence of iNKT activation on CD1d versus CD80 or B7H2
    Study

    n: not reported in source

    Colorectal cancer (CRC) cells with iNKT cells
    Outcome group
    Immune response · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    However, neutralization assay revealed iNKT cells' activation depended on CD1d expression rather than CD80 or B7H2.
  7. 07LabIn vitro (cells)Mechanism

    Inhibition of the Erk/MAPK pathway greatly attenuated the upregulation of CD1d by thymosin alpha‑1 in colorectal cancer cells.

    In plain wordsIn lab tests, blocking the Erk/MAPK pathway largely stopped thymosin alpha‑1 from raising CD1d on colon cancer cells.

    Outcome
    Not applicableErk/MAPK dependence of thymosin alpha 1 induced CD1d upregulation
    Study

    n: not reported in source

    Colorectal cancer (CRC) cells
    Outcome group
    Immune response · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Mechanistically, inhibition of Erk/MAPK pathway greatly attenuated the upregulation of CD1d by TA.

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 3Current

    10 Oct 2026, 08:55 UTC

    Study results updated

  2. Version 2

    9 Oct 2026, 03:03 UTC

    Study data updated · source update from Europe PMC

  3. Version 1

    9 Oct 2026, 03:02 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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