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Study · Animal study (in vivo) · mouse · 2015

5 results

Thymosin α1 promotes the activation of myeloid-derived suppressor cells in a Lewis lung cancer model by upregulating Arginase 1.

Yuan C, Zheng Y, Zhang B, Shao L, Liu Y, Tian T, Gu X, Li X, Fan K

Biochemical and biophysical research communications23 Jun 2015Cited by 11 (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 study5

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In a mouse Lewis lung cancer model, thymosin alpha‑1 used alone increased CD8+ T cells.

    In plain wordsIn mice with lung cancer, thymosin alpha‑1 alone increased CD8+ T cells.

    Outcome
    IncreaseCD8+ T cells
    Study

    mousen: not reported in source

    Lewis lung cancer model
    Outcome group
    Immune response · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Tα1 used alone elevated CD8(+) T cells, but failed to inhibit tumor growth.
    1 context sentence
    Summary · context
    Using a Lewis lung caner model, here we report that Tα1 used alone elevated CD8(+) T cells, but failed to inhibit tumor growth.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In a mouse Lewis lung cancer model, thymosin alpha‑1 used alone failed to inhibit tumor growth.

    In plain wordsIn mice with lung cancer, thymosin alpha‑1 alone did not slow tumor growth.

    Outcome
    No significant changeTumor growth
    Study

    mousen: not reported in source

    Lewis lung cancer model
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Tα1 used alone elevated CD8(+) T cells, but failed to inhibit tumor growth.
    1 context sentence
    Summary · context
    Using a Lewis lung caner model, here we report that Tα1 used alone elevated CD8(+) T cells, but failed to inhibit tumor growth.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In a mouse Lewis lung cancer model, immunosuppressive myeloid-derived suppressor cells produced more Arginase 1 in response to thymosin alpha‑1, leading to stronger suppression of anti-tumor immunity.

    In plain wordsIn mice with lung cancer, thymosin alpha‑1 made suppressor immune cells produce more Arginase 1, which weakened anti-tumor immunity.

    Outcome
    IncreaseArginase 1 production in myeloid-derived suppressor cells
    Study

    mousen: not reported in source

    Lewis lung cancer model
    Outcome group
    Immune response · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Furthermore, immunosuppressive myeloid-derived suppressor cells (MDSCs) showed heightened Arginase 1 production in response to Tα1 treatment, which led to stronger suppression of anti-tumor immunity.
    1 context sentence
    Summary · context
    Using a Lewis lung caner model, here we report that Tα1 used alone elevated CD8(+) T cells, but failed to inhibit tumor growth.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In a mouse Lewis lung cancer model, the thymosin alpha‑1 induced upregulation of ARG1 depended on TLR/MyD88 signaling.

    In plain wordsIn mice with lung cancer, the rise in ARG1 after thymosin alpha‑1 depended on a signaling pathway called MyD88.

    Outcome
    Not applicableDependence of ARG1 upregulation on TLR/MyD88 signaling
    Study

    mousen: not reported in source

    Lewis lung cancer model
    Outcome group
    Receptor activity and mechanism · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    the upregulation of ARG1 was dependent on TLRs/MyD88 signaling
    1 context sentence
    Summary · context
    Using a Lewis lung caner model, here we report that Tα1 used alone elevated CD8(+) T cells, but failed to inhibit tumor growth.

Studies that did not test the peptide alone1

In this study, Thymosin alpha-1 was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Thymosin alpha-1.

  1. 05AnimalNot a test of Thymosin alpha-1 aloneAnimal study (in vivo)Efficacy outcome

    In a mouse Lewis lung cancer model, blocking MyD88 signaling abrogated the enhanced ARG1 expression and restored the anti-tumor efficacy of thymosin alpha‑1.

    In plain wordsIn mice with lung cancer, blocking MyD88 signaling together with thymosin alpha‑1 restored the anti-tumor effect.

    Outcome
    DecreaseAnti-tumor efficacy of Tα1 with MyD88 blockade
    Study

    mousen: not reported in source

    Lewis lung cancer model
    Comparator
    Thymosin alpha 1 without MyD88 blockade
    Outcome group
    Tumor growth · Cancer

    Source sentences

    Summary
    blocking MyD88 signaling abrogated the enhanced ARG1 expression and restored the anti-tumor efficacy of Tα1.
    1 context sentence
    Summary · context
    Using a Lewis lung caner model, here we report that Tα1 used alone elevated CD8(+) T cells, but failed to inhibit tumor growth.

    In this study, Thymosin alpha-1 was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Thymosin alpha-1.

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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