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Study · In vitro (cells) · 2022

8 results

Thymosin α-1 Reverses M2 Polarization of Tumor-Associated Macrophages during Efferocytosis.

Wei YT, Wang XR, Yan C, Huang F, Zhang Y, Liu X, Wen ZF, Sun XT, Zhang Y, Chen YQ, Gao R, Pan N, Wang LX

Cancer research1 May 2022Cited by 72 (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 study8

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

  1. 01LabIn vitro (cells)Mechanism

    In breast tumor-associated macrophages exposed to apoptotic cells, thymosin alpha‑1 reversed M2 polarization during efferocytosis.

    In plain wordsIn cells, thymosin alpha‑1 reversed a tumor-supporting state of immune cells called M2 polarization.

    Outcome
    DecreaseM2 polarization of IL10-producing tumor-associated macrophages during efferocytosis
    Study

    n: not reported in source

    Tumor-associated macrophages exposed to apoptotic tumor cells (efferocytosis)
    Outcome group
    Immune response · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Here we report that, in the breast tumor microenvironment, thymosin α-1 (Tα-1) significantly reverses M2 polarization of IL10-producing tumor-associated macrophages (TAM) during efferocytosis induced by apoptotic cells.
  2. 02LabIn vitro (cells)Mechanism

    In macrophage and apoptotic tumor cell systems, thymosin alpha‑1 bound to phosphatidylserine on apoptotic tumor cells and was internalized by macrophages.

    In plain wordsIn cells, thymosin alpha‑1 bound to dying tumor cells and was taken up by immune cells called macrophages.

    Outcome
    Not applicableBinding to phosphatidylserine on apoptotic tumor cells and uptake by macrophages
    Study

    n: not reported in source

    Macrophages and apoptotic tumor cells
    Outcome group
    Receptor activity and mechanism · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Tα-1, which bound to phosphatidylserine on the surface of apoptotic tumor cells and was internalized by macrophages
  3. 03LabIn vitro (cells)Mechanism

    In macrophages exposed to apoptotic tumor cells, thymosin alpha‑1 activated SHIP1 through the lysosomal TLR7/MyD88 pathway.

    In plain wordsIn cells, thymosin alpha‑1 switched on an immune signal called SHIP1 through the TLR7/MyD88 pathway.

    Outcome
    IncreaseSHIP1 activation through the lysosomal TLR7/MyD88 pathway
    Study

    n: not reported in source

    Macrophages and apoptotic tumor cells
    Outcome group
    Receptor activity and mechanism · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    triggered the activation of SH2-containing inositol 5'-phosphatase 1 (SHIP1) through the lysosomal Toll-like receptor 7 (TLR7)/MyD88 pathway
  4. 04LabIn vitro (cells)Mechanism

    In macrophages exposed to apoptotic tumor cells, thymosin alpha‑1 led to dephosphorylation of efferocytosis-activated TBK1.

    In plain wordsIn cells, thymosin alpha‑1 reduced the activity of an immune enzyme called TBK1.

    Outcome
    DecreaseDephosphorylation of efferocytosis-activated TBK1
    Study

    n: not reported in source

    Macrophages and apoptotic tumor cells
    Outcome group
    Receptor activity and mechanism · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    subsequently resulting in dephosphorylation of efferocytosis-activated TBK1 and reduction of efferocytosis-induced IL10.
  5. 05LabIn vitro (cells)Mechanism

    In macrophages exposed to apoptotic tumor cells, thymosin alpha‑1 reduced efferocytosis-induced IL10.

    In plain wordsIn cells, thymosin alpha‑1 lowered the immune-suppressing signal IL10 that dying-cell clearance had caused.

    Outcome
    DecreaseEfferocytosis-induced IL10
    Study

    n: not reported in source

    Macrophages and apoptotic tumor cells
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    and reduction of efferocytosis-induced IL10.

Studies that did not test the peptide alone3

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. 06AnimalNot a test of Thymosin alpha-1 aloneAnimal study (in vivo)Efficacy outcome

    In an in vivo breast cancer model, thymosin alpha‑1 combined with epirubicin chemotherapy markedly suppressed tumor growth.

    In plain wordsIn an animal breast cancer model, thymosin alpha‑1 together with epirubicin chemotherapy strongly slowed tumor growth.

    Outcome
    DecreaseTumor growth in breast cancer model
    Study

    n: not reported in source

    In vivo breast cancer model
    Outcome group
    Tumor growth · Cancer

    Source sentences

    Summary
    Tα-1 combined with epirubicin chemotherapy markedly suppressed tumor growth in an in vivo breast cancer model by reducing macrophage-derived IL10 and enhancing the number and function of tumor-infiltrating CD4+ and CD8+ T cells.

    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.

  2. 07AnimalNot a test of Thymosin alpha-1 aloneAnimal study (in vivo)Mechanism

    In an in vivo breast cancer model, thymosin alpha‑1 combined with epirubicin reduced macrophage-derived IL10.

    In plain wordsIn an animal breast cancer model, thymosin alpha‑1 together with epirubicin lowered IL10 made by macrophages.

    Outcome
    DecreaseMacrophage-derived IL10
    Study

    n: not reported in source

    In vivo breast cancer model
    Outcome group
    Inflammation markers · Immune and inflammation

    Source sentences

    Summary
    Tα-1 combined with epirubicin chemotherapy markedly suppressed tumor growth in an in vivo breast cancer model by reducing macrophage-derived IL10

    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.

  3. 08AnimalNot a test of Thymosin alpha-1 aloneAnimal study (in vivo)Mechanism

    In an in vivo breast cancer model, thymosin alpha‑1 combined with epirubicin enhanced the number and function of tumor-infiltrating CD4+ and CD8+ T cells.

    In plain wordsIn an animal breast cancer model, thymosin alpha‑1 together with epirubicin increased the number and function of T cells inside tumors.

    Outcome
    IncreaseNumber and function of tumor-infiltrating CD4+ and CD8+ T cells
    Study

    n: not reported in source

    In vivo breast cancer model
    Outcome group
    Immune response · Immune and inflammation

    Source sentences

    Summary
    Tα-1 combined with epirubicin chemotherapy markedly suppressed tumor growth in an in vivo breast cancer model by reducing macrophage-derived IL10 and enhancing the number and function of tumor-infiltrating CD4+ and CD8+ T cells

    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, 08:19 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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