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Study · Animal study (in vivo) · mouse · 2025

11 results

Plasmacytoid dendritic cells alleviate allergic asthma via airway epithelial cell-dependent thymosin β4 expression.

Li Y, Chen Z, Han M, Duan Z, Li R, Cui X, Ge H, Shu Y, Li H, He R

The Journal of allergy and clinical immunology18 Feb 2025Cited by 5 (Europe PMC)

PMID39978686 (opens in a new tab)DOI10.1016/j.jaci.2025.01.047 (opens in a new tab)PepBankPUB-39978686
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 study11

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In BDCA2-DTR mice with allergic asthma, Tβ4 supplementation reversed the exacerbation of asthmatic phenotypes caused by pDC depletion.

    In plain wordsIn mice with allergic asthma, thymosin beta‑4 reversed the worsening of asthma signs that followed removal of pDC cells.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseAsthmatic phenotypes after Tβ4 supplementation
    Study

    mousen: not reported in source

    house mite dust-induced allergic asthma
    Outcome group
    Respiratory function · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Importantly, Tβ4 supplementation reversed the exacerbation of asthmatic phenotypes in BDCA2-DTR mice.
  2. 02AnimalAnimal study (in vivo)Mechanism

    Through reduced CCL2 expression, Tβ4 reduced the recruitment of inflammatory monocyte-derived cells.

    In plain wordsThrough lower CCL2, thymosin beta‑4 reduced the arrival of inflammatory immune cells.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseInflammatory monocyte-derived cell recruitment
    Study

    mousen: not reported in source

    house mite dust-induced allergic asthma
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Mechanistically, Tβ4 inhibited IL-4/IL-13-induced phosphorylation of Janus kinase 1 and signal transducer and activator of transcription 6 and downstream early growth response 2 expression in macrophages, thereby reducing CCL2 expression and subsequent inflammatory monocyte-derived cell recruitment.
  3. 03LabIn vitro (cells)Mechanism

    In macrophages, Tβ4 inhibited IL-4/IL-13-induced phosphorylation of Janus kinase 1.

    In plain wordsIn macrophage cells, thymosin beta‑4 reduced IL-4/IL-13-driven activation of the enzyme Janus kinase 1.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseJAK1 phosphorylation in macrophages
    Study

    n: not reported in source

    macrophages
    Outcome group
    Receptor activity and mechanism · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Mechanistically, Tβ4 inhibited IL-4/IL-13-induced phosphorylation of Janus kinase 1 and signal transducer and activator of transcription 6 and downstream early growth response 2 expression in macrophages, thereby reducing CCL2 expression and subsequent inflammatory monocyte-derived cell recruitment.
  4. 04LabIn vitro (cells)Mechanism

    In macrophages, Tβ4 inhibited IL-4/IL-13-induced phosphorylation of STAT6.

    In plain wordsIn macrophage cells, thymosin beta‑4 reduced IL-4/IL-13-driven activation of the signal protein STAT6.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseSTAT6 phosphorylation in macrophages
    Study

    n: not reported in source

    macrophages
    Outcome group
    Receptor activity and mechanism · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Mechanistically, Tβ4 inhibited IL-4/IL-13-induced phosphorylation of Janus kinase 1 and signal transducer and activator of transcription 6 and downstream early growth response 2 expression in macrophages, thereby reducing CCL2 expression and subsequent inflammatory monocyte-derived cell recruitment.
  5. 05LabIn vitro (cells)Mechanism

    In macrophages, Tβ4 inhibited downstream early growth response 2 expression induced by IL-4/IL-13.

    In plain wordsIn macrophage cells, thymosin beta‑4 lowered the level of the protein early growth response 2.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseEGR2 expression in macrophages
    Study

    n: not reported in source

    macrophages
    Outcome group
    Receptor activity and mechanism · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Mechanistically, Tβ4 inhibited IL-4/IL-13-induced phosphorylation of Janus kinase 1 and signal transducer and activator of transcription 6 and downstream early growth response 2 expression in macrophages, thereby reducing CCL2 expression and subsequent inflammatory monocyte-derived cell recruitment.
  6. 06LabIn vitro (cells)Mechanism

    In macrophages, Tβ4 reduced CCL2 expression.

    In plain wordsIn macrophage cells, thymosin beta‑4 lowered production of the signal protein CCL2.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseCCL2 expression in macrophages
    Study

    n: not reported in source

    macrophages
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Mechanistically, Tβ4 inhibited IL-4/IL-13-induced phosphorylation of Janus kinase 1 and signal transducer and activator of transcription 6 and downstream early growth response 2 expression in macrophages, thereby reducing CCL2 expression and subsequent inflammatory monocyte-derived cell recruitment.

Natural levels measured4

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

  1. 07HumanEndogenous levelObservational studyOther

    Serum Tβ4 levels were decreased in humans with ongoing allergic asthma.

    In plain wordsIn people with allergic asthma, the body's own thymosin beta‑4 level in blood was lower.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseSerum Tβ4 in humans with allergic asthma
    Study

    n: not reported in source

    Outcome group
    Immune response · Respiratory

    Source sentences

    Summary
    Unexpectedly, decreased serum Tβ4 levels were detected in mice and humans with ongoing allergic asthma.

    This result measures the body's own Thymosin beta-4 (human). Nobody was given the peptide. It is not evidence about taking it.

  2. 08AnimalEndogenous levelAnimal study (in vivo)Mechanism

    In asthmatic mouse lung pDCs, Tβ4 was among the most upregulated genes.

    In plain wordsIn mice with asthma, the body's own thymosin beta‑4 gene was strongly switched on in lung pDC cells.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseTβ4 expression in asthmatic lung pDCs
    Study

    mousen: not reported in source

    house mite dust-induced allergic asthma
    Outcome group
    Immune response · Respiratory

    Source sentences

    Summary
    RNA-sequencing analysis revealed that the anti-inflammatory peptide thymosin β4 (Tβ4) was among the most upregulated genes in asthmatic lung pDCs.

    This result measures the body's own Thymosin beta-4 (human). Nobody was given the peptide. It is not evidence about taking it.

  3. 09AnimalEndogenous levelAnimal study (in vivo)Mechanism

    In asthmatic mice, airway epithelial cell-derived IL-33 was required for upregulating Tβ4 expression in pDCs.

    In plain wordsIn mice with asthma, the signal IL-33 from airway cells was needed to raise the body's own thymosin beta‑4 in pDC cells.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseIL-33 dependence of Tβ4 expression in pDCs
    Study

    mousen: not reported in source

    house mite dust-induced allergic asthma
    Outcome group
    Immune response · Respiratory

    Source sentences

    Summary
    Airway epithelial cell-derived IL-33 was required for upregulating Tβ4 expression in pDCs, which represented the main source of Tβ4 in asthmatic lungs.

    This result measures the body's own Thymosin beta-4 (human). Nobody was given the peptide. It is not evidence about taking it.

  4. 10AnimalEndogenous levelAnimal study (in vivo)Other

    Serum Tβ4 levels were decreased in mice with ongoing allergic asthma.

    In plain wordsIn mice with allergic asthma, the body's own thymosin beta‑4 level in blood was lower.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseSerum Tβ4 in mice with allergic asthma
    Study

    mousen: not reported in source

    house mite dust-induced allergic asthma
    Outcome group
    Immune response · Respiratory

    Source sentences

    Summary
    Unexpectedly, decreased serum Tβ4 levels were detected in mice and humans with ongoing allergic asthma.

    This result measures the body's own Thymosin beta-4 (human). Nobody was given the peptide. It is not evidence about taking it.

Studies that did not test the peptide alone1

In this study, Thymosin beta-4 (human) 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 beta-4 (human).

  1. 11AnimalNot a test of Thymosin beta-4 (human) aloneAnimal study (in vivo)Mechanism

    In asthmatic lungs, alveolar macrophages were identified as the major source of CCL2 and the target of Tβ4.

    In plain wordsIn mice with allergic asthma, alveolar macrophages were identified as the main target of thymosin beta‑4 in the lungs.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    Not applicableAlveolar macrophages as target of Tβ4
    Study

    mousen: not reported in source

    house mite dust-induced allergic asthma
    Outcome group
    Receptor activity and mechanism · Respiratory

    Source sentences

    Summary
    Alveolar macrophages were identified as the major source of CCL2 and the target of Tβ4 in asthmatic lungs.

    In this study, Thymosin beta-4 (human) 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 beta-4 (human).

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.

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