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Thymosin-alpha-1

Thymalfasin, Zadaxin, Thymosin α1

Quick Stats
Studies 759
Trials 63
Score 1
2004 pubmed

Thymosin alpha 1 activates dendritic cells for antifungal Th1 resistance through toll-like receptor signaling.

Romani. Luigina L; Bistoni. Francesco F; Gaziano. Roberta R; Bozza. Silvia S; Montagnoli. Claudia C; Perruccio. Katia K; Pitzurra. Lucia L; Bellocchio. Silvia S; Velardi. Andrea A; Rasi. Guido G; Di Francesco. Paolo P; Garaci. Enrico E

Key Findings

  • Thymosin‑alpha‑1 triggers dendritic cell maturation and IL‑12 production via p38/NF‑kB and MyD88‑dependent Toll‑like receptor pathways
  • This activation leads to a stronger Th1‑type immune response against the fungus Aspergillus fumigatus
  • In mice that received hematopoietic transplants, the peptide improved survival by protecting against invasive aspergillosis

Practical Outcomes

  • For biohackers, the results are interesting but not directly usable. The work is pre‑clinical, so there’s no clear protocol, dosage, or safety data for humans. Until human studies are done, it’s not a practical supplement for boosting immunity against fungal infections.

Summary

The study shows that the peptide thymosin‑alpha‑1 can help immune cells called dendritic cells mature and produce signals that boost a type of antifungal defense in mice, especially after a bone‑marrow transplant, but it’s all in animal models and doesn’t give any human dosing or safety info.

Abstract

Dendritic cells (DCs) show a remarkable functional plasticity in the recognition of Aspergillus fumigatus and orchestrate the antifungal immune resistance in the lungs. Here, we show that thymosin alpha 1, a naturally occurring thymic peptide, induces functional maturation and interleukin-12 production by fungus-pulsed DCs through the p38 mitogen-activated protein kinase/nuclear factor (NF)-kappaB-dependent pathway. This occurs by signaling through the myeloid differentiation factor 88-dependent pathway, involving distinct Toll-like receptors. In vivo, the synthetic peptide activates T-helper (Th) cell 1-dependent antifungal immunity, accelerates myeloid cell recovery, and protects highly susceptible mice that received hematopoietic transplants from aspergillosis. By revealing the unexpected activity of an old molecule, our finding provides the rationale for its therapeutic utility and qualify the synthetic peptide as a candidate adjuvant promoting the coordinated activation of the innate and adaptive Th immunity to the fungus.

Study Information

Provider

pubmed

Year

2004

Date

2004-02-24T00:00:00.000Z

DOI

10.1182/blood-2003-11-4036