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LL-37

Cathelicidin, hCAP-18, FALL-39, CAP-18

Quick Stats
Studies 2230
Trials 95
Score 1
2005 pubmed

LL-37 enhances adaptive antitumor immune response in a murine model when genetically fused with M-CSFR (J6-1) DNA vaccine.

An. Li-Li LL; Yang. Ying-Hua YH; Ma. Xiao-Tong XT; Lin. Yong-Min YM; Li. Ge G; Song. Yu-Hua YH; Wu. Ke-Fu KF

Key Findings

  • Genetically fusing LL‑37 to the M‑CSFR DNA vaccine increased both antibody and cytotoxic immune responses in mice
  • The fused vaccine extended survival of mice challenged with tumor cells expressing M‑CSFR
  • Co‑administration of LL‑37 without fusion did not improve survival, indicating the fusion is necessary

Practical Outcomes

  • For now, this study is a proof‑of‑concept that LL‑37 can act as an adjuvant when genetically linked to a DNA vaccine, but it offers no direct, actionable steps for biohackers or self‑experimenters. It suggests future vaccine designs might benefit from peptide fusions, yet human applications are far off.

Summary

Scientists attached the immune‑boosting peptide LL‑37 directly to a DNA vaccine targeting a cancer‑related receptor in mice, and this combo sparked stronger antibody and killer‑cell responses and helped the mice live longer after tumor exposure. Simply giving LL‑37 alongside the vaccine didn’t work, showing the fusion is crucial. The work is still early‑stage animal research and not a ready‑to‑use protocol for people.

Abstract

DNA vaccine against M-CSFR(J6-1) (macrophage colony-stimulating factor receptor cloned from the J6-1 leukemic cell line) has shown both protective and therapeutic effects. In this study, to explore the adjuvant effects of LL-37 to M-CSFR(J6-1) DNA vaccines, we constructed genetically fused vaccines encoding M-CSFR(J6-1) and LL-37(pF). After immunizing BALB/c mice, specific humoral and cellular immune responses were detected. Compared with pR (encoding the extracellular region of M-CSFR(J6-1)), pF was more effective in inducing humoral and cytotoxic immune response, prolonging survival of mice challenged with SP2/0-CSFR(J6-1) tumor cells, and inducing IFN-gamma and IL-4 release by splenocytes. In this study, we also constructed pLL37 (encoding the mature LL-37) and coadministrated pLL37 and pR to see whether the genetic fusion was necessary. We found that compared with pR alone, pLL37+pR could not prolong survival of mice challenged with SP2/0-CSFR(J6-1) tumor cells. Our results suggest that when genetically fused with M-CSFR(J6-1), LL-37 could enhance adaptive immune response against M-CSFR(J6-1) in a murine model challenged with tumor cells bearing M-CSFR(J6-1).

Study Information

Provider

pubmed

Year

2005

Date

2005-01-11T00:00:00.000Z

DOI

10.1016/j.leukres.2004.11.009