Menu
Peptide Database
Results
No peptides found
Featured

Use search to browse all 100+ peptides

LL-37

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

Quick Stats
Studies 2230
Trials 95
Score 2
2016 pubmed 30 citations

Cutting Edge: LL-37-Mediated Formyl Peptide Receptor-2 Signaling in Follicular Dendritic Cells Contributes to B Cell Activation in Peyer's Patch Germinal Centers.

Kim. Sae-Hae SH; Kim. Yu Na YN; Jang. Yong-Suk YS

Key Findings

  • s patches express the receptor Fpr2.",
  • ,

Practical Outcomes

  • While the work is mechanistic and done in animal models, it hints that boosting LL‑37 or FPR2 activity could help strengthen gut mucosal immunity. No dosage, safety, or human data are provided, so biohackers should treat this as a scientific insight rather than a ready‑to‑use protocol and await further research before trying supplementation.

Summary

The study shows that the antimicrobial peptide LL-37 can talk to a gut immune receptor (FPR2) on special cells that help B‑cells work. This signaling makes the gut produce more signals (CXCL13 and BAFF) that tell B‑cells to grow and make IgA antibodies, which protect the intestine.

Abstract

Peyer's patches (PPs) are the major mucosal immune-inductive site, and germinal centers (GCs) in PPs determine the quality of the Abs produced. PP GCs are continuously induced by the gut microbiota, and their maintenance contributes to the induction of strong IgA responses to Ags. In this study, we investigated the role of formyl peptide receptor (FPR)-mediated signaling in the maintenance of PP GCs, because FPRs recognize the microbiota and initiate an innate immune response by chemotaxis. We found that follicular dendritic cells (FDCs), a key organizer of B cell follicles and GCs in mucosal immunity, express Fpr2. Additionally, Fpr2-mediated signaling in PP FDCs promoted Cxcl13 and B cell activating factor expression, as well as B cell proliferation and activation. Therefore, we suggest that Fpr2-mediated signaling in FDCs plays a key role in GC maintenance in PPs and results in an Ag-specific IgA response in the gut mucosal immune compartment.

Study Information

Provider

pubmed

Year

2016

Date

2016-12-14T00:00:00.000Z

DOI

10.4049/jimmunol.1600886

Citations

30

References

29