Level D· Scientific groundwork from lab and animal studiesAnimal StudyEurope PMCOpen access

Chemokine Receptor-6 Promotes B-1 Cell Trafficking to Perivascular Adipose Tissue, Local IgM Production and Atheroprotection

Srikakulapu P., Upadhye A., Drago F., Perry HM., Bontha SV., McSkimming C.

Animal Study, published in Front Immunol (2021) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Animal Study
Journal
Front Immunol (2021)
Reported sample size
—
Source database
Europe PMC
PMID
33679793
PMCID
PMC7933012
DOI
10.3389/fimmu.2021.636013
Citations
25

Abstract (original English)

Chemokine receptor-6 (CCR6) mediates immune cell recruitment to inflammatory sites and has cell type-specific effects on diet-induced atherosclerosis in mice. Previously we showed that loss of CCR6 in B cells resulted in loss of B cell-mediated atheroprotection, although the B cell subtype mediating this effect was unknown. Perivascular adipose tissue (PVAT) harbors high numbers of B cells including atheroprotective IgM secreting B-1 cells. Production of IgM antibodies is a major mechanism whereby B-1 cells limit atherosclerosis development. Yet whether CCR6 regulates B-1 cell number and production of IgM in the PVAT is unknown. In this present study, flow cytometry experiments demonstrated that both B-1 and B-2 cells express CCR6, albeit at a higher frequency in B-2 cells in both humans and mice. Nevertheless, B-2 cell numbers in peritoneal cavity (PerC), spleen, bone marrow and PVAT were no different in ApoE -/- CCR6 -/- compared to ApoE -/- CCR6 +/+ mice. In contrast, the numbers of atheroprotective IgM secreting B-1 cells were significantly lower in the PVAT of ApoE -/- CCR6 -/- compared to ApoE -/- CCR6 +/+ mice. Surprisingly, adoptive transfer (AT) of CD43 - splenic B cells into B cell-deficient μ MT -/- ApoE -/- mice repopulated the PerC with B-1 and B-2 cells and reduced atherosclerosis when transferred into ApoE -/- CCR6 +/+ sIgM -/- mice only when those cells expresse

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
Coronary VesselsAdipose TissueB-Lymphocyte SubsetsCells, CulturedAnimalsMice, KnockoutHumansMiceApolipoproteins EImmunoglobulin M

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