Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMedOpen access

Adipose-derived mesenchymal stromal cells modulate experimental autoimmune arthritis by inducing an early regulatory innate cell signature.

Lopez-Santalla M., Menta R., Mancheño-Corvo P., Lopez-Belmonte J., DelaRosa O., Bueren JA.

Animal Study on Autoimmune Research, published in Immun Inflamm Dis (2016) — 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
Immun Inflamm Dis (2016)
Country
England
Reported sample size
—
Source database
PubMed
PMID
27957329
PMCID
PMC4879467
DOI
10.1002/iid3.106
Citations
20

Abstract (original English)

Modulation of innate immune responses in rheumatoid arthritis and other immune-mediated disorders is of critical importance in the clinic since a growing body of information has shown the key contribution of dysregulated innate responses in the progression of the disease. Mesenchymal stromal cells (MSCs) are the focus of intensive efforts worldwide due to their key role in tissue regeneration and modulation of inflammation. In this study, we define innate immune responses occurring during the early course of treatment with a single dose of expanded adipose-derived MSCs (eASCs) in established collagen-induced arthritis. eASCs delay the progression of the disease during the early phase of the disease. This is accompanied by a transient induction of Ly6C + monocytes that differentiate into IL10 + F4/80 + cells in arthritic mice. Strikingly, the induced IL10 + F4/80 + myeloid cells preferentially accumulated in the draining lymph nodes. This effect was accompanied with a concomitant declining of their frequencies in the spleens. Our results show that eASCs attenuate the arthritic process by inducing an early innate cell signature that involves a transient induction of Ly6C + monocytes in periphery that differentiate into IL10 + F4/80 + macrophages. Our findings demonstrate that early regulatory innate cell responses, involving the monocyte compartment, are targeted by the eASCs dur

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
Adipose TissueAdiposityAnimalsArthritis, ExperimentalAutoimmune DiseasesCell DifferentiationMesenchymal Stem Cell TransplantationMesenchymal Stem CellsMiceMonocytes

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