Document Detail

Human adipose tissue-derived mesenchymal stromal cells promote B-cell motility and chemoattraction.
MedLine Citation:
PMID:  25240680     Owner:  NLM     Status:  Publisher    
BACKGROUND AIMS: Mesenchymal stromal cells hold special interest for cell-based therapy because of their tissue-regenerative and immunosuppressive abilities. B-cell involvement in chronic inflammatory and autoimmune pathologies makes them a desirable target for cell-based therapy. Mesenchymal stromal cells are able to regulate B-cell function; although the mechanisms are little known, they imply cell-to-cell contact.
METHODS: We studied the ability of human adipose tissue-derived mesenchymal stromal cells (ASCs) to attract B cells.
RESULTS: We show that ASCs promote B-cell migration through the secretion of chemotactic factors. Inflammatory/innate signals do not modify ASC capacity to mediate B-cell motility and chemotaxis. Analysis of a panel of B cell-related chemokines showed that none of them appeared to be responsible for B-cell motility. Other ASC-secreted factors able to promote cell motility and chemotaxis, such as the cytokine interleukin-8 and prostaglandin E2, did not appear to be implicated.
CONCLUSIONS: We propose that ASC promotion of B-cell migration by undefined secreted factors is crucial for ASC regulation of B-cell responses.
Laura Barrio; Victor Delgado Cuevas; Ramón Menta; Pablo Mancheño-Corvo; Olga delaRosa; Wilfried Dalemans; Eleuterio Lombardo; Yolanda R Carrasco
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-9-17
Journal Detail:
Title:  Cytotherapy     Volume:  -     ISSN:  1477-2566     ISO Abbreviation:  Cytotherapy     Publication Date:  2014 Sep 
Date Detail:
Created Date:  2014-9-21     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100895309     Medline TA:  Cytotherapy     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2014 International Society for Cellular Therapy. Published by Elsevier Inc. All rights reserved.
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