Human adipose tissue-derived mesenchymal stromal cells promote B-cell motility and chemoattraction.
Laura Barrio, Victor Delgado Cuevas, Ramón Menta, Pablo Mancheño-Corvo, Olga delaRosa, Wilfried Dalemans, Eleuterio Lombardo, Yolanda R Carrasco
Author Information
Laura Barrio: B Cell Dynamics Laboratory, Department of Immunology and Oncology, Centro Nacional de Biotecnología (CNB)-CSIC, UAM-Campus Cantoblanco, Madrid, Spain.
Victor Delgado Cuevas: B Cell Dynamics Laboratory, Department of Immunology and Oncology, Centro Nacional de Biotecnología (CNB)-CSIC, UAM-Campus Cantoblanco, Madrid, Spain.
Ramón Menta: TiGenix SAU, Parque Tecnológico de Madrid, Madrid, Spain.
Pablo Mancheño-Corvo: TiGenix SAU, Parque Tecnológico de Madrid, Madrid, Spain.
Olga delaRosa: TiGenix SAU, Parque Tecnológico de Madrid, Madrid, Spain.
Wilfried Dalemans: TiGenix NV, Leuven, Belgium.
Eleuterio Lombardo: TiGenix SAU, Parque Tecnológico de Madrid, Madrid, Spain.
Yolanda R Carrasco: B Cell Dynamics Laboratory, Department of Immunology and Oncology, Centro Nacional de Biotecnología (CNB)-CSIC, UAM-Campus Cantoblanco, Madrid, Spain. Electronic address: ycarrasco@cnb.csic.es.
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.
