Open AccessHuman Adipose Tissue‐Derived Mesenchymal Stem Cells Abrogate Plasmablast Formation and Induce Regulatory B Cells Independently of T Helper Cells
Author(s) -
Franquesa M.,
Mensah F. K.,
Huizinga R.,
Strini T.,
Boon L.,
Lombardo E.,
DelaRosa O.,
Laman J. D.,
Grinyó J. M.,
Weimar W.,
Betjes M. G. H.,
Baan C. C.,
Hoogduijn M. J.
Publication year - 2015
Publication title -
stem cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.159
H-Index - 229
eISSN - 1549-4918
pISSN - 1066-5099
DOI - 10.1002/stem.1881
Subject(s) - biology , immune system , mesenchymal stem cell , cd40 , b 1 cell , b cell , regulatory b cells , cd38 , microbiology and biotechnology , cd19 , stem cell , immunology , stromal cell , naive b cell , adipose tissue , cellular differentiation , interleukin 21 , antibody , t cell , antigen presenting cell , cytotoxic t cell , cancer research , in vitro , endocrinology , cd34 , biochemistry , gene
Mesenchymal or stromal stem cells (MSC) interact with cells of the immune system in multiple ways. Modulation of the immune system by MSC is believed to be a therapeutic option for autoimmune disease and transplant rejection. In recent years, B cells have moved into the focus of the attention as targets for the treatment of immune disorders. Current B‐cell targeting treatment is based on the indiscriminate depletion of B cells. The aim of this study was to examine whether human adipose tissue‐derived MSC (ASC) interact with B cells to affect their proliferation, differentiation, and immune function. ASC supported the survival of quiescent B cells predominantly via contact‐dependent mechanisms. Coculture of B cells with activated T helper cells led to proliferation and differentiation of B cells into CD19 + CD27 high CD38 high antibody‐producing plasmablasts. ASC inhibited the proliferation of B cells and this effect was dependent on the presence of T cells. In contrast, ASC directly targeted B‐cell differentiation, independently of T cells. In the presence of ASC, plasmablast formation was reduced and IL‐10‐producing CD19 + CD24 high CD38 high B cells, known as regulatory B cells, were induced. These results demonstrate that ASC affect B cell biology in vitro, suggesting that they can be a tool for the modulation of the B‐cell response in immune disease. S tem C ells 2015;33:880–891