Mesenchymal stem cells from human bone marrow or adipose tissue differently modulate mitogen-stimulated B-cell immunoglobulin production in vitro.
Mesenchymal stem cells (MSC) have been characterized as multipotent cells which are able to differentiate into several mesodermal and nonmesodermal lineage cells and this feature along with their extensive growth and comprehensive immunomodulatory properties establish them as a promising tool for therapeutic applications, including cell-based tissue engineering and treatment of immune-mediated disorders. Although bone marrow (BM) is the most common MSC source, cells with similar characteristics have been shown to be present in several other adult tissues. Adipose tissue (AT), large quantities of which can be easily obtained, represents an attractive alternative to BM in isolating adipose tissue-derived MSC (AT-MSC). BM-MSCs and AT-MSCs share some immunomodulatory properties as they are both not inherently immunogenic and suppress the proliferation of alloantigen- or mitogen-stimulated T-cells. Our purpose was to comparatively examine under appropriate in vitro conditions, phenotypes, morphology and some functional properties of BM-MSCs and AT-MSCs, such as differentiation potential and especially the ability to suppress the immunoglobulin production by mitogen-stimulated B-cells. While the morphological, immunophenotypical, colony-forming and adipogenic characteristics of both types of cells were almost identical, AT-MSCs showed less potential for osteogenic differentiation than BM-MSCs. We found that AT-MSCs not only inhibited the Ig-production but also suppressed this B-cell function to a much greater extent compared to BM-MSC. This finding supports the potential role of AT-MSCs as an alternative to BM-MSCs for clinical purposes.
Bochev
Ivan
I
Department of Molecular Immunology, Institute of Biology and Immunology of Reproduction, Bulgarian Academy of Sciences,73 Tzarigradsko shosse, 1113 Sofia, Bulgaria.
Elmadjian
Gabriel
G
Kyurkchiev
Dobroslav
D
Tzvetanov
Liubomir
L
Altankova
Iskra
I
Tivchev
Peter
P
Kyurkchiev
Stanimir
S
D050156:Adipogenesis / Q000187:drug effects; D000273:Adipose Tissue / Q000166:cytology* / Q000187:drug effects; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000917:Antibody Formation / Q000187:drug effects / Q000276:immunology*; D015703:Antigens, CD / Q000378:metabolism; D001402:B-Lymphocytes / Q000166:cytology / Q000187:drug effects* / Q000276:immunology*; D001854:Bone Marrow Cells / Q000166:cytology* / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D002469:Cell Separation; D048430:Cell Shape / Q000187:drug effects; D002478:Cells, Cultured; D003114:Colony-Forming Units Assay; D000071063:Endoglin; D005347:Fibroblasts / Q000166:cytology / Q000187:drug effects; D006801:Humans; D016130:Immunophenotyping; D059630:Mesenchymal Stem Cells / Q000166:cytology* / Q000187:drug effects; D008875:Middle Aged; D008934:Mitogens / Q000494:pharmacology*; D010012:Osteogenesis / Q000187:drug effects; D011956:Receptors, Cell Surface / Q000378:metabolism; D014746:Vimentin / Q000378:metabolism
D015703:Antigens, CD; C064206:ENG protein, human; D000071063:Endoglin; D008934:Mitogens; D011956:Receptors, Cell Surface; D014746:Vimentin