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Evidence for the Involvement of Galectin‐3 in Mesenchymal Stem Cell Suppression of Allogeneic T‐Cell Proliferation
Author(s) -
Sioud M.,
Mobergslien A.,
Boudabous A.,
Fløisand Y.
Publication year - 2010
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.2010.02378.x
Subject(s) - biology , mesenchymal stem cell , progenitor cell , microbiology and biotechnology , galectin 1 , gene knockdown , immune system , haematopoiesis , stem cell , cd34 , innate immune system , immunology , cell culture , genetics
Human bone marrow‐derived mesenchymal stem cells (MSC) are multipotent non‐hematopoietic progenitors that have regulatory activity on immune cells. NOD‐ and Toll‐like receptors (NLR, TLR) have several roles in immunity, including those relevant to pathogen recognition and shaping the course of immune responses by controlling gene expression. We have shown that these innate immune receptors are expressed by hematopoietic CD34+ progenitors and MSC. To uncover genes critical in MSC function, first we have used microarray to screen for potential transcripts whose levels are altered in response to NOD‐1 and TLR‐2 activation, and second we validated some candidate genes using real‐time RT‐PCR, Western blots and cellular assays. Amongst the altered genes, galectin‐3 was upregulated at both mRNA and protein levels in response to TLR‐2 activation. Interestingly, MSC secreted galectin‐3, a protein known to modulate T‐cell proliferation, gene expression, cell adhesion and migration. Knockdown of galectin‐3 in MSC using small interfering RNA (siRNA) reduced the immunosuppressive effect of MSC on mixed lymphocyte cultures when compared to cells treated with an irrelevant siRNA ( P < 0.05). Collectively, the data emphasize a new role of galectin‐3 in the immunomodulatory function of MSC and indicate that NOD signalling pathway is also functional in these cells.