Open AccessReciprocal Interactions Between Human Mesenchymal Stem Cells and γδ T Cells Or Invariant Natural Killer T Cells
Author(s) -
Prigione Ignazia,
Benvenuto Federica,
Bocca Paola,
Battistini Luca,
Uccelli Antonio,
Pistoia Vito
Publication year - 2009
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 - 10.1634/stemcells.2008-0687
Subject(s) - mesenchymal stem cell , biology , natural killer t cell , cytotoxic t cell , microbiology and biotechnology , interleukin 21 , immunology , antigen presenting cell , t cell , immune system , interleukin 12 , in vitro , biochemistry
The immunomodulatory activities of human mesenchymal stem cells (MSCs) provide a rational basis for their application in the treatment of immune‐mediated diseases, such as graft versus host disease and multiple sclerosis. The effects of MSCs on invariant natural killer T (iNKT) and γδ T cells, both involved in the pathogenesis of autoimmune diseases, are unknown. Here, we investigated the effects of MSCs on in vitro expansion of these unconventional T‐cell populations. MSCs inhibited iNKT (Vα24 + Vβ11 + ) and γδ T (Vδ2 + ) cell expansion from peripheral blood mononuclear cells in both cell‐to‐cell contact and transwell systems. Such inhibition was partially counteracted by indomethacin, a prostaglandin E 2 inhibitor. Block of indoleamine 2,3‐deoxygenase and transforming growth factor β1 did not affect Vα24 + Vβ11 + and Vδ2 + cell expansion. MSCs inhibited interferon‐γ production by activated Vα24 + Vβ11 + and impaired CD3‐mediated proliferation of activated Vα24 + Vβ11 + and Vδ2 + T cells, without affecting their cytotoxic potential. MSCs did not inhibit antigen processing/presentation by activated Vδ2 + T cells to CD4 + T cells. In contrast, MSCs were lysed by activated Vδ2 + T cells through a T‐cell receptor‐dependent mechanism. These results are translationally relevant in view of the increasing interest in MSC‐based therapy of autoimmune diseases. S TEM C ELLS 2009;27:693–702