Suppression effect on IFN‑γ of adipose tissue‑derived mesenchymal stem cells isolated from β2‑microglobulin‑deficient mice
Author(s) -
Junko Masuda,
E. TakayamaMuromachi,
Tatsuo Ichinohe,
Warren Strober,
Masako MizunoKamiya,
Tomokatsu Ikawa,
Atsushi Kitani,
Harumi Kawaki,
Ivan J. Fuss,
Hiroshi Kawamoto,
Akimasa Seno,
Arun Vaidyanath,
Naoki Umemura,
Akifumi Mizutani,
Tomonari Kasai,
Yasuko Honjo,
Ayano Satoh,
Hiroshi Murakami,
Yoshimoto Katsura,
Nobuo Kondoh,
Masaharu Seno
Publication year - 2018
Publication title -
experimental and therapeutic medicine
Language(s) - English
Resource type - Journals
eISSN - 1792-1015
pISSN - 1792-0981
DOI - 10.3892/etm.2018.6689
Subject(s) - mesenchymal stem cell , biology , immunology , stem cell , adipose tissue , bone marrow , haematopoiesis , cancer research , microbiology and biotechnology , endocrinology
Administration of bone marrow-derived mesenchymal stem cells (MSCs) is a possible treatment for graft-versus-host disease (GVHD) following allogeneic hematopoietic stem cell transplantation and other inflammatory conditions. To address the mechanism of immunosuppression by MSCs, in particular those derived from adipose tissue (AMSCs), AMSCs were isolated from three different mouse strains, and the suppressive capacity of the AMSCs thus obtained to suppress interferon (IFN)-γ generation in mixed lymphocyte reaction cultures serving as an in vitro model of GVHD were assessed. It was revealed that the AMSCs had a potent capacity to suppress IFN-γ production regardless of their strain of origin and that such suppression was not associated with production of interleukin-10. In addition, the results demonstrated that β2-microglobulin (β2m)-deficient AMSCs from β2m -/- mice were also potent suppressor cells, verifying the fact that the mechanism underlying the suppression by AMSCs is independent of major histocompatibility complex (MHC) class I expression or MHC compatibility. As AMSCs appear to have immunosuppressive properties, AMSCs may be a useful source of biological suppressor cells for the control of GVHD in humans.
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