An article
published this year in “PLOS ONE” using our AnnexinV-DY634, by our customers
from Fundación Inbiomed, Foundation for Stem Cell Research, Mesenchymal Stem
Cell Laboratory, San Sebastián, Spain, in the study of how
IFNγ Regulates Activated Vδ2+ T Cells through a Feedback Mechanism Mediated by Mesenchymal Stem Cells.
Congrats and Thanks.
Summary:
γδ T cells play a
role in a wide range of diseases such as autoimmunity and cancer. The majority
of circulating human γδ T lymphocytes express a Vγ9Vδ2+ (Vδ2+) T cell receptor
(TCR) and following activation release pro-inflammatory cytokines. In this
study, we show that IFNγ, produced by Vδ2+ cells, activates mesenchymal stem
cell (MSC)-mediated immunosupression, which in turn exerts a negative feedback
mechanism on γδ T cell function ranging from cytokine production to
proliferation. Importantly, this modulatory effect is limited to a short period
of time (<24 hours) post-T cell activation, after which MSCs can no longer
exert their immunoregulatory capacity. Using genetically modified MSCs with the
IFNγ receptor 1 constitutively silenced, we demonstrate that IFNγ is essential
to this process. Activated γδ T cells induce expression of several factors by
MSCs that participate in the depletion of amino acids. In particular, we show
that indolamine 2,3-dioxygenase (IDO), an enzyme involved in L-tryptophan
degradation, is responsible for MSC-mediated immunosuppression of Vδ2+ T cells.
Thus, our data demonstrate that γδ T cell responses can be immuno-modulated by
different signals derived from MSC.
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