Data from: Effect of mitochondrial oxidative stress on regulatory T cell manufacturing for clinical application in transplantation: Results from a pilot study

The manufacturing process of regulatory T (Treg) cells for clinical
application begins with the positive selection of CD25þ cells using
superparamagnetic iron oxide nanoparticle (SPION)-conjugated anti-CD25
antibodies (spCD25) and immunomagnetic cell separation technology. Our
findings revealed that the interaction of spCD25 with its cell target
induced the internalization of the complex spCD25–interleukin-2 receptor.
Accumulation of intra- cellular spCD25 triggered oxidative stress, causing
delayed Treg expansion and temporary reduction in suppressor activity.
This activation delay hindered the efficient generation of clinically
competent cells. During this early phase, Treg cells exhibited elevated
mitochondrial superoxide and lipid peroxidation levels, with a concomitant
decrease in mitochondrial respiration rates. The results uncovered the
increased mitochondrial unfolded protein response. This protective,
redox-sensitive activity is inherent in Tregs when contrasted with
homologous, spCD25-treated, conventional T cells. Although the temporary
effects of spCD25 on clinically competent cells did not impede their use
in a safety/feasibility pilot study with kidney transplant recipients, it
is reasonable to anticipate a potential reduction in their therapeutic
efficacy. The mechanistic understanding of the adverse effects triggered
by spCD25 is crucial for improving the manufacturing process of clinically
competent Treg cells, a pivotal step in the successful implementation of
immune cell therapy in transplantation.