These findings extend CREMα effects to yet another immune cell subset, myeloid DCs, which express reduced levels of CD86 that is caused by trans-repression through CREMα. This in turn decreases the ability of these cells to transduce co-stimulatory signals towards T lymphocytes. In line with the trans-repressive effects of CREMα on IL-2 and TCR ζ chain production, this constitutes another (indirect) mechanism by which CREMα severely impairs T cell survival and function. It remains to be elucidated whether this mechanism plays a role in the pathogenesis of SLE, because lupus patients display increased CD86 levels on myeloid DCs [57]. Furthermore, it is yet unknown whether the expression of CREM itself is deregulated in myeloid DCs from lupus patients.
