It is well documented that T cells from SLE patients express increased levels of tyrosine kinase (Syk) which contribute to aberrant T cell signaling in these individuals. In vitro findings suggest CREMα as a strong repressor of Syk gene transcription that is caused by the recruitment to a CRE within the Syk promoter. At first, this might appear contradictory in the context of the classic ‘SLE T cell phenotype’. Yet, the Syk promoter exhibits reduced histone H3 acetylation in SLE T cells, translating into reduced accessibility for the transcriptional repressor CREMα [54].
