These data point to disrupted T effector cell differentiation and the Wnt/β-catenin pathway as contributors to immune dysfunction in SLE while further supporting a central role for the type I interferon pathway in lupus.
Although myeloid-specific loss of β-catenin does not seem to be important for lupus development, the potential role of this transcription factor in other leukocytes and renal cells remain to be elucidated.