TY - JOUR
T1 - Leukocyte beta-catenin expression is disturbed in systemic lupus erythematosus
AU - Orme, Jacob J.
AU - Du, Yong
AU - Vanarsa, Kamala
AU - Wu, Tianfu
AU - Satterthwaite, Anne B.
AU - Mohan, Chandra
PY - 2016/8
Y1 - 2016/8
N2 - Wnt/β-catenin signaling is relatively understudied in immunity and autoimmunity. β-catenin blocks inflammatory mediators and favors tolerogenic dendritic cell (DC) phenotypes. We show here that leukocytes from lupus-prone mice and SLE patients express diminished β-catenin transcriptional activity, particularly in myeloid cells, although other leukocytes revealed similar trends. Serum levels of DKK-1, an inhibitor under transcriptional control of Wnt/β-catenin, were also decreased in lupus-prone mice. Surprisingly, however, preemptive deletion of β-catenin from macrophages appears to have no effect on lupus development, even in mice with varying genetic loads for 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.
AB - Wnt/β-catenin signaling is relatively understudied in immunity and autoimmunity. β-catenin blocks inflammatory mediators and favors tolerogenic dendritic cell (DC) phenotypes. We show here that leukocytes from lupus-prone mice and SLE patients express diminished β-catenin transcriptional activity, particularly in myeloid cells, although other leukocytes revealed similar trends. Serum levels of DKK-1, an inhibitor under transcriptional control of Wnt/β-catenin, were also decreased in lupus-prone mice. Surprisingly, however, preemptive deletion of β-catenin from macrophages appears to have no effect on lupus development, even in mice with varying genetic loads for 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.
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U2 - 10.1371/journal.pone.0161682
DO - 10.1371/journal.pone.0161682
M3 - Article
C2 - 27548498
AN - SCOPUS:84984819409
VL - 11
JO - PLoS ONE
JF - PLoS ONE
SN - 1932-6203
IS - 8
M1 - e0161682
ER -