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2016 ; 7
(42
): 68086-68096
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Jiang XX
; Liu Y
; Li H
; Gao Y
; Mu R
; Guo J
; Zhang J
; Yang YM
; Xiao F
; Liu B
; Wang C
; Shen B
; Chen SY
; Li Z
; Yang G
Oncotarget
2016[Oct]; 7
(42
): 68086-68096
PMID27590507
show ga
The aberrant expansion of B1a cells has been observed in several murine
autoimmune disease models; however, the mechanism of such proliferation of B1a
cells is still limited. Here, we identify that Myb Like, SWIRM And MPN Domains 1
(MYSM1), a histone H2A deubiquitinase, plays an intrinsic role in the
proliferation of B1a cells where MYSM1 deficiency results in the increased
proliferation of B1a cells in mice. We demonstrate that MYSM1 recruits c-Myc to
the promoter of miR-150 and stimulates the transcription of miR-150. Our further
investigation shows that miR-150 decreases FMS-like tyrosine kinase 3 (FLT3) in
B1a cells. In agreement with our animal studies, the percentage of FLT3+ B1 cells
in Systemic Lupus Erythematosus (SLE) patients is significantly higher than
healthy control. Thus, this study uncovers a novel pathway MYSM1/miR-150/FLT3
that inhibits proliferation of B1a, which may be involved in the pathogenesis of
SLE.
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