Expression of murine Unc93b1 is up-regulated by interferon and estrogen signaling: implications for sex bias in the development of autoimmunity

作者: Ravichandran Panchanathan , Hongzhu Liu , Divaker Choubey

DOI: 10.1093/INTIMM/DXT015

关键词:

摘要: The endoplasmic reticulum transmembrane protein, Unc93b1, is essential for trafficking of endosomal TLRs from the to endosomes. A genetic defect in human UNC93B1 gene associated with immunodeficiency. However, systemic lupus erythematosus (SLE) patients express increased levels protein B cells. Because SLE and certain mouse models exhibits a sex bias serum type I interferons are disease activity, we investigated whether female hormone estrogen (E2) or I interferon signaling could up-regulate expression murine Unc93b1 gene. We found that steady-state mRNA were measurably higher immune cells (CD3 + , B220 CD11b CD11c ) isolated C57BL/6 (B6) females than agematched males. Moreover, treatment E2 interferons (IFN-α, IFN-β IFN-γ) significantly protein. Accordingly, deficiency receptor-α STAT1 decreased Interestingly, appreciably B6.Nba2 lupusprone mice compared age-matched B6 females. Furthermore, interferon- E2-inducible p202 macrophage cell line (RAW264.7) whereas knockdown reduced levels. To our knowledge, observations demonstrate first time activation interferon up-regulates Unc93b1.

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