Article Text

Download PDFPDF

LP-094 Repression of Id3 aggravates lupus phenotypes in murine models via aberrant B cell differentiation
  1. Youngjae Park1,
  2. Da Som Kim2,3,
  3. Mi-La Cho2 and
  4. Seung-Ki Kwok1,2
  1. 1Department of Internal Medicine, Seoul St. Mary’s hospital, The Catholic University of Korea, Republic of Korea
  2. 2The Rheumatism Research Center, The Catholic University of Korea, Republic of Korea
  3. 3Department of Biomedicine and Health Sciences, College of Medicine, The Catholic University of Korea, Republic of Korea


Background Id3 is a member of the inhibitor of DNA binding (Id) family which is a helix-loop-helix protein acting as a transcriptional regulator. Previous studies have reported that Id3 plays an essential role in the development and function of regulatory T cells in lupus. However, its role in B cells remains unclarified.

Methods To investigate the role of Id3 in B cells, we generated C57BL/6 mice with a CD19Cre-mediated B cell-specific depletion of Id3 as well as mice (Id3-/-) with a conventional knockout of Id3. In these mice, we evaluated the presentation of lupus-mimicking phenotypes and changes in immune cell populations. Additionally, we assessed the influences of B cell-specific Id3 depletion in lupus-induced mice by R848.

Results In Id3-/- mice, proportions of effector T cells such as Th1, Th2, and Th17 cells were elevated whereas those of regulatory T cells were lower than in control mice. Furthermore, proportions of plasma cells were significantly elevated in Id3-/- mice. These mice presented with increased inflammation in kidney tissues, resembling lupus nephritis. An elevated proportion of plasma cells was replicated in mice with B cell-specific Id3 depletion. Induction using R848 exacerbated lupus-like manifestations including increased proteinuria and higher serum immunoglobulin levels in B cell-specific Id3-depleted mice than in control mice. In an in vitro study, CD19+ B cells from Id3-/- mice were more differentiated into plasma cells than those from control mice. In contrast, there were no significant differences in other B cell subsets.

Conclusions Genetic suppression of Id3 in murine models exacerbated lupus-like phenotypes with aberrant B cell differentiation. These findings may imply a potential role of Id3 in the pathogenesis of lupus.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See:

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.