Intravenous Ig Regulates Anti-Desmoglein 3 IgG Production in B220 Antibody-Producing Cells in Mice with Pemphigus Vulgaris

Yuko Kase, Hayato Takahashi, Hiromi Ito, Aki Kamata, Masayuki Amagai, Jun Yamagami

Research output: Contribution to journalArticlepeer-review

Abstract

Intravenous Ig (IVIG) is a treatment option for intractable cases of pemphigus vulgaris (PV), an autoimmune blistering disease caused by autoantibodies against desmoglein 3 (DSG3). To investigate the efficacy of IVIG on autoantibody secretion, we produced PV model mice by adoptive transfer of immunized Dsg3−/− splenocytes to Rag2−/− mice. We found that circulating anti-DSG3 IgG ELISA titer decreased in PV model mice after 5 days of treatment with IVIG compared with PBS-treated mice, whereas the F(ab’)2 fragment did not suppress the anti-DSG3 IgG titer. enzyme-linked immunospot assay revealed that IVIG treatment reduced the frequency of anti-DSG3 antibody–secreting cells in the spleen but not in lymph nodes and bone marrow. Moreover, this reduction was observed only in the splenic B220 fraction but not in the B220+ fraction. Furthermore, IVIG decreased the serum levels of anti-DSG3 IgG, even after a significant reduction of its titer, owing to antibody-mediated CD20+ B cell depletion. In addition, IVIG suppressed anti-DSG3 IgG production in B220CD138+ plasma cells derived from PV model mice ex vivo. These results indicate that IVIG reduced autoantibody production in B220 cells containing plasma cells in PV model mice, and this function may indicate one of the mechanisms of action of IVIG on PV.

Original languageEnglish
JournalJournal of Investigative Dermatology
DOIs
Publication statusAccepted/In press - 2021

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Dermatology
  • Cell Biology

Fingerprint

Dive into the research topics of 'Intravenous Ig Regulates Anti-Desmoglein 3 IgG Production in B220 Antibody-Producing Cells in Mice with Pemphigus Vulgaris'. Together they form a unique fingerprint.

Cite this