Clinical Rheumatology

, Volume 37, Issue 7, pp 1783–1790 | Cite as

Decreased IgG4 ACPA levels in responders and increased CD1c+ classical dendritic cells in non-responders of patients with rheumatoid arthritis under therapy

  • Robby Engelmann
  • Sven Nekarda
  • Daniela Kuthning
  • Christian Kneitz
  • Brigitte Müller-Hilke
Original Article


The treatment options for patients suffering from rheumatoid arthritis expanded over the last years. However, reliable biomarkers to guide therapy decisions are still warranted. Therefore, we here evaluated the value of antibodies against citrullinated peptide antigens (ACPA) IgG subclasses and peripheral blood antigen presenting cells as biomarkers to monitor and predict therapy response of patients with rheumatoid arthritis. Thirty-four ACPA-positive RA patients were enrolled and monitored for 3 months after therapy begin. ACPA IgG1 and IgG4 serum levels were quantified by ELISA. Phenotyping of the B cell, monocytic, and dendritic cell lineages was performed via flow cytometry. Three months after therapy begin, the responders showed a significant decrease in IgG4 ACPA levels, and this was independent of the individual treatment regimen. The non-responders showed a significant increase in CD1c+ classical dendritic cells (cDC). Furthermore, the baseline disease activity score 28 and the baseline percentage of cDC allowed for some prediction of future therapy responses. We here suggest IgG4 ACPA levels as biomarkers to monitor therapy response in RA. The increase in CD1c+ cDC among non-responders to therapy remains enigmatic and requires future elucidation of the underlying mechanisms.


Antigens B-lymphocytes CD1 Dendritic cells Enzyme-linked immunosorbent assay Flow cytometry IgG subclasses IgG4 



We thank Matthias Richter for providing patient samples and data.


This work was supported by the Pfizer Inc. under grant number WI170970. The funding agency had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Compliance with ethical standards

Conflict of interest

This work was supported by the Pfizer Inc. The funding agency had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. C.K. received consulting and lecture fees from Pfizer Inc. All other authors have no further financial relationship with the sponsor and declare no additional conflicts of interest.

Supplementary material

10067_2018_4053_MOESM1_ESM.pdf (1.6 mb)
ESM 1 (PDF 1593 kb)


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Copyright information

© International League of Associations for Rheumatology (ILAR) 2018

Authors and Affiliations

  1. 1.Institute of ImmunologyRostock University Medical CenterRostockGermany
  2. 2.Klinikum Südstadt RostockRostockGermany

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