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01.12.2015 | Research article | Ausgabe 1/2015 Open Access

BMC Musculoskeletal Disorders 1/2015

Human adipose-derived mesenchymal stem cells attenuate collagen antibody-induced autoimmune arthritis by inducing expression of FCGIIB receptors

BMC Musculoskeletal Disorders > Ausgabe 1/2015
Hyoju Yi, Kwi Young Kang, Youngkyun Kim, Hyerin Jung, Yeri Alice Rim, Narae Park, Juryun Kim, Seung Min Jung, Sung-Hwan Park, Ji Hyeon Ju
Wichtige Hinweise
Hyoju Yi and Kwi Young Kang contributed equally to this work.

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

HY, YK, NP, JK carried out the molecular studies. HJ carried out the tissue staining and immunostaining. HJ, YAR carried out animal experiments. JHJ, KYK, SHP, SMJ participated in the design of the study and performed the statistical analysis. HY, KYK, JHJ conceived of the study. KYK, HY helped to draft the manuscript. All authors read and approved the final manuscript.



Adipose-derived stem cells (ASCs) are mesenchymal stem cells (MSCs) derived from adipose tissue. MSCs have multiple properties including anti-inflammatory and immunomodulatory effects in various disease models and human diseases. However, the mechanisms underlying this wide range of effects need to be explored.


Collagen antibody-induced arthritis (CAIA) is a unique model in which arthritis is rapidly and strongly induced. ASCs were intraperitoneally infused into CAIA mice before or after arthritis induction. The serum levels of various cytokines, adipokines, and chemokines were measured. The expression of FC gamma receptors (FCGRs) was investigated in peritoneal macrophages ex vivo. RAW264.7 cells and ASCs were co-cultured to elucidate the direct and indirect role of ASCs on FCGR expression.


ASCs attenuated arthritis in CAIA mice. Serum levels of tumor necrosis factor α, interleukin (IL)-15, resistin, and leptin were reduced in ASC-treated CAIA mice, whereas serum levels of IL-6 and adiponectin were not affected. In peritoneal macrophages isolated from ASC-treated mice, expression of FCGRIIB, which is immunoinhibitory, was higher than that of FCGRI. Co-culture of ASCs with RAW264.7 cells modulated the expression of FCGRs. The expression patterns and timings of peak expression differed among FCGRs. Expression of FCGRIIB was higher and peaked earlier than that of FCGRI. FCGRIII expression was not affected by this co-culture.


This is a study to show that ASCs have anti-arthritic effects in CAIA mice. Modulation of FCGRs by ASCs might be a therapeutic mechanism in this antibody-associated arthritis model.
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