Interferon-inducible Mx1 protein is highly expressed in renal tissues from treatment-naïve lupus nephritis, but not in those under immunosuppressive treatment

Abstract

Objectives: The aim of this study was to clarify the consequences of Mx1, one of the IFN-inducible proteins, in the peripheral blood as well as in renal tissues in patients with systemic lupus erythematosus (SLE).

Patients and methods: Mx1 protein concentrations in (PBMCs) from 18 SLE patients mostly in their stable disease status, 11 IgA nephropathy (IgAN) patients, 5 ANCA-associated vasculitis (AAV) patients and 16 healthy controls were measured using enzyme-linked immunosorbent assay (ELISA). Mx1 expression in renal specimens from 18 patients with lupus nephritis (LN), 18 with IgAN and 10 with AAV were evaluated using immunohistochemistry.

Results: Mx1 protein concentrations in lysates of PBMCs were significantly higher in SLE patients compared with those in other three groups. Mx1-positive area in renal tissues was significantly dominant in both glomeruli and renal tubules of LN compared with other renal diseases. Renal Mx1 protein levels were lower in LN after immunosuppressive treatment, compared with those from immunosuppressant-naïve patients.

Conclusion: Mx1 levels were upregulated in lupus peripheral blood even when their disease activities were stable. On the other hand, Mx1 was highly expressed in kidneys from patients with LN before treatment, which was decreased after immunosuppressive treatment. These results suggest that Mx1 is a potential marker for the diagnosis of SLE in the peripheral blood and also for the activity of lupus nephritis in the kidney.

Keywords:

• Systemic lupus erythematosus
• lupus nephritis
• type I interferon
• Mx1

Acknowledgements

The authors acknowledge all the members of the Rheumatology Division and Nephrology Division of Hokkaido University Hospital, and also the laboratory assistants and technicians.

Conflict of interest

Atsumi T received personal fees from Chugai during the conduct of the study; grants and personal fees from Astellas, Takeda, Mitsubishi Tanabe, Chugai and Pfizer; grants from Daiichi Sankyo and Otsuka; and personal fees from Eisai and AbbVie, outside the submitted work. TA received grants and personal fees from Astellas; grants and personal fees from Takeda; grants and personal fees from Mitsubishi Tanabe; grants and personal fees from Chugai; grants and personal fees from Pfizer; grants and personal fees from Daiichi Sankyo; grants from Otsuka, personal fees from Eisai, personal fees from AbbVie, outside the submitted work.

Additional information

Funding

This study was partly supported by Japan Agency for Medical Research and Development.