Sialoadhesin deficiency does not influence the severity of lupus nephritis in New Zealand Black x New Zealand White F1 mice

Dana Kidder, Hannah E. Richards, Paul A. Lyons, Paul R. Crocker (Corresponding Author)

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Systemic lupus erythematosus (SLE) is a chronic inflammatory condition with multisystem involvement. One of the key features of the disease is the upregulation of type I interferons, resulting in the so-called “interferon signature”. Recent flow cytometric and transcriptomic studies identified Sialoadhesin (Sn, CD169) as an important interferon-induced blood monocyte biomarker in diseased patients. To investigate a potential causative role of Sn in SLE, we generated NZBWF1 (New Zealand Black x New Zealand White F1) mice lacking Sn and compared onset and progression of disease with NZBWF1 expressing normal levels of Sn.

Sn expression in renal tissues of pre-diseased and diseased NZBWF1 mice was evaluated by Quantitative real time PCR (QPCR) and immunohistochemistry. Sn−/− NZBWF1 mice were generated by speed congenics. Disease severity of Sn+/+ and Sn−/− NZBWF1 mice was assessed by serum immunoassays, flow cytometry, light microscopy and immunohistochemistry.

Renal tissues from proteinuric NZBWF1 mice exhibited a significant upregulation of Sn mRNA and protein expression following disease onset. Further immunohistochemical analysis showed that Sn+ macrophages assumed a distinct periglomerular distribution and, unlike CD68+ macrophages, were not present within the glomeruli. Analysis of disease severity in Sn −/− and Sn +/+ NZBWF1 mice revealed no significant differences in the disease progression between the two groups although Sn-deficient mice showed a more rapid onset of proteinuria.

These data confirm a positive correlation of Sn with disease activity. However, Sn deficiency does not have a significant effect on the severity and progression of lupus nephritis in the NZBWF1 mouse model.
Original languageEnglish
Article numberR175
Number of pages9
JournalArthritis Research & Therapy
Issue number6
Publication statusPublished - 1 Nov 2013

Bibliographical note

This work was supported by a Wellcome Trust Clinical Fellowship 087078 (to DK) and Wellcome Trust Senior Fellowship 081882MA (to PRC). PAL was funded by a Wellcome Trust Programme Grant (083650/Z/07/Z). We thank the Renal Unit in Ninewells Hospital, Dundee, Scotland, UK, for their support with the immunohistochemistry analysis.


  • Systemic Lupus Erythematosus
  • Experimental Autoimmune Encephalomyelitis
  • Lupus Nephritis
  • Active Systemic Lupus Erythematosus
  • Histological Severity


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