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Immunoregulatory Role of CD1d in the Hydrocarbon Oil-Induced Model of Lupus Nephritis¹

Jun-Qi Yang^2,*, Avneesh K. Singh^2,, Michael T. Wilson, Minoru Satoh, Aleksandar K. Stanic, Jang-June Park, Seokmann Hong^3,, Stephan D. Gadola, Akiei Mizutani, Srinivasa R. Kakumanu^*, Westley H. Reeves, Vincenzo Cerundolo, Sebastian Joyce, Luc Van Kaer and Ram Raj Singh^4,*

^* Department of Internal Medicine, Autoimmunity and Tolerance Laboratory, University of Cincinnati College of Medicine, Cincinnati, OH 45267; Department of Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232; Department of Medicine, University of Florida, Gainesville, FL 32610; Tumor Immunology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford, United Kingdom

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease that is accompanied by the emergence of autoreactive T cells and a reduction in regulatory T cells. Humans and mice with SLE have reduced numbers of CD1d-restricted NK T cells, suggesting a role for these cells in the regulation of SLE. In this study, we show that CD1d deficiency exacerbates lupus nephritis induced by the hydrocarbon oil pristane. This exacerbation in disease is associated with: 1) reduced TNF- and IL-4 production by T cells, especially during the disease induction phase; and 2) expansion of marginal zone B cells. Strikingly, inoculation of pristane in wild-type mice resulted in reduced numbers and/or functions of NK T cells and CD1d-expressing dendritic cells. These findings suggest that CD1d may play an immunoregulatory role in the development of lupus in the pristane-induced model.

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