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C1q inhibits immune complex-induced interferon-[alpha] production in plasmacytoid dendritic cells: A novel link between C1q deficiency and systemic lupus erythematosus pathogenesis
Arthritis & Rheumatism, 10/05/09

Lood C et al. – The findings contribute to the understanding of why C1q deficiency is such a strong risk factor for SLE and suggest an explanation for the up–regulation of the type I IFN system seen in SLE patients.

Exclusive Author Commentary
Christian Lood, 10/08/09

C1q deficiency has since many years been associated with development of SLE and the major hypothesis for this association is decreased clearance of apoptotic cells. However, recent published data from our group (Gullstrand et al 2009) demonstrated that there could be alternative explainations for the strong association between C1q deficiency and SLE. Here, we could demonstrate a novel function of C1q in the regulation of immune complex-induced interferon-alpha production by plasmacytoid dendritic cells. These findings are important for the understanding of the role of C1q in protection against development of lupus, and may also be important when exploring new therapeutic strategies aiming to down-regulate the activated plasmacytoid dendritic cells in SLE patients

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