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Interferon Signaling Useful Target in Mouse Lupus

Blocking signaling may reduce inflammatory response

THURSDAY, Dec. 27 (HealthDay News) -- Inhibiting downstream signaling through the interferon-α receptor may reduce the inflammatory response in a mouse model of systemic lupus erythematosus, according to a report published online Dec. 16 in Nature Immunology.

Lu Wang, Ph.D., from the Hospital for Special Surgery in New York City, and colleagues examined the function of the calcium-dependent kinases CaMK and Pyk2 in signaling through immunoreceptor tyrosine-based activation motif (ITAM)-coupled receptors. The role of CaMK and Pyk2 were examined in interferon-α signaling in the spleen, lymph nodes and kidneys in a mouse model of systemic lupus erythematosus, an autoimmune disease where type I interferons have been linked to pathogenesis.

The researchers found that CaMK and Pyk2 were involved in signaling through integrins and an ITAM-containing adaptor, and involved in augmenting Jak-1 activation and STAT1-dependent gene expression induced by interleukin-10 and interferon-α. In the mouse lupus model, interferon-α induced phosphorylation of STAT1, which was suppressed by a CaMK inhibitor.

"Inhibition of CaMK and Pyk2 diminished the STAT1-mediated inflammatory effects of interferons, including in vivo in a mouse model of the interferon-driven disease systemic lupus erythematosus," Wang and colleagues conclude. "Thus, CaMK and Pyk2 may be therapeutic targets whose inhibition downregulates the inflammatory properties of cytokines."

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