The evidence seemed convincing that a protein called interleukin-12 is a major contributor to autoimmune disorders. But a report in this week's Nature (Vol. 421, No. 6924, pp. 744-748, dated 13 February 2003) argues that interleukin-12 has been wrongly accused, at least in the case of a brain autoimmune disease in mice. The real culprit in autoimmune inflammation, say Daniel J. Cua of DNAX Research Inc., Palo Alto, California, and colleagues is the protein's close relative interleukin-23.
Antibodies that block interleukin-12 have been widely used in mouse models of autoimmune disease and are being tested in humans. It now seems that interleukin-23 should also be considered a target, as the antibodies against interleukin-12 might serendipitously block this cytokine too.
"Certainly there is far more complexity here than initially envisioned, but this gives ample opportunity for intervention," say Wendy T. Watford and John J. O'Shea of the National Institutes of Arthritis, Musculoskeletal and Skin Disease, National Institutes of Health, Bethesda, Maryland, in an accompanying News and Views article.
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