The enigmatic role of interleukin-12 in the pathogenesis of Sjögren's syndrome: comment on the article by Vosters et al.

Vosters et al (1) recently reported that autoimmunityprone interleukin-12 (IL-12)–transgenic mice represent a new model of Sjo¨gren’s syndrome (SS) (1). IL-12–transgenic animals were generated by expressing the biologically active IL-12 p70 heterodimer under the control of the thyroglobulin promoter. The mice exhibited high serum levels of IL-12, and IL-12– dependent lymphocytic infiltration of the thyroid, the lungs, and the salivary and the lacrimal glands, mimicking human SS (2). Vosters and colleagues demonstrated that salivary flow was reduced in IL-12–transgenic mice compared with wild-type controls. Salivary glands showed increased lymphocytic infiltration with reduced numbers of acini, and serum anti-SSB/La antibodies (a serologic hallmark of SS [3]) were consistently detected, together with antinuclear antibodies (ANAs).