The Journal of Experimental Medicine
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Published online 25 April 2005 doi:10.1084/jem.20050473
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 201, Number 9, 1479-1486
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ARTICLE

 Role of interleukin-1 (IL-1) in the pathogenesis of systemic onset juvenile idiopathic arthritis and clinical response to IL-1 blockade

Virginia Pascual1,2, Florence Allantaz1, Edsel Arce1, Marilynn Punaro2,3, and Jacques Banchereau1

1 Baylor Institute for Immunology Research, Dallas, TX 75204
2 Texas Scottish Rite Hospital for Children, Dallas, TX 75219
3 UT Southwestern Medical Center, Dallas, TX 75390

CORRESPONDENCE Virginia Pascual: Virginip{at}Baylorhealth.edu OR Jacques Banchereau: Jacquesb{at}Baylorhealth.edu

Systemic onset juvenile idiopathic arthritis (SoJIA) encompasses ~10% of cases of arthritis that begin in childhood. The disease is unique in terms of clinical manifestations, severity of joint involvement, and lack of response to tumor necrosis factor blockade. Here, we show that serum from SoJIA patients induces the transcription of innate immunity genes, including interleukin (IL)-1 in healthy peripheral blood mononuclear cells (PBMCs). Upon activation, SoJIA PBMCs release large amounts of IL-1ß. We administered recombinant IL-1 receptor antagonist to nine SoJIA patients who were refractory to other therapies. Complete remission was obtained in seven out of nine patients and a partial response was obtained in the other two patients. We conclude that IL-1 is a major mediator of the inflammatory cascade that underlies SoJIA and that this cytokine represents a target for therapy in this disease.

Abbreviations used: ESR, erythrocyte sedimentation rate; IL-1Ra, IL-1R antagonist; JIA, juvenile idiopathic arthritis; MTX, methotrexate; SLE, systemic lupus erythematosus; SoJIA, systemic onset juvenile idiopathic arthritis.

V. Pascual and F. Allantaz contributed equally to this work.


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