Nature Medicine
11, 933 - 935 (2005)
Published online: 28 August 2005; | doi:10.1038/nm1291
PI3K inhibition blocks glomerulonephritis and extends lifespan in a mouse model of systemic lupusDomingo F Barber1, Almira Bartolomé1, Carmen Hernandez1, Juana M Flores2, Clara Redondo3, Cristina Fernandez-Arias1, Montserrat Camps4, Thomas Rückle4, Matthias K Schwarz4, Santiago Rodríguez1, Carlos Martinez-A1, Dimitrios Balomenos1, Christian Rommel4
& Ana C Carrera11
Department of Immunology and Oncology, and Animal Facility, Centro Nacional de Biotecnología/CSIC, Universidad Autónoma de Madrid, Cantoblanco, Madrid E-28049, Spain. 2
Department of Animal Medicine and Surgery, Veterinary School, Universidad Complutense de Madrid, Madrid, E-28040 Spain. 3
Hospital Ramón y Cajal, Carretera de Colmenar Viejo Km 9, Madrid, E-28034, Spain. 4
Serono Pharmaceutical Research Institute, Serono International S.A., Geneva, Switzerland CH-1211.
Correspondence should be addressed to Ana C Carrera acarrera@cnb.uam.es Systemic lupus erythematosus (SLE) is a chronic inflammatory disease generated by deregulation of T cell−mediated B-cell activation, which results in glomerulonephritis and renal failure. Disease is treated with immunosuppressants and cytostatic agents that have numerous side effects. Here we examine the use of inhibitors of phosphoinositide 3-kinase (PI3K)  , a lipid kinase that regulates inflammation, in the MRL-lpr mouse model of SLE. Treatment reduced glomerulonephritis and prolonged lifespan, suggesting that P13K may be a useful target in the treatment of chronic inflammation.
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