PI3Kγ inhibition blocks glomerulonephritis and extends lifespan in a mouse model of systemic lupus

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 examin...

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Published inNature medicine Vol. 11; no. 9; pp. 933 - 935
Main Authors Carrera, Ana C, Barber, Domingo F, Bartolomé, Almira, Hernandez, Carmen, Flores, Juana M, Redondo, Clara, Fernandez-Arias, Cristina, Camps, Montserrat, Rückle, Thomas, Schwarz, Matthias K, Rodríguez, Santiago, Martinez-A, Carlos, Balomenos, Dimitrios, Rommel, Christian
Format Journal Article
LanguageEnglish
Published Nature Publishing Group 01.09.2005
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Summary: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) γ, a lipid kinase that regulates inflammation, in the MRL-lpr mouse model of SLE. Treatment reduced glomerulonephritis and prolonged lifespan, suggesting that P13Kγ may be a useful target in the treatment of chronic inflammation.
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ISSN:1078-8956
1546-170X
DOI:10.1038/nm1291