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Novel and enhanced IL-1 gene expression in autoimmune mice with lupus

Boswell, Jaquie M. and Yui, Mary A. and Endres, Stefan and Burt, David W. and Kelley, Vicki E. (1988) Novel and enhanced IL-1 gene expression in autoimmune mice with lupus. Journal of Immunology, 141 (1). pp. 118-124. ISSN 0022-1767.

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IL-1 is a pleiotropic factor encoded for by at least two genes, alpha and beta, and capable of eliciting a broad set of immunologic and inflammatory events. MRL/MP-lpr (MRL-lpr) mice are an appealing model for studies of renal injury inasmuch as disease in this strain is spontaneous, rapid, predictable, and regulated by the lpr gene. Infiltration of macrophages and the proliferation of the glomerular mesangial cells are prominent features of renal disease. Because both mesangial cells and macrophages can synthesize IL-1, the purpose of this study was to determine whether enhanced IL-1 gene expression is associated with lupus nephritis in the MRL-lpr mouse model. Glomerular macrophages, abundant in the kidneys of MRL-lpr mice but rarely present in the kidney of congenic MRL/MP-++(MRL-++) mice, were isolated and cultured and found to express a 10-fold increase in both IL-1 alpha and IL-1 beta mRNA transcripts as compared with MRL-++ and MRL-lpr mesangial cells. IL-1 alpha was not detected in the total RNA extracted from freshly excised kidney, whereas IL-1 beta transcripts were detected in both the renal cortex of MRL-lpr as well as MRL-++ animals. A previously undetected truncated 1200 nucleotide IL-1 beta transcript together with the conventional 1600 nucleotide IL-1 beta transcript was found in kidneys from MRL-lpr and was abundantly expressed in glomeruli of MRL-lpr mice with lupus nephritis. Isolated glomeruli from MRL-lpr mice with nephritis produce IL-1, whereas in normal glomeruli from MRL-++ and C3H/FeJ mice this cytokine was not detected. Glomerular macrophages and mesangial cells cultured from MRL-lpr mice with nephritis both secrete IL-1. These studies indicate that IL-1 beta gene expression and IL-1 protein are increased in the kidneys of autoimmune mice with lupus nephritis and is generated, at least in part, by glomerular macrophages. We speculate that an alteration in IL-1 beta gene expression may be responsible for causing a cascade of events leading to acute and chronic renal injury.

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Yui, Mary A.0000-0002-3136-2181
Additional Information:© 1988 American Association of Immunologists. Received for publication January 19. 1988. Accepted for publication April 8, 1988. This work was supported by the National Institutes of Health Grant AM 36149 and the Pennsylvania Lupus Foundation. We thank Drs. Terry B. Strom and Charles B. Carpenter for helpful suggestions and reviewing this manuscript. We also thank Corinne Kennedy for her careful secretarial assistance. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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NIHAM 36149
Pennsylvania Lupus FoundationUNSPECIFIED
Issue or Number:1
Record Number:CaltechAUTHORS:20170303-162003195
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Usage Policy:No commercial reproduction, distribution, display or performance rights in this work are provided.
ID Code:74744
Deposited By: Donna Wrublewski
Deposited On:18 Mar 2017 03:57
Last Modified:03 Oct 2019 16:42

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