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Increased macrophage colony-stimulating factor in neonatal and adult autoimmune MRL-lpr mice

Yui, Mary A. and Brissette, William H. and Brennan, Daniel C. and Wuthrich, Rudolf P. and Rubin-Kelley, Vicki E. (1991) Increased macrophage colony-stimulating factor in neonatal and adult autoimmune MRL-lpr mice. American Journal of Pathology, 139 (2). pp. 255-261. ISSN 0002-9440. PMCID PMC1886069. https://resolver.caltech.edu/CaltechAUTHORS:20170303-145305364

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Abstract

Abnormal macrophages in MRL-lpr mice are implicated in the pathogenesis of autoimmune disease. These mice die of lupus nephritis by 5 to 6 months of age. This study reports that MRL-lpr mice have an increased level of circulating macrophage colony-stimulating factor (M-CSF) detectable as early as 1 week of age. Macrophage colony-stimulating factor decreased between 2 and 4 months and then steadily increased beginning at 4 months of age. In contrast, M-CSF was not detected in sera from congenic MRL-++ mice, normal C3H/FeJ mice, two other mouse strains with the lpr gene (B6-lpr and C3H-lpr), or another lupus model, the NZB/W mouse. These observations indicate that the lpr gene alone is not responsible for inducing this growth factor, and elevated M-CSF is not required for all forms of murine lupus. The entire source of serum M-CSF is not clear. The unique T cells regulated by the lpr gene are not responsible for the increased serum M-CSF levels, as no M-CSFs could be detected in supernatants from cultured lymph nodes from MRL-lpr mice, and the steady-state levels of M-CSF mRNA in lymph nodes and spleens in MRL-lpr, C3H-lpr mice and in their respective congenic strains were similar. The steady-state M-CSF mRNA transcripts in liver, lung, and bone marrow in MRL-lpr, MRL-++, and C3H/FeJ mice were also similar. Macrophage colony-stimulating factor transcripts were clearly elevated in the kidneys of MRL-lpr mice, suggesting a renal source of circulating M-CSF. The increase of M-CSF might be responsible for the increased numbers and enhanced functions of macrophages, which in turn cause tissue destruction in MRL-lpr mice.


Item Type:Article
Related URLs:
URLURL TypeDescription
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1886069/PubMed CentralArticle
ORCID:
AuthorORCID
Yui, Mary A.0000-0002-3136-2181
Additional Information:© American Association of Pathologists. Accepted for publication March 12, 1991. The authors thank Drs. C. B. Carpenter and David L. Perkins for carefully reviewing this manuscript. Supported by NIH grants DK-36149, DK-40839, and CA-48626 (to Vicki Rubin-Kelley), Al-07918 (to Daniel Brennan), and a grant from the Jules and Gwen Knapp Chartable Foundation. Rudolph Wuthrich is a recipient of a grant from the Swiss National Science Foundation.
Funders:
Funding AgencyGrant Number
NIHDK-36149
NIHDK-40839
NIHCA-48626
NIHAl-07918
Jules and Gwen Knapp Chartable FoundationUNSPECIFIED
Swiss National Science Foundation (SNSF)UNSPECIFIED
Issue or Number:2
PubMed Central ID:PMC1886069
Record Number:CaltechAUTHORS:20170303-145305364
Persistent URL:https://resolver.caltech.edu/CaltechAUTHORS:20170303-145305364
Usage Policy:No commercial reproduction, distribution, display or performance rights in this work are provided.
ID Code:74726
Collection:CaltechAUTHORS
Deposited By: Donna Wrublewski
Deposited On:03 Mar 2017 23:40
Last Modified:03 Oct 2019 16:42

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