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• W2022479433 abstract "One of the characteristic features of the lupus syndrome in humans and mice is the organ-specific accumulation of leukocytes within a variety of different tissues; however, the etiology of this phenomenon remains unclear. The work presented here determined the role of intercellular adhesion molecule (ICAM)-1 in the development of pulmonary leukocyte accumulation by generating MRL/MpJ-Faslpr mice that are genetically deficient in this critical adhesion molecule. Interestingly, these MRL/MpJ-Faslpr ICAM-1 knockout mice exhibit prolonged survival times compared to littermates expressing ICAM-1. We have determined that lack of ICAM-1 completely abrogates the development of pulmonary inflammation but does not prevent the development of autoantibodies, lymphadenopathy, and glomerulonephritis. Furthermore, the lack of pulmonary inflammation was found to be due to decreased migration of leukocytes to the lung rather than decreased in situ proliferation of cells." @default.
• W2022479433 created "2016-06-24" @default.
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• W2022479433 date "1997-09-01" @default.
• W2022479433 modified "2023-10-18" @default.
• W2022479433 title "Intercellular adhesion molecule-1 deficiency prolongs survival and protects against the development of pulmonary inflammation during murine lupus." @default.
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• W2022479433 doi "https://doi.org/10.1172/jci119647" @default.
• W2022479433 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/508271" @default.
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