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Research Article Free access | 10.1172/JCI119647

Intercellular adhesion molecule-1 deficiency prolongs survival and protects against the development of pulmonary inflammation during murine lupus.

C M Lloyd, J A Gonzalo, D J Salant, J Just, and J C Gutierrez-Ramos

Millennium Pharmaceuticals Inc., Cambridge, Massachusetts 02139, USA.

Find articles by Lloyd, C. in: JCI | PubMed | Google Scholar

Millennium Pharmaceuticals Inc., Cambridge, Massachusetts 02139, USA.

Find articles by Gonzalo, J. in: JCI | PubMed | Google Scholar

Millennium Pharmaceuticals Inc., Cambridge, Massachusetts 02139, USA.

Find articles by Salant, D. in: JCI | PubMed | Google Scholar

Millennium Pharmaceuticals Inc., Cambridge, Massachusetts 02139, USA.

Find articles by Just, J. in: JCI | PubMed | Google Scholar

Millennium Pharmaceuticals Inc., Cambridge, Massachusetts 02139, USA.

Find articles by Gutierrez-Ramos, J. in: JCI | PubMed | Google Scholar

Published September 1, 1997 - More info

Published in Volume 100, Issue 5 on September 1, 1997
J Clin Invest. 1997;100(5):963–971. https://doi.org/10.1172/JCI119647.
© 1997 The American Society for Clinical Investigation
Published September 1, 1997 - Version history
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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.

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