Manifestations of inflammatory arthritis are critically dependent on LFA-1

Gerald M. Watts, Frank J M Beurskens, Ines Martin-Padura, Christie M. Ballantyne, Lloyd B. Klickstein, Michael B. Brenner, David M. Lee

Research output: Contribution to journalArticlepeer-review


Leukocyte infiltration of synovial fluid and tissues is the hallmark of inflammatory arthritis. Selectins and β2 integrins have been implicated in the multistep process of leukocyte adhesion to vascular endothelium. However, previous work has revealed disparate requirements for leukocyte recruitments to specific anatomic locales. Moreover, the mechanisms regulating recruitment of leukocytes to the joint in inflammatory arthritis models are not fully understood. We hypothesized that β2 integrins, expressed on leukocytes, might play a pathogenic role in synovial inflammation. Using mice deficient in all β2 integrins (CD18 null mice), we demonstrate that expression of these heterodimeric adhesion molecules is critical for arthritis induction in the K/B x N serum transfer model. Using null-allele mice and blocking mAbs, we demonstrate specifically that CD11a/CD18 (LFA-1) is absolutely required for the development of arthritis in this model. Blocking mAbs further revealed an ongoing requirement for LFA-1 I-domain adhesive function in disease perpetuation. These findings suggest that the LFA-1 I-domain forms an attractive target for treatment of human inflammatory arthritis.

Original languageEnglish
Pages (from-to)3668-3675
Number of pages8
JournalJournal of Immunology
Issue number6
Publication statusPublished - Mar 15 2005

ASJC Scopus subject areas

  • Immunology


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