i M, Shannon JM, et al. Maintenance of the mouse type II cell phenotype in vitro. Am J Physiol Lung Cell Mol Physiol 283: L256264. Kannan S, Audet A, Knittel J, Mullegama S, Gao GF, et al. Src kinase Lyn is crucial for Pseudomonas aeruginosa internalization into lung cells. Eur J Immunol 36: 17391752. Graham RC, Jr., Lundholm U, Karnovsky MJ Cytochemical Demonstration of Peroxidase Activity with 3-Amino-9-Ethylcarbazole. J Histochem Cytochem 13: 150152. Teiken JM, Audettey JL, Laturnus DI, Zheng S, Epstein PN, et al. Podocyte loss in aging OVE26 diabetic mice. Anat Rec 291: 114121. Wu M, Pasula R, “9357531 Smith PA, Martin WJ, 2nd Mapping alveolar binding sites in vivo using phage peptide libraries. Gene Ther 10: 14291436. Wu M, Sherwin T, Brown WL, Stockley PG Delivery of antisense oligonucleotides to leukemia cells by RNA bacteriophage capsids. Nanomedicine 1: 6776. Kannan S, Audet A, Huang H, Chen LJ, Wu M Cholesterol-rich membrane rafts and Lyn are involved in phagocytosis during Pseudomonas aeruginosa infection. J Immunol 180: 23962408. 12 Rheumatoid arthritis is a chronic inflammatory autoimmune disease of the joints that is characterized by a marked thickening of the synovium due to neovascularization, fibroblast proliferation, and the recruitment of macrophages and other immune cells. The local production of enzymes and cytokines, and the activation of osteoclasts cause 
cartilage degradation and bone erosion, finally leading to joint destruction and functional disability. Fibroblast-like synoviocytes are unique cells of mesenchymal origin that constitute the intimal lining, which comprises 23 cell layers in normal conditions but can increase up to 15 layers in RA. Due to the border position between synovial tissue and synovial fluid, FLS obtain signals from both compartments and affect synovial tissue homeostasis in many ways. Moreover, it is increasingly appreciated that FLS contribute to the pathogenesis of RA by regulating inflammatory processes and, more directly, by eroding cartilage. A cell surface marker that defines FLS is CD55. The presence of CD55 in the intimal lining was initially reported by Medof et al.. Later work by Stevens et al. and Edwards and Wilkinson identified CD55 as a marker with an apparent specificity for “8813645 intimal fibroblasts in synovial disease. CD55, also known as decay-accelerating factor, is a broadly expressed cell surface molecule that protects cells from self-inflicted damage mediated by complement activation. CD55 controls complement by accelerating the decay of C3/C5 convertases. In line with this well-established function, CD55-deficient mice develop increased complement-mediated autoimmunity in a variety of antibody-driven models. Next to its role as a complement regulator, CD55 is a binding partner of CD97, an adhesion-type G protein-coupled receptor abundantly expressed on almost all leukocytes. AdhesionGPCRs are nonclassical heptahelical receptors that facilitate cell and matrix interactions of various cell types. CD97-positive macrophages closely associate with CD55-expressing FLS in the synovial intima. Using CD97-specific multivalent fluorescent probes, we previously demonstrated the ability of CD97 to interact with CD55 on FLS in RA synovium. Based on the MEK162 sitespecific expression of CD55 and CD97, and the finding that CD97 facilitates leukocyte adhesion in vitro, we postulated that the CD55 Expression on Synovial Fibroblasts interaction of CD97 intimal macrophages with CD55 FLS might facilitat
