| First Author | Bullard DC | Year | 1999 |
| Journal | J Immunol | Volume | 163 |
| Issue | 5 | Pages | 2844-9 |
| PubMed ID | 10453030 | Mgi Jnum | J:57086 |
| Mgi Id | MGI:1343665 | Doi | 10.4049/jimmunol.163.5.2844 |
| Citation | Bullard DC, et al. (1999) Acceleration and increased severity of collagen-induced arthritis in P-selectin mutant mice. J Immunol 163(5):2844-9 |
| abstractText | P-selectin plays an important role in leukocyte adherence to microvascular endothelium and is expressed in synovial tissue from patients with rheumatoid arthritis (RA). However, the contribution of P-selectin to the initiation and chronicity of joint inflammation is not well understood. In these studies, collagen-induced arthritis (CIA) was induced in P-selectin mutant (-/-) mice to explore the role of P-selectin in the development of joint inflammation. Surprisingly, CIA onset was accelerated and severity was increased in P-selectin mutant mice, compared with wild-type mice (+/+). Increased levels of anti-type II collagen IgG were detected in both nonarthritic and arthritic P-selectin mutant mice from days 14-91. In addition, splenocytes isolated from immunized and nonimmunized P-selectin mutant mice produced significantly less IL-2 and IL-4, but significantly higher levels of IL-10 and IL-5 than splenocytes from wild-type mice. These observations show that P-selectin-mediated leukocyte rolling is not required for the development of murine CIA and that P-selectin expression exerts a controlling effect on the development of Ag-driven inflammatory joint disease, possibly by mediating the recruitment and/or trafficking of specific leukocyte subtypes into lymphoid tissue or inflammatory foci. |
