| First Author | Kleinau S | Year | 1999 |
| Journal | J Immunol | Volume | 162 |
| Issue | 7 | Pages | 4266-70 |
| PubMed ID | 10201957 | Mgi Jnum | J:53569 |
| Mgi Id | MGI:1332942 | Doi | 10.4049/jimmunol.162.7.4266 |
| Citation | Kleinau S, et al. (1999) Importance of CD23 for collagen-induced arthritis: delayed onset and reduced severity in CD23-deficient mice. J Immunol 162(7):4266-70 |
| abstractText | Increased expression of the low affinity receptor for IgE, FcepsilonRII/CD23 has been observed in rheumatoid arthritis. In view of this, we have investigated the expression and influence of CD23 in collagen-induced arthritis (CIA), an animal model for rheumatoid arthritis. CD23+ cells were analyzed in lymph nodes of DBA/1 mice immunized with bovine collagen type II (BCII) in CFA or with CFA only. The percentage of CD23+ lymph node cells was increased in both BCII/CFA- and CFA-immunized mice at 1, 3, and 7 wk after immunization compared with unimmunized mice, indicating a role for the adjuvant to trigger general inflammation and CD23 expression. To investigate the functional role of CD23 in CIA, CD23-deficient mice on the DBA/1 genetic background were studied. After immunization with BCII/CFA, these mice developed CIA with delayed onset and reduced severity compared with wild-type mice. These findings suggest that an increased number of CD23+ cells is part of an inflammatory response and that CD23 expression is of pathogenic importance in the arthritic process. |
