| First Author | Sancho D | Year | 2006 |
| Journal | J Leukoc Biol | Volume | 80 |
| Issue | 6 | Pages | 1233-41 |
| PubMed ID | 16921025 | Mgi Jnum | J:116596 |
| Mgi Id | MGI:3694546 | Doi | 10.1189/jlb.1205749 |
| Citation | Sancho D, et al. (2006) CD69 targeting differentially affects the course of collagen-induced arthritis. J Leukoc Biol 80(6):1233-41 |
| abstractText | CD69 expression is induced following activation of leukocytes at inflammatory sites and plays a negative regulatory role in the development of collagen-induced arthritis (CIA). To evaluate potential strategies of CD69 targeting in chronic inflammatory diseases, two different anti-CD69 mAbs were generated and their effects on CIA were studied. Administration of the IgG1 anti-CD69 mAb 2.2 to DBA/1 mice with CIA led to an exacerbation of the disease, correlated with down-modulation of CD69 from the cell surface, and reproduced the phenotype of the CD69(-/-) mouse in wild-type animals. In contrast, treatment with the IgG2a anti-CD69 mAb 2.3 was effective in ameliorating CIA when administered in the early or intermediate phases of the disease, causing a decreased production of proinflammatory cytokines in inflammatory foci. Monoclonal antibody 2.3 induces partial depletion of CD69+ cells in vivo. Moreover, adoptive transfer of type-II collagen (CII)-sensitized cells treated with mAb 2.3 to deplete CD69+ cells did not result in arthritis. The attenuation of inflammation correlates with reduced lymphocyte proliferative response in response to CII and with a reduction in the frequency of CII-specific T cells producing IFN-gamma. We thus conclude that CD69 targeting by mAbs can either enhance or dampen the immune response. |
