| First Author | Pizzolla A | Year | 2013 |
| Journal | Am J Pathol | Volume | 183 |
| Issue | 4 | Pages | 1144-55 |
| PubMed ID | 23911657 | Mgi Jnum | J:200919 |
| Mgi Id | MGI:5510270 | Doi | 10.1016/j.ajpath.2013.06.019 |
| Citation | Pizzolla A, et al. (2013) A Glucose-6-Phosphate Isomerase Peptide Induces T and B Cell-Dependent Chronic Arthritis in C57BL/10 Mice: Arthritis without Reactive Oxygen Species and Complement. Am J Pathol 183(4):1144-55 |
| abstractText | Immunization with human glucose-6-phosphate isomerase (hG6PI) protein or with several of its peptides induces arthritis in DBA/1 mice. We investigated G6PI peptide-induced arthritis in C57BL/10 mice and the effect of oxidative burst on disease. To study the arthritogenicity of G6PI peptides and its immune dependency, we used genetically modified and congenic mice on the C57BL/10 background and in vitro T- and B-cell assays. hG6PI325-339 peptide induced arthritis in C57BL/10 mice. The disease was associated with major histocompatibility complex class II and was dependent on T cells, B cells, and complement C5. Th1 and Th17 cells primed with the hG6PI325-339 peptide cross-reacted with the murine G6PI protein. The severity of the disease increased in mice carrying a mutation in Ncf1 (Ncf1 */ *), which abolishes the NADPH oxidase 2 complex oxidative burst. Ncf1 */ * mice developed arthritis also on immunization with the mouse G6PI325-339 peptide and in the absence of C5. The antibody responses to the G6PI protein and peptides were minimal in both Ncf1 */ * and wild-type mice. Herein is described G6PI peptide as the first peptide to induce arthritis in C57BL/10 mice. The differences between the wild-type and Ncf1 */ * mice suggest that an alternative complement-independent arthritogenic pathway could be operative in the absence of oxidative burst. |
