| First Author | Axtell RC | Year | 2004 |
| Journal | J Immunol | Volume | 173 |
| Issue | 5 | Pages | 2928-32 |
| PubMed ID | 15322150 | Mgi Jnum | J:92725 |
| Mgi Id | MGI:3054339 | Doi | 10.4049/jimmunol.173.5.2928 |
| Citation | Axtell RC, et al. (2004) Cutting edge: critical role for CD5 in experimental autoimmune encephalomyelitis: inhibition of engagement reverses disease in mice. J Immunol 173(5):2928-32 |
| abstractText | The induction phase of experimental autoimmune encephalomyelitis (EAE) in mice is T cell dependent and coreceptors that regulate T cell activation modulate disease development. We report here that mice lacking CD5, an important modulator of T cell activation, exhibit significantly delayed onset and decreased severity of EAE. The resistance to EAE in CD5(-/-) mice was not due to the inability of T cells to respond efficiently to stimulation with MOG(35-55) but was associated with the presence of elevated frequency of apoptotic activated T cells in spleens and DLN. We also observed a net decrease in peripheral activated CD4(+) T cells in CD5(-/-) spleens and DLN 10 days after immunization. We further show that in vivo blockade of CD5 engagement after induction of EAE by soluble CD5-Fc, a treatment that induces elimination of activated T cells, promoted recovery from EAE. Our studies indicate that CD5 regulates survival of activated T cells and provides a target for treatment of T cell-dependent autoimmune diseases such as multiple sclerosis. |
