| First Author | Roger T | Year | 1993 |
| Journal | Immunology | Volume | 80 |
| Issue | 4 | Pages | 661-3 |
| PubMed ID | 8307618 | Mgi Jnum | J:15958 |
| Mgi Id | MGI:64057 | Citation | Roger T, et al. (1993) Mls-1 and Mls-2 superantigens do not control susceptibility to collagen-induced arthritis in HI and HII mice. Immunology 80(4):661-3 |
| abstractText | The HI mouse line is sensitive to collagen-induced arthritis (CIA), whereas HII is refractory, although both express the H-2q permissive haplotype. The two lines also share the same T-cell receptor (TcR) gene haplotypes for alpha and beta chains. The distribution of mouse mammary tumour viruses (MMTV), which encode endogenous superantigens (SAg) such as minor leucocyte-stimulating antigens (Mls) known to modulate the available TcR-V beta repertoire, was investigated in the two lines. Mls-1 is present in HI-susceptible mice, while Mls-2 and Mls-2-like SAg are absent in both lines. This suggests that Mls antigens play no significant role in the resistance to CIA. Moreover, HI and HII exhibit close V beta gene usage as assessed by fluorescence staining with 11 V beta-specific monoclonal antibodies (mAb). These results indicate that mechanisms other than clonal deletion based on V beta expression and induced by SAg are involved in the resistance of H-2q-positive mice to experimental arthritis. Yet, a slightly reduced level of V beta 5+ T cells is observed in HII animals which might correlate with the presence of Mtv-6 and Mtv-9 proviruses. |
