Suppr超能文献

Mls-1和Mls-2超抗原并不控制HI和HII小鼠对胶原诱导性关节炎的易感性。

Mls-1 and Mls-2 superantigens do not control susceptibility to collagen-induced arthritis in HI and HII mice.

作者信息

Roger T, Boudaly S, Couderc J, Seman M

机构信息

Laboratoire d'Immunodifférenciation, Université Denis Diderot, Paris, France.

出版信息

Immunology. 1993 Dec;80(4):661-3.

Abstract

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.

摘要

HI小鼠品系对胶原诱导的关节炎(CIA)敏感,而HII则具有抗性,尽管两者都表达H-2q允许单倍型。这两个品系在α和β链的T细胞受体(TcR)基因单倍型上也相同。研究了编码内源性超抗原(SAg)的小鼠乳腺肿瘤病毒(MMTV)的分布,已知这些超抗原如微小白细胞刺激抗原(Mls)可调节可用的TcR-Vβ库,研究对象为这两个品系。Mls-1存在于HI易感小鼠中,而Mls-2和Mls-2样SAg在两个品系中均不存在。这表明Mls抗原在对CIA的抗性中不起重要作用。此外,通过用11种Vβ特异性单克隆抗体(mAb)进行荧光染色评估,HI和HII表现出相近的Vβ基因使用情况。这些结果表明,基于Vβ表达并由SAg诱导的克隆缺失以外的机制参与了H-2q阳性小鼠对实验性关节炎的抗性。然而,在HII动物中观察到Vβ5 + T细胞水平略有降低,这可能与Mtv-6和Mtv-9前病毒的存在有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3c5/1422239/ed0730d0c0dd/immunology00091-0154-a.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验