Bourgeois Christine, Stockinger Brigitta
Division of Molecular Immunology, The National Institute for Medical Research, The Ridgeway, Mill Hill, London NW7 1AA, U.K.
J Immunol. 2006 Oct 1;177(7):4558-66. doi: 10.4049/jimmunol.177.7.4558.
Lymphopenia has been associated with autoimmune pathology and it has been suggested that lymphopenia-induced proliferation of naive T cells may be responsible for the development of immune pathology. In this study we demonstrate that lymphopenia-induced proliferation is restricted to conditions of extreme lymphopenia, because neither naive nor memory T cells transferred into T cell-depleted hosts proliferate unless the depletion exceeds 90% of the peripheral repertoire. Memory CD4 T cells as well as regulatory CD4 T cells proved to be relatively resistant to depletion regimes, and both subsets restrict the expansion and phenotypic conversion of naive T cells by an IL-7R-dependent mechanism. It therefore seems unlikely that lymphopenia-induced proliferation of peripheral T cells causes deleterious side effects that result in immune pathology in states of partial and transient lymphopenia.
淋巴细胞减少与自身免疫病理相关,有人提出淋巴细胞减少诱导的初始T细胞增殖可能是免疫病理发展的原因。在本研究中,我们证明淋巴细胞减少诱导的增殖仅限于极端淋巴细胞减少的情况,因为除非外周库的耗竭超过90%,否则转入T细胞耗竭宿主的初始T细胞和记忆T细胞均不会增殖。记忆CD4 T细胞以及调节性CD4 T细胞被证明对耗竭方案相对抗性,并且这两个亚群通过IL-7R依赖机制限制初始T细胞的扩增和表型转换。因此,淋巴细胞减少诱导的外周T细胞增殖似乎不太可能导致有害的副作用,从而在部分和短暂淋巴细胞减少状态下导致免疫病理。