Page S T, Bogatzki L Y, Hamerman J A, Malissen M, Perlmutter R M, Pullen A M
Howard Hughes Medical Institute, and Department of Immunology, University of Washington, Seattle 98195, USA.
Int Immunol. 1999 Feb;11(2):169-77. doi: 10.1093/intimm/11.2.169.
A pre-TCR-CD3 signal is required for the efficient maturation of CD4- CD8- thymocytes to the CD4+ CD8+ stage. This study addressed whether a similar signal is required for maturation of intestinal intraepithelial lymphocytes (IEL) that may develop extrathymically. We have shown previously that IEL from mice deficient for CD3- associated zeta chains include an immature population of CD3- CD8alphaalpha+ cells expressing cytoplasmic TCR beta chains but lacking detectable surface TCRalphabeta, CD16 and B220. Here we stimulated the appearance of such IEL in epsilon+/- zeta-/- mice by expression of an activated Lck transgene or in vivo treatment with anti-CD3epsilon. Anti-CD3epsilon treatment of RAG-deficient animals also yielded CD16- B220- IEL. In contrast, expression of a TCRbeta transgene in rag-1(-/-) mice did not stimulate the appearance of CD3- CD8alphaalpha+ CD16- B220- cells. Taken together these data indicate that although anti-CD3epsilon treatment and LckF505 assist in catalyzing a CD16+ B220+ --> CD16- B220- transition, these manipulations are not equivalent to a pre-TCR signal in IEL lymphocytes.
前TCR-CD3信号是CD4-CD8-胸腺细胞高效成熟至CD4+CD8+阶段所必需的。本研究探讨了肠上皮内淋巴细胞（IEL）在胸腺外发育成熟是否需要类似信号。我们之前已经表明，来自缺乏CD3相关ζ链的小鼠的IEL包括一群未成熟的CD3-CD8αα+细胞，这些细胞表达细胞质TCRβ链，但缺乏可检测到的表面TCRαβ、CD16和B220。在此，我们通过表达活化的Lck转基因或用抗CD3ε进行体内处理，刺激ε+/-ζ-/-小鼠中此类IEL的出现。用抗CD3ε处理RAG缺陷动物也产生了CD16-B220-IEL。相比之下，在rag-1（-/-）小鼠中表达TCRβ转基因并未刺激CD3-CD8αα+CD16-B220-细胞的出现。综合这些数据表明，尽管抗CD3ε处理和LckF505有助于催化CD16+B220+→CD16-B220-转变，但这些操作并不等同于IEL淋巴细胞中的前TCR信号。
