Leitner W, Bergmann E S, Thalhamer J
Walter Reed Army Institute of Research, Department of Immunology, Washington, DC 20307-5100.
Res Exp Med (Berl). 1994;194(4):221-30. doi: 10.1007/BF02576383.
Splenic regeneration represents an interesting phenomenon both in relation to its role as a model system (to study the development of the complex three-dimensional architecture of an immunological organ) and because of the clinical application, namely autotransplantation of spleen. The latter is one of the attempts to restore splenic functions after splenectomy, which is known to increase a life-long risk of fatal sepsis. However, splenic functions of autotransplanted splenic tissue are known to be highly dependent on the recovery of the complex microenvironment and immunoarchitecture of the splenic compartments during the regeneration processes, but the elements inducing splenic reorganization are still unknown. Therefore, the present work investigates whether splenic stroma depleted of cells is able to induce regenerative processes after implantation. In addition, we tried to recombine stromal tissue with selected cell populations to study their influence. Cell-free stromal tissue induced angiogenesis and to a lesser extent also attracted the immigration of lymphocytes during the first 60 days of regeneration. However, after this period of regeneration, the transplants began to degenerate and were resorbed. The recombination of stromal tissue with mitogen-stimulated spleen cells only resulted in intensifying the degenerative processes, and all implants were resorbed after 120 days. Except that in the first 30 days there were some accumulations of lymphocytes that resembled primitive follicles, no splenic compartments such as red pulp, periarteriolar lymphoid sheath, or marginal zone could be detected in any of the transplants. From these results it can be concluded that splenic stroma can induce the primary events of splenic regeneration (like angiogenesis), but is not able to provide an appropriate microenvironment and immunoarchitecture for a correct repopulation and differentiation of cells. Furthermore, the recombination experiments point to a minor role of T-cells and possibly an important role for accessory cells in splenic regeneration.
脾脏再生是一个有趣的现象，这不仅体现在它作为一个模型系统（用于研究免疫器官复杂三维结构的发育）的作用上，还因其临床应用，即脾脏自体移植。后者是脾切除术后恢复脾脏功能的一种尝试，已知脾切除会增加终生致命性败血症的风险。然而，已知自体移植的脾脏组织的脾脏功能高度依赖于再生过程中脾脏各部分复杂微环境和免疫结构的恢复，但诱导脾脏重组的因素仍然未知。因此，本研究调查了去除细胞的脾脏基质在植入后是否能够诱导再生过程。此外，我们试图将基质组织与选定的细胞群体重组，以研究它们的影响。在再生的前60天，无细胞的基质组织诱导了血管生成，在较小程度上也吸引了淋巴细胞的迁移。然而，在这个再生期之后，移植物开始退化并被吸收。基质组织与有丝分裂原刺激的脾细胞重组仅导致退化过程加剧，所有植入物在120天后均被吸收。除了在最初30天有一些类似原始滤泡的淋巴细胞聚集外，在任何移植物中都未检测到脾髓、动脉周围淋巴鞘或边缘区等脾脏部分。从这些结果可以得出结论，脾脏基质可以诱导脾脏再生的初级事件（如血管生成），但无法为细胞的正确重新填充和分化提供合适的微环境和免疫结构。此外，重组实验表明T细胞在脾脏再生中的作用较小，而辅助细胞可能起重要作用。
