Atkins R C, Ford W L
J Exp Med. 1975 Mar 1;141(3):664-80. doi: 10.1084/jem.141.3.664.
A systemic graft-vs.-host (GVH) reaction was initiated by the intravenous injection of parental strain thoracic duct lymphocytes (TDL) into irradiated F1 hybrid recipients with in-dwelling thoracic duct cannulae. The migration of the donor lymphocytes was followed by labeling them in vitro with either [3H] or [14C]uridine and measuring radioactivity by scintillation counting of the spleen and lymph nodes of the recipients removed 24 h after injection and in TDL collected throughout this period. The localization of labeled cells was always compared to that of a reference population of nonreactive lymphocytes, e.g. F1 hybrid, labeled with the alternative isotope (Fig. 1). A consistent surplus of the reactive label was found in the spleen which was balanced by a deficit of the reactive label in TDL; lymph nodes gave intermediate values. The same distribution pattern was noted when the reference population was a specifically unresponsive population of the parental strain. This differential distribution depends on recognition of the recipient's Ag-B antigens because when normal lymphocytes were injected together with specifically unresponsive lymphocytes into a "third party" F1 hybrid (against which both populations were reactive) there was no surplus of the normal cells in the spleen and no deficit in the lymph. Moreover in an Ag-B identical strain combination there was no detectable difference in the distribution of reactive and nonreactive populations. The distribution of a labeled reaction population can be accounted for if a substantial minority of cells are immobilized in the spleen and lymph nodes as a consequence of antigen recognition (Fig. 3). When the donor cells in the spleen were assayed 24 h after injection there was paradoxically a slight reduction in their specific GVH activity, which is at least partly because they are under-represented in a single cell suspension. The size of the splenic surplus (23%) and the thoracic duct deficit (12%) suggested that the minority of nonimmune lymphocytes which recognize each Ag-B complex carry 12% of the radioactive label in the original population. It is argued that this provides a near estimate of the frequency of T lymphocytes which can recognize each Ag-B antigenic complex.
通过将亲代品系胸导管淋巴细胞（TDL）静脉注射到带有内置胸导管插管的经照射的F1杂种受体中，引发了全身性移植物抗宿主（GVH）反应。通过在体外使用[3H]或[14C]尿苷标记供体淋巴细胞，并在注射后24小时取出受体的脾脏和淋巴结进行闪烁计数来测量放射性，从而追踪供体淋巴细胞的迁移情况，并在整个期间收集TDL进行测量。标记细胞的定位总是与用另一种同位素标记的非反应性淋巴细胞参考群体（例如F1杂种）的定位进行比较（图1）。在脾脏中发现反应性标记始终存在过剩，而在TDL中反应性标记则不足；淋巴结给出的是中间值。当参考群体是亲代品系的特异性无反应群体时，也观察到相同的分布模式。这种差异分布取决于对受体Ag-B抗原的识别，因为当将正常淋巴细胞与特异性无反应淋巴细胞一起注射到“第三方”F1杂种（两种群体对其均有反应）中时，脾脏中没有正常细胞过剩，淋巴中也没有不足。此外，在Ag-B相同的品系组合中，反应性和非反应性群体的分布没有可检测到的差异。如果由于抗原识别，相当一部分少数细胞固定在脾脏和淋巴结中，那么标记反应群体的分布就可以得到解释（图3）。注射后24小时对脾脏中的供体细胞进行检测时，矛盾的是其特异性GVH活性略有降低，这至少部分是因为它们在单细胞悬液中的代表性不足。脾脏过剩量（23%）和胸导管不足量（12%）的大小表明，识别每种Ag-B复合物的少数非免疫淋巴细胞在原始群体中携带12%的放射性标记。有人认为，这提供了对能够识别每种Ag-B抗原复合物的T淋巴细胞频率的近似估计。
