Fitzgerald P A, Bennett M
Cancer Invest. 1983;1(2):139-49. doi: 10.3109/07357908309042416.
Cytolytic T lymphocyte (CTL) functions were compared in mice between the ages of 2 and 30 months. The stimulator cells were H-2 allogeneic spleen or tumor cells, parental-strain spleen cells, or syngeneic tumor cells. Effector cells capable of lysing syngeneic tumor cells were shown to be T cells and not NK cells. The cell-mediated lympholysis (CML) responses by spleen cells of aged mice were near normal against H-2 allogeneic spleen or tumor cells but were defective against syngeneic tumor cells or parental-strain spleen cells. The defective syngeneic tumor CML response was observed at various responder:stimulator ratios and at various days of incubation. The defect was in the nonadherent, and not in the adherent, fraction of spleen cells. Suppressor cells were detected in spleens of 30 month, but not of 18 month old mice. Aged mice were more susceptible than young mice to small inocula of syngeneic C57BL EL-4 lymphoma cells. The immunogenicity of irradiated spleen cells of old mice had not changed for the F1 antiparent CML response. Splenic CML responses of young mice treated with 89Sr demonstrated a similar pattern, i.e., good responses to H-2 allogeneic stimulator cells but poor responses to syngeneic tumor cells or to parental-strain spleen cells. This loss of certain CTL functions influenced by marrow dependent cells can partially explain the increased susceptibility of old animals to tumors.
对2至30月龄小鼠的细胞毒性T淋巴细胞（CTL）功能进行了比较。刺激细胞为H-2同种异体脾细胞或肿瘤细胞、亲代品系脾细胞或同基因肿瘤细胞。能够裂解同基因肿瘤细胞的效应细胞被证明是T细胞而非自然杀伤（NK）细胞。老年小鼠脾细胞介导的细胞溶解（CML）反应对H-2同种异体脾细胞或肿瘤细胞接近正常，但对同基因肿瘤细胞或亲代品系脾细胞存在缺陷。在不同的反应细胞：刺激细胞比例和不同的孵育天数下均观察到同基因肿瘤CML反应存在缺陷。缺陷存在于脾细胞的非黏附部分，而非黏附部分。在30月龄小鼠的脾脏中检测到了抑制细胞，但18月龄小鼠的脾脏中未检测到。老年小鼠比年轻小鼠对同基因C57BL EL-4淋巴瘤细胞的小剂量接种更敏感。老年小鼠经照射的脾细胞对F1抗亲代CML反应的免疫原性未发生改变。用89Sr处理的年轻小鼠的脾脏CML反应表现出类似的模式，即对H-2同种异体刺激细胞反应良好，但对同基因肿瘤细胞或亲代品系脾细胞反应较差。这种受骨髓依赖性细胞影响的某些CTL功能丧失可以部分解释老年动物对肿瘤易感性增加的原因。
