Masahiro Mieno

The Roles of CD8+ and CD4+ Cells in Tumor Rejection

In vivo administrations of anti‐Lyt‐2.2 (CDS) mAb and anti‐L3T4 (CD4) mAb selectively eliminated CD8+ cells amd CD4+ cells, respectively. The relative potencies of CD8+ cells and CD4+ cells and their roles in primary tumor rejections were studied by investigating the effects of these mAbs on tumor growth. CD8+ cells were themselves fully capable of mediating rejection in 5 different tumor rejection systems: two radiation leukemia virus (RadLV)‐induced leukemias, B6RV2 and BALBRVD, a radiation‐induced leukemia BALBRL♂1, and a plasmacytoma BALBMOPC‐70A in CB6F1 mice, and a Friend virus‐induced leukemia B6FBL‐3 in B6 mice. On the other hand, CD4+ cells were capable of resisting tumor growth of B6FBL‐3, but not of the other four tumors. Furthermore, for efficient rejection of CB6F1UV+˚l sarcoma by CB6F1 mice, synergy of CDS+ and CD4+ cells was necessary. Blocking of UV+˚ 1 rejection was abrogated by delayed administration of anti‐L3T4 (CD4) mAb but not anti‐Lyt‐2.2 (CDS) mAb, indicating the involvement of CD4+ cells in only the initial phase of rejection.

Effects of Exogenous Acetylcholine upon Adrenal 17-Hydroxycorticosteroid Secretion of Intact and Head X-Irradiated Dogs

Adrenocortical response to exogenous acetylcholine (Ach) was investigated, under anesthetized conditions, in intact, hypophysectomized and head X-irradiated dogs. Intravenous injection of Ach (1 mg/kg b.w.) to intact dogs resulted in marked increases in the secretion of 17-hydroxycorticosteroids (17-OHCS) by the adrenal gland. The maximum response was seen at 10 min after the injection and a return to preinjection levels tended to occur by 60 min. This effect was abolished completely by hypophysectomy. In dogs whose heads had been irradiated with 200 and 1,000 R of X-rays 1 day previously, a considerably lower response to Ach was found; 17-OHCS output at the time when the secretion had been maximum was 44--53% less than that in non-irradiated dogs.