Harada M, Matsunaga K, Oguchi Y, Iijima H, Tamada K, Abe K, Takenoyama M, Ito O, Kimura G, Nomoto K
Department of Virology, Kyushu University, Fukuoka, Japan.
Int J Cancer. 1997 Jan 27;70(3):362-72. doi: 10.1002/(sici)1097-0215(19970127)70:3<362::aid-ijc19>3.0.co;2-h.
We investigated both the effect and the mechanism of oral (p.o.) administration of PSK, a protein-bound polysaccharide derived from Basidiomycetes, on the anti-tumor T-cell response in gut-associated lymphoid tissue (GALT). The p.o. administration of PSK significantly suppressed the growth of colon 26 carcinoma (C-26) inoculated into the subserosal space of the cecum (i.c.), and augmented the tumor-neutralizing activity of the draining mesenteric lymph node (LN) cells. PSK treatment also significantly decreased the levels of immunosuppressive factors such as plasma transforming growth factor (TGF)-beta in the i.c. C-26-inoculated mice. We also evaluated the improving effect of PSK on the anti-tumor T-cell response in GALT by utilizing B7-transfected P815 mastocytoma (B7/P815). The PSK treatment promoted the rejection of i.c.-inoculated B7/P815 and restored the CD4+ T-cell-dependent proliferative response of the draining mesenteric LN cells against in vitro restimulation. Furthermore, the treatment also decreased the TGF-beta production but increased the IFN-gamma production of these cells. The p.o. administration of PSK, however, showed no effect in the CD8+ T-cell-dependent cytolytic activity of the draining mesenteric LN cells after in vitro restimulation. Overall, these results indicate that the p.o. administration of PSK can improve the impaired anti-tumor CD4+ T-cell response in GALT, mainly through a suppression of TGF-beta production and a restoration of IFN-gamma production.
我们研究了口服源自担子菌的蛋白结合多糖PSK对肠道相关淋巴组织（GALT）中抗肿瘤T细胞反应的影响及其机制。口服PSK可显著抑制接种于盲肠浆膜下间隙（i.c.）的结肠26癌（C-26）的生长，并增强引流肠系膜淋巴结（LN）细胞的肿瘤中和活性。PSK治疗还显著降低了i.c.接种C-26的小鼠体内免疫抑制因子如血浆转化生长因子（TGF）-β的水平。我们还利用B7转染的P815肥大细胞瘤（B7/P815）评估了PSK对GALT中抗肿瘤T细胞反应的改善作用。PSK治疗促进了i.c.接种的B7/P815的排斥，并恢复了引流肠系膜LN细胞对体外再刺激的CD4 + T细胞依赖性增殖反应。此外，该治疗还降低了这些细胞的TGF-β产生，但增加了IFN-γ产生。然而，口服PSK对体外再刺激后引流肠系膜LN细胞的CD8 + T细胞依赖性细胞溶解活性没有影响。总体而言，这些结果表明，口服PSK可以改善GALT中受损的抗肿瘤CD4 + T细胞反应，主要是通过抑制TGF-β产生和恢复IFN-γ产生。
