Ponvert C, Galoppin L, Canu P
Université René Descartes (Paris V), Laboratoire d'Immunoallergologie, Faculté de Médecine Cochin, Port Royal, France.
Cancer Lett. 1994 Sep 30;85(1):125-31. doi: 10.1016/0304-3835(94)90248-8.
There is evidence that mast cells and their degranulation products are involved in resistance against tumours. Previously, we have shown that tumour incidence and growth were inversely correlated with basal histamine levels, i.e. mast cell numbers, in tissues of W/Wv (mast cell-deficient), Wv/+ (partially mast cell-depleted), and +/+ (mast cell-sufficient) mice, and that histamine levels were increased in numerous tissues of tumour-bearing animals, including C57BL/6 and C3H mice, Sprague-Dawley and Commentry rats. The aim of this work was to analyse the incidence and growth of a grafted tumour (fibrosarcoma MC-B6-1) in W/+ mice, as compared with W/Wv, Wv/+ and +/+ mice, and to study the modifications in tissue histamine levels in W/+, W/Wv, Wv/+ and +/+ tumour-grafted mice, in order to determine whether or not these modifications were correlated with resistance to tumours. We report confirmation that tumour incidence and growth are inversely correlated with basal tissue histamine levels in W/Wv, Wv/+, and +/+ fibrosarcoma-bearing mice. However, in W/+ mice (normal tissue histamine levels), tumour incidence was the same as in Wv/+ mice. Histamine levels in tissues of W/Wv, Wv/+, W/+ and +/+ tumour bearing mice were not significantly different from those in controls. They were higher in some tissues of Wv/+ mice rejecting the tumour than in Wv/+ mice not rejecting the tumour. However, in W/+ and +/+ mice, histamine levels were not significantly different, and even tended to be lower in most tissues of mice rejecting the tumour than in mice accepting the tumour. Overall, these results suggest that resistance to tumours cannot be ascribed solely to mast cells, and that other mechanisms may also be involved. Thus, further experiments are needed to clarify the exact role of mast cells and mast cell-derived mediators and cytokines in the defence against tumours.
有证据表明肥大细胞及其脱颗粒产物参与了抗肿瘤反应。此前,我们已经证明,在W/Wv(肥大细胞缺陷型)、Wv/+(部分肥大细胞缺失型)和+/+(肥大细胞充足型)小鼠的组织中,肿瘤发生率和生长与基础组胺水平呈负相关,即与肥大细胞数量呈负相关,并且在包括C57BL/6和C3H小鼠、Sprague-Dawley和Commentry大鼠在内的荷瘤动物的许多组织中,组胺水平升高。这项工作的目的是分析与W/Wv、Wv/+和+/+小鼠相比,W/+小鼠中移植肿瘤(纤维肉瘤MC-B6-1)的发生率和生长情况,并研究W/+、W/Wv、Wv/+和+/+肿瘤移植小鼠组织中组胺水平的变化,以确定这些变化是否与抗肿瘤能力相关。我们报告证实,在W/Wv、Wv/+和+/+荷纤维肉瘤小鼠中,肿瘤发生率和生长与基础组织组胺水平呈负相关。然而,在W/+小鼠(正常组织组胺水平)中,肿瘤发生率与Wv/+小鼠相同。W/Wv、Wv/+、W/+和+/+荷瘤小鼠组织中的组胺水平与对照组相比无显著差异。在排斥肿瘤的Wv/+小鼠的某些组织中,组胺水平高于未排斥肿瘤的Wv/+小鼠。然而,在W/+和+/+小鼠中,组胺水平无显著差异,甚至在排斥肿瘤的小鼠的大多数组织中,组胺水平往往低于接受肿瘤的小鼠。总体而言,这些结果表明,抗肿瘤能力不能仅归因于肥大细胞,还可能涉及其他机制。因此,需要进一步的实验来阐明肥大细胞以及肥大细胞衍生的介质和细胞因子在抗肿瘤防御中的确切作用。