This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Fukase, S. Articles by Sendo, F. Search for Related Content PubMed PubMed Citation Articles by Fukase, S. Articles by Sendo, F.

Tumor Cytotoxicity of Polymorphonuclear Leukocytes in Beige Mice: Linkage of High Responsiveness to Linear ß-1,3-D-Glucan with the Beige Gene¹

Department of Pathology [S. F., T. I., S. A.] and Department of Parasitology [F. S.], Yamagata University School of Medicin, Iida, Zao, Yamagata 990-23, Japan

Beige mice (bg/bg) have many functional defects in their leukocytes and these phenotypes are inherited autosomal recessively. We studied the tumor cytotoxicity of polymorphonuclear leukocytes (PMN) obtained from bg/bg. The intensity of tumor cytotoxicity of PMN induced by linear ß-1,3-D-glucan was significantly higher in bg/bg PMN than in PMN of heterozygous control mice (bg/+). To analyze this phenomenon more precisely from the genetic viewpoint, we determined the tumor cytotoxicity of PMN from mice obtained by several mating experiments. (a) The intensity of linear ß-1,3-D-glucan-induced PMN cytotoxicity was found to be genetically defined and linked completely with the beige gene. In litter mates obtained from bg/+() x bg/bg(), bg/bg() x bg/+(), and bg/+() x bg/+() mating, PMN from only bg/bg showed significantly higher tumor cytotoxicity than those from bg/+ or mice that do not possess the beige gene (+/+). (b) The tumor cytotoxicity induced by other stimulants (phorbol myristate acetate and cytokines) was not significantly higher in bg/bg than bg/+ or +/+ PMN. It was concluded that the high responsiveness to linear ß-1,3-D-glucan in terms of tumor cytotoxicity of PMN was determined by the locus that is linked to the beige gene and is expressed autosomal recessively.

¹ This work was supported in part by a Grant-in-Aid for Specific Research (No. 61015009) from the Ministry of Education, Science and Culture of Japan.

² To whom requests for reprints should be addressed.

Received 2/17/87. Revised 6/18/87. Accepted 6/23/87.