Resistance of H-2 heterozygous mice to parental tumors. II. Characterization of Hh-1 controlled hybrid resistance to syngeneic fibrosarcomas and the EL-4 lymphoma.

Resistance of H-2 heterozygous mice to parental tumors. II. Characterization of Hh-1 controlled hybrid resistance to syngeneic fibrosarcomas and the EL-4 lymphoma.
复制标题

H-2杂合小鼠对亲本肿瘤的抵抗力。

DOI:
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发表时间:
1977
影响因子:
4.4
通讯作者:
L. Wicker
L. Wicker
中科院分区:
医学2区
文献类型:
--
作者:
E. Clark;R. Harmon;L. Wicker

文献摘要

被引文献

相似文献

Hybrid resistance to the C57BL lymphoma EL-4 and to two 3-methylcholanthrene-induced B10.A(4R) fibrosarcomas of recent origin was studied in H-2 heterozygous mice. Histocompatible tumor recipients were derived from mating C57BL/10, B10.A, and H-2 a /H-2 b intra- H-2 recombinant mice in such a way as to provide heterozygosity at defined portions of the H-2 complex. Hybrid resistance was assessed by comparing the mean survival times and tumor incidence of H-2 heterozygotes with those of homozygous 4R (sarcomas) or B10 (EL-4) mice. The results reveal that heterozygosity at the D end of the H-2 complex controls hybrid resistance to fibrosarcomas as well as to lymphomas. Evidence is discussed which suggests that the locus controlling hybrid resistance, Hh-1 , is located within the H-2 complex between the S and D regions. Hh-1 -controlled hybrid resistance was clearly demonstrable when tumor cells were inoculated by the intraperitoneal route but was not detected if tumor cells were injected subcutaneously. Both Hh-1 -controlled hybrid resistance and its in vitro correlate, natural cytotoxicity, appear to be most strongly expressed in the peritoneum. Pretreatment of Hh-1 heterozygous mice with Hh-1-H-2D b parental spleen cells consistently reduced tumor resistance compared to mice pretreated with reciprocal parental Hh-1-H-2D d splenocytes. This suggests that Hh-1 codes for or regulates the expression of cell-surface antigens found on normal H-2 b parental cells. In addition, we have found that other H-2 genes, probably I region immune response genes, also influence fibrosarcoma growth in F 1 hybrid hosts. Thus, several loci within the H-2 complex appear to play a role in the polygenic control of the immune response to fibrosarcomas.