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Critical Reviews™ in Immunology
インパクトファクター: 1.352 5年インパクトファクター: 3.347 SJR: 0.657 SNIP: 0.55 CiteScore™: 2.19

ISSN 印刷: 1040-8401
ISSN オンライン: 2162-6472

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Critical Reviews™ in Immunology

DOI: 10.1615/CritRevImmunol.v14.i3-4.60
pages 337-353

Genes for Control of Spread of the Tumor and Mycobacterium tuberculosis Infection in the Mouse

Igor K. Egorov
The Jackson Laboratory, Bar Harbor, Maine 04609
Boris V. Nickonenko
The Jackson Laboratory, Bar Harbor, Maine 04609

要約

In this review, new data are interpreted that provide some answers to the question of why the immune system fails to respond to metastatic cancers. A function such as an element of the immune response is expected to be under the control of a gene. To find a gene, a mutant is required. Complex screens have been designed and used to detect mouse mutants resisting spread of transplantable tumors (in a spontaneous metastasis assay). Curiously, both mutants with increased and decreased resistance to spread of the tumor have been found. S-27 is a strongly resistant mutant linked to MHC; this mutation also affected some responses to Mycobacterium tuberculosis infection. A long sought link between malignant transformation and vaccination against mycobacterial diseases is discovered in this mutant. A search for a molecule responsible for effects of the S-27 mutation resulted in an unexpected finding. The S-27 mutant carries complex nucleotide alterations at the junction between the signal sequence and the sequences coding for the mature MHC class II Aβ polypeptide chain. Antigen recognition region of the Aβ molecule is not affected by this mutation. Some concepts developed during the course of this study are illustrated in Figures 1 to 4.


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