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Critical Reviews™ in Immunology
Impact-faktor: 1.352 5-jähriger Impact-Faktor: 3.347 SJR: 0.657 SNIP: 0.55 CiteScore™: 2.19

ISSN Druckformat: 1040-8401
ISSN Online: 2162-6472

Volumes:
Volumen 39, 2019 Volumen 38, 2018 Volumen 37, 2017 Volumen 36, 2016 Volumen 35, 2015 Volumen 34, 2014 Volumen 33, 2013 Volumen 32, 2012 Volumen 31, 2011 Volumen 30, 2010 Volumen 29, 2009 Volumen 28, 2008 Volumen 27, 2007 Volumen 26, 2006 Volumen 25, 2005 Volumen 24, 2004 Volumen 23, 2003 Volumen 22, 2002 Volumen 21, 2001 Volumen 20, 2000 Volumen 19, 1999 Volumen 18, 1998 Volumen 17, 1997 Volumen 16, 1996 Volumen 15, 1995 Volumen 14, 1994

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

ABSTRAKT

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.