Abstract
During the past several years an active interest has developed in genetic regulation of host susceptibility and resistance to both infection and malignancy.1 The potential role of genetic makeup of individuals as a major determinant of susceptibility to a variety of infectious agents receives strong support from epidemiologic data. Concomitantly, the widespread development of genetically defined strains of mutant, congenic, and recombinant inbred mice have made it possible for investigators to make new advances in this field. According to Skamene,l this allows for detailed mapping of the murine genome, resulting in the identification of the various chromosomal loci controlling resistance and susceptibility to a given infectious or oncogenic stimulus. This strategy has already resulted in the identification of several chromosomal loci involved in regulation of various traits. As Skamene points out, resistance genes to various infectious or malignant agents appear to map to the same locus1. This suggests that there may be common mechanisms of host resistance to combat a variety of unrelated agents. Once these various genes have been identified, we can then begin to investigate the various cellular and molecular mechanisms that underlie the traits of resistance and susceptibility, thereby developing a better understanding of host defense mechanisms along with the potential for developing remedial measures.
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Berk, R.S. (1993). Genetic Regulation of the Murine Corneal and Non-Corneal Response to Pseudomonas aeruginosa . In: Campa, M., Bendinelli, M., Friedman, H. (eds) Pseudomonas aeruginosa as an Opportunistic Pathogen. Infectious Agents and Pathogenesis. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3036-7_10
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DOI: https://doi.org/10.1007/978-1-4615-3036-7_10
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