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Genetic Control of Natural Resistance to Trypanosoma rhodesiense: Transfer of Resistance with Bone Marrow or Spleen Cells
Hellen C. Greenblatt, Terry A. Potter and David L. Rosenstreich
The Journal of Infectious Diseases
Vol. 151, No. 5 (May, 1985), pp. 911-916
Published by: Oxford University Press
Stable URL: http://www.jstor.org/stable/30135966
Page Count: 6
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Inbred strains of mice differ greatly in their innate resistance to Trypanosoma rhodesiense, the etiologic agent of African sleeping sickness. BALB/c mice are very susceptible to this organism, whereas C57BL/6 mice are highly resistant. This difference is regulated by at least three distinct genes. An adoptive transfer study was performed in order to determine the tissue site of expression of these genes. Three inbred mouse strains (C57BL/6J, C3H.SW/SnJ, and BALB.B) that differ in resistance to T. rhodesiense, but are histocompatible at the H-2 locus, were used in the study. The adoptive transfer of normal bone marrow cells from C57BL/6J (resistant) mice into X-irradiated BALB.B (susceptible) mice rendered the recipient mice resistant to a subsequent experimental challenge with T. rhodesiense. Conversely, the transfer of bone marrow cells from BALB.B mice into irradiated C57BL/6J mice rendered the latter mice susceptible. Resistance could also be adoptively transferred from C57BL/6J mice to a second susceptible strain, C3H.SW/SnJ, by using either bone marrow or spleen cells. These findings demonstrate that although multiple genes control innate resistance to T. rhodesiense, all or most of these genes appear to control the development or function of cells whose progenitors reside in the spleen and bone marrow.
The Journal of Infectious Diseases © 1985 Oxford University Press