TY - JOUR
T1 - Genetic control of natural resistance to trypanosoma rhodesiense
T2 - Transfer of resistance with bone marrow or spleen cells
AU - Greenblatt, Hellen C.
AU - Potter, Terry A.
AU - Rosenstreich, David L.
N1 - Funding Information:
Received for publication June 22, 1984, and in revised form November 19, 1984. This work was supported in part by grants from the United Nations Development Programme/World Bank/World Health Organization Special Programme for Research and Training in Tropical Diseases (TDR), by Grant AI-17934 from the National Institute of Allergy and Infectious Diseases, and by grant P30CA-133from the AECOM Cancer Center Core Grant (National Cancer Institute). We thank Stanley Williams for his technical assistance, Dr. Frank Lilly and Michael Jeffers for the BALB.B mice, and Dr. Ethel Jacobson for the allotyping of chimeric mice. Please address requests for reprints to Dr. Hellen C. Greenblatt, Clinical Sciences Incorporated, 30 Troy Road, Whippany, New Jersey 07981.
PY - 1985/5
Y1 - 1985/5
N2 - 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.
AB - 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.
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U2 - 10.1093/infdis/151.5.911
DO - 10.1093/infdis/151.5.911
M3 - Article
C2 - 3886807
AN - SCOPUS:0021993501
SN - 0022-1899
VL - 151
SP - 911
EP - 916
JO - Journal of Infectious Diseases
JF - Journal of Infectious Diseases
IS - 5
ER -