Hybrid resistance is the prevention of proliferation of grafts of H-2 homozygous normal or neoplastic hemopoietic cells by F1 hybrid mice heterozygous at H-2. This observation goes against the laws of transplantation genetics, which state that histocompatibility antigens are inherited in a codominant fashion. The hybrid or hemopoietic histocompatibility (Hh) antigens recognized have not been characterized chemically even though the determinants map at H-2D.
One aim here is to generate monoclonal antibodies to Hh antigens. The effector cells responsible for hybrid resistance include natural killer cells (NK), which probably function in surveillance against tumors. Cells other than NK cells are also probably involved and may have the specific receptors for Hh antigens.
A second aim i s to generate monoclonal antibodies against the effector cells involved in hybrid resistance responses. To enhance the success of the above two aims, we aim to develop an in vitro assay for hybrid resistance. The potential importance of the work may relate to antiself immunity (autoimmunity and tumor surveillance), since the parent and the F1 share the structural genes for the same Hh antigen. (SR)

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Project (R01)
Project #
5R01CA036922-03
Application #
3174586
Study Section
(SSS)
Project Start
1984-03-01
Project End
1987-02-28
Budget Start
1986-03-01
Budget End
1987-02-28
Support Year
3
Fiscal Year
1986
Total Cost
Indirect Cost
Name
University of Texas Sw Medical Center Dallas
Department
Type
Schools of Medicine
DUNS #
City
Dallas
State
TX
Country
United States
Zip Code
75390
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Catalina, F; Speciale, S G; Kumar, V et al. (2001) Food restriction-like effects of dietary dehydroepiandrosterone. Hypothalamic neurotransmitters and metabolites in male C57BL/6 and (C57BL/6 x DBA/2)F1 mice. Exp Biol Med (Maywood) 226:208-15
Austin Taylor, M; Bennett, M; Kumar, V et al. (2000) Functional defects of NK cells treated with chloroquine mimic the lytic defects observed in perforin-deficient mice. J Immunol 165:5048-53

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