Abstract

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)

  Funding Agency

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

  Institution

Name
University of Texas Sw Medical Center Dallas
Department
Type
Schools of Medicine
DUNS #
City
Dallas
State
TX
Country
United States
Zip Code
75390

  Publications

Johansson, Maria H; Taylor, Mesha A; Jagodic, Maja et al. (2006) Mapping of quantitative trait loci determining NK cell-mediated resistance to MHC class I-deficient bone marrow grafts in perforin-deficient mice. J Immunol 177:7923-9
Catalina, Fernando; Milewich, Leon; Kumar, Vinay et al. (2003) Dietary dehydroepiandrosterone inhibits bone marrow and leukemia cell transplants: role of food restriction. Exp Biol Med (Maywood) 228:1303-20
Taylor, Mesha Austin; Ward, Brant; Schatzle, John D et al. (2002) Perforin- and Fas-dependent mechanisms of natural killer cell-mediated rejection of incompatible bone marrow cell grafts. Eur J Immunol 32:793-9
Morris, Margaret A; Liu, Jingxuan; Arora, Veera et al. (2002) B6 strain Ly49I inhibitory gene expression on T cells in FVB.Ly49IB6 transgenic mice fails to prevent normal T cell functions. J Immunol 169:3661-6
Morris, Margaret A; Koulich, Elena; Liu, Jingxuan et al. (2002) Definition of additional functional ligands for Ly49I(B6) using FVBLy49I(B6) transgenic mice and B6 natural killer cell effectors. Transplantation 74:1449-54
Murphy, W J; Koh, C Y; Raziuddin, A et al. (2001) Immunobiology of natural killer cells and bone marrow transplantation: merging of basic and preclinical studies. Immunol Rev 181:279-89
Daniels, K A; Devora, G; Lai, W C et al. (2001) Murine cytomegalovirus is regulated by a discrete subset of natural killer cells reactive with monoclonal antibody to Ly49H. J Exp Med 194:29-44
Taylor, M A; Chaudhary, P M; Klem, J et al. (2001) Inhibition of the death receptor pathway by cFLIP confers partial engraftment of MHC class I-deficient stem cells and reduces tumor clearance in perforin-deficient mice. J Immunol 167:4230-7
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

Showing the most recent 10 out of 61 publications