The number of mouse Tcra-V gene segments varies from one individual to another and is estimated to be about 100. Southern blot analysis revealed that most of the Tcra-V are organized in clusters composed of copies of Tcra-V belonging to different subfamilies. We analyzed in detail a Tcra-V subfamily and looked for new Tcra-V in order to improve the knowledge of the mouse Tcra locus organization. A series of genomic clones derived from the B10.A mouse strain enclosing these clusters was used to determined the structure of all the Tcra-V2. We were able to identify ten Tcra-V2. This study showed that the Tcra-V2 can be organized into three structural subgroups. The distribution of the genes along the Tcra locus, plus their structural organization, indicates that successive duplications occurred during the processes of expansion and contraction of the Tcra-V gene subfamilies. Several Tcra-V2 are also identical, indicating recent duplications. The most divergent Tcra-V2 differ by 7.4% nucleotides, leading to 5.2% differences in amino acid contents.
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http://dx.doi.org/10.1007/BF02602560 | DOI Listing |
J Agric Food Chem
June 2010
National Institute of Health Sciences, Setagaya-ku, Tokyo, Japan.
Type-I allergic disorders and particularly food hypersensitivities are becoming increasingly common worldwide. This study investigated whether dietary enrichment with carotenoids inhibited oral sensitization to an antigen and the development of food allergies. The effects of a diet high in carotenoids were investigated in B10A mice that were orally sensitized to ovalbumin (OVA).
View Article and Find Full Text PDFJ Heart Lung Transplant
July 2007
Department of Cardiac Surgery, National Heart and Lung Institute, London, UK.
Background: Cardiac allograft vasculopathy (CAV) is the pre-eminent cause of late cardiac allograft failure. It is characterized by a concentric intimal hyperplasia, which we designate transplant intimal hyperplasia (TIH). To date, blockade of the adhesion molecule lymphocyte function-associated antigen-1 (LFA-1) has been shown to be effective in preventing TIH in experimental models of transplantation, but only when combined with other immunosuppressants.
View Article and Find Full Text PDFClin Exp Immunol
December 2006
Department of Cardiac Surgery, National Heart and Lung Institute, Imperial College London, Hammersmith Hospital, London, UK.
Transplant coronary artery disease is the pre-eminent cause of late cardiac allograft failure. It is primarily characterized by a concentric intimal hyperplasia, which we designate transplant intimal hyperplasia (TIH). Although the pathogenesis of TIH is predominately immune driven, the specific role of alloantibodies in the disease process remains undefined.
View Article and Find Full Text PDFFEMS Immunol Med Microbiol
June 2006
Department of Experimental Medicine, McGill University, Montreal, QC, Canada.
Modulation of immune responses using Toll-like receptor (TLR) ligands is fast becoming one of the main new approaches for the treatment of infectious and allergic diseases. Characterizing the role of genetic factors in modulating responses to these ligands will be crucial in determining the efficacy of a particular treatment. Our previous findings have shown that treatment of Mycobacterium bovis BCG infection with a synthetic TLR7 ligand resulted in a reduction of the splenic bacterial load only in mice carrying a wild-type allele of Nramp1.
View Article and Find Full Text PDFJ Invest Dermatol
April 2006
Department of Human Genetics, Montreal General Hospital Research Institute, McGill University, Montreal, Quebec, Canada.
Control of macrophage functions by natural resistance-associated macrophage protein 1 (NRAMP1) has proven to be important for murine resistance to several intracellular pathogens, including Mycobacterium bovis BCG and Salmonella typhimurium, although the exact molecular mechanism of its action remains unknown. We identified secretory leukocyte protease inhibitor (SLPI) as a novel candidate gene whose expression is dependent on Nramp1 gene expression using B10A.Nramp1+/+ and B10A.
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