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      Allorecognition in the Tasmanian Devil ( Sarcophilus harrisii), an Endangered Marsupial Species with Limited Genetic Diversity


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          Tasmanian devils ( Sarcophilus harrisii) are on the verge of extinction due to a transmissible cancer, devil facial tumour disease (DFTD). This tumour is an allograft that is transmitted between individuals without immune recognition of the tumour cells. The mechanism to explain this lack of immune recognition and acceptance is not well understood. It has been hypothesized that lack of genetic diversity at the Major Histocompatibility Complex (MHC) allowed the tumour cells to grow in genetically similar hosts without evoking an immune response to alloantigens. We conducted mixed lymphocyte reactions and skin grafts to measure functional MHC diversity in the Tasmanian devil population. The limited MHC diversity was sufficient to produce measurable mixed lymphocyte reactions. There was a wide range of responses, from low or no reaction to relatively strong responses. The highest responses occurred when lymphocytes from devils from the east of Tasmania were mixed with lymphocytes from devils from the west of Tasmania. All of the five successful skin allografts were rejected within 14 days after surgery, even though little or no MHC I and II mismatches were found. Extensive T-cell infiltration characterised the immune rejection. We conclude that Tasmanian devils are capable of allogeneic rejection. Consequently, a lack of functional allorecognition mechanisms in the devil population does not explain the transmission of a contagious cancer.

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          Allograft theory: transmission of devil facial-tumour disease.

          The Tasmanian devil, a large carnivorous Australian marsupial, is under threat from a widespread fatal disease in which a malignant oral-facial tumour obstructs the animal's ability to feed. Here we show that the chromosomes in these tumours have undergone a complex rearrangement that is identical for every animal studied. In light of this remarkable finding and of the known fighting behaviour of the devils, we propose that the disease is transmitted by allograft, whereby an infectious cell line is passed directly between the animals through bites they inflict on one another.
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            Genetic basis for species vulnerability in the cheetah.

            A population genetic survey of over 200 structural loci previously revealed that the South African cheetah (Acinonyx jubatus jubatus) has an extreme paucity of genetic variability, probably as a consequence of a severe population bottleneck in its recent past. The genetic monomorphism of the species is here extended to the major histocompatibility complex, since 14 reciprocal skin grafts between unrelated cheetahs were accepted. The apparent consequences of such genetic uniformity to the species include (i) great difficulty in captive breeding, (ii) a high degree of juvenile mortality in captivity and in the wild, and (iii) a high frequency of spermatozoal abnormalities in ejaculates. The species vulnerability of the cheetah was demonstrated by an epizootic of coronavirus-associated feline infectious peritonitis in an Oregon breeding colony in 1983. Exposure and spread of the coronavirus, which has a very low morbidity in domestic cats (approximately 1 percent), has decimated a heretofore productive and healthy captive population. The extreme genetic monomorphism, especially at the major histocompatibility complex, and the apparent hypersensitivity of the cheetah to a viral pathogen may be related, and provide a biological basis for understanding the adaptive significance of abundant genetic variation in outbred mammalian species.
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              Cleavage of parallel-stranded DNA duplex by peplomycin metal complexes.

              Peplomycin-mediated degradation of parallel-stranded (ps) duplex was investigated. It was found that Co- and Fe-peplomycins degraded ps DNA duplex by 4'-hydrogen abstraction at 5'-GPy (pyrimidine) site in a similar manner to that of antiparallel B-DNA. While the orientation of two strands of ps and B-form DNA duplexes are reversed, peplomycin metal complex can bind to ps DNA duplex to cause oxidative DNA damage. These results indicate that peplomycin metal complex mainly interacts with one strand which is damaged.

                Author and article information

                Role: Editor
                PLoS One
                PLoS ONE
                Public Library of Science (San Francisco, USA )
                21 July 2011
                : 6
                : 7
                : e22402
                [1 ]Menzies Research Institute Tasmania, University of Tasmania, Tasmania, Australia
                [2 ]Faculty of Veterinary Science, University of Sydney, New South Wales, Australia
                [3 ]School of Medicine, University of Tasmania, Tasmania, Australia
                [4 ]Royal Hobart Hospital, Department of Pathology, Tasmania, Australia
                La Jolla Institute of Allergy and Immunology, United States of America
                Author notes

                Conceived and designed the experiments: AK KB GMW. Performed the experiments: AK YC FK BW. Analyzed the data: AK YC KB SD GMW. Wrote the paper: AK GMW. Read and commented on the manuscript: AK YC FK BW SD KB GMW.

                Kreiss et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
                : 27 May 2011
                : 21 June 2011
                Page count
                Pages: 8
                Research Article
                Major Histocompatibility Antigens
                Immunologic Subspecialties
                Tumor Immunology
                Major Histocompatibility Complex
                Clinical Immunology
                Immunologic Subspecialties
                Tumor Immunology
                Major Histocompatibility Complex
                Veterinary Science
                Veterinary Medicine
                Veterinary Immunology



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