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Immunodepression in Babesia microti infections

Published online by Cambridge University Press:  06 April 2009

Anne C. Purvis
Affiliation:
Department of Zoology, University of London, King's College, Strand, London WC2R 2LS

Extract

Infection with the avirulent piroplasm Babesia microti in mice is accompanied by a marked depression in the ability of the mice to mount an immune response to sheep red blood cells. The period of immunodepression begins 3 days after peak parasitaemia and is maximal 4 days later. There-after, there is a slow return to normal immune responsiveness, correlated with the gradual disappearance of the parasites from the blood. Both IgM and IgG responses are depressed. Cell-mediated responses as determined by contact sensitivity to oxazolone and allograft survival are apparently unaffected. Phagocytic activity as measured by carbon clearance tests is increased, and is correlated with the parasitaemia.

Type
Research Article
Copyright
Copyright © Cambridge University Press 1977

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References

Argyris, P. F. (1967). Role of macrophages in antibody production. Immune response to sheep red blood cells. Journal of Immunology 99, 744–50.CrossRefGoogle ScholarPubMed
Corsini, A. C., Clayton, C., Askonas, B. A. & Ogilvie, B. M. (1977). Loss of B cell potential in mice infected with Trypanosoma brucei. Clinical and Experimental Immunology, (in the Press).Google ScholarPubMed
Cox, F. E. G. (1976). Increased virulence of trypanosome infections in mice with malaria or piroplasmosis: immunological considerations. In Second International Symposium on the Biochemistry of Parasites and Host-Parasite Relationships (ed. van der Bossche, H.), pp. 421–6. Amsterdam: Elsevier.Google Scholar
Cox, F. E. G. (1977). Interactions between trypanosomes and piroplasms in mice. Protozoology 3, 129–34.Google Scholar
Cunningham, A. J. & Szenberg, A. (1968). Further improvements in the plaque technique for detecting single antibody-forming cells. Immunology 14, 599.Google ScholarPubMed
Dresser, D. W. & Wortis, H. H. (1965). A localized haemolysis in gel method for detection of cells producing 7S antibody. Use of an antiglobulin serum to detect cells producing antibody with low haemolytic efficiency. Nature, London 208, 859–61.CrossRefGoogle Scholar
Goodwin, L. G., Green, D. G., Guy, M. W. & Voller, A. (1972). Immunosuppression during trypanosomiasis. British Journal of Experimental Pathology 53, 40–3.Google ScholarPubMed
Greenwood, B. M. (1974). Possible role of a B cell mitogen in hypergammaglobulinaemia in malaria and trypanosomiasis. Lancet 1, 435–6.CrossRefGoogle Scholar
Greenwood, B. M., Playfair, J. H. L. & Torrigiani, G. (1971). Immunosuppression in murine malaria. 1. General characteristics. Clinical and Experimental Immunology 8, 467–78.Google Scholar
Holmes, P. H., Mammo, E., Thomson, A., Knight, P. A., Lucken, R., Murray, P. K., Murray, M., Jennings, F. W. & Urquhart, G. M. (1974). Immunosuppression in bovine trypanosomiasis. Veterinary Record, July 27, 86–7.CrossRefGoogle Scholar
Hudson, K. M., Byner, C., Freeman, J. & Terry, R. J. (1976). Immunodepression, high IgM levels and evasion of the immune response in murine trypanosomiasis. Nature, London 264, 256–8.CrossRefGoogle ScholarPubMed
Jayawardena, A. N. & Waksman, B. H. (1977). Suppressor cells in experimental trypanosomiasis. Nature, London 265, 539–41.CrossRefGoogle Scholar
Loose, L. D., Cook, J. A. & Di, Luzio N. R. (1972). Malarial immunosuppression. A macrophage mediated defect. Proceedings of the Helminthological Society of Washington 39 (special issue), 484–91.Google Scholar
Loose, L. D. & Di Luzio, N. R. (1976). A temporal relationship between reticulo-endothelial system phagocytic alterations and antibody responses in mice infected with Plasmodium berghei (NYU-strain). American Journal of Tropical Medicine and Hygiene 25, 221–8.CrossRefGoogle Scholar
Miller, J. F. A. p. & Mitchell, G. F. (1968). Cell to cell interaction in the immune response. 1. Haemolysin-forming cells in neonatally thymectomized mice reconstituted with thymus or thoracic duct lymphocytes. Journal of Experimental Medicine 128, 801–20.CrossRefGoogle ScholarPubMed
Moran, C. J., De Rivera, V. S. & Turk, J. L. (1973). The immunological significance of histological changes in the spleen and liver in mouse malaria. Clinical and Experimental Immunology 13, 467–78.Google ScholarPubMed
Murry, P. K., Jennings, F. W., Murray, M. & Urquhart, G. M. (1974). The nature of immunosuppression in Trypanosoma brucei infections in mice. 2. The role of the T and B lymphocytes. Immunology 27, 825–40.Google Scholar
Phillips, R. S. & Wakelin, D. (1976). Trichuris muris: effect of concurrent infections with rodent piroplasms on immune expulsion from mice. Experimental Parasitology 39, 95100.CrossRefGoogle ScholarPubMed
Salaman, M. H., Wedderburn, N. & Bruce-Chwatt, L. J. (1969). The immunodepressive effect of a murine plasmodium and its interaction with murine oncogenic viruses. Journal of General Microbiology 59, 383–91.CrossRefGoogle ScholarPubMed
Strickland, G. T., Voller, R. A., Pettit, L. E. & Fleck, D. G. (1972). Immunodepression associated with concomitant toxoplasma and malarial infections in mice. The Journal of Infectious Diseases 126, 5460.CrossRefGoogle ScholarPubMed
Stuart, A. E., Habeshaw, J. A. & Davidson, A. E. (1973). Phagocytes in vitro. In Handbook of Experimental Immunology, 2nd ed. (ed. Weir, D. M.), pp. 24.124.26. Oxford: Blackwell.Google Scholar
Voller, A. & O'Neill, P. (1971). Immunofluorescence method suitable for large scale application to malaria. Bulletin of the World Health Organization 45, 524–9.Google ScholarPubMed
Warren, H. S. & Weidanz, W. P. (1976). Malarial immunodepression in vitro: adherent spleen cells are functionally defective as accessory cells in the response to horse erythrocytes. European Journal of Immunology 6, 816–19.CrossRefGoogle ScholarPubMed