By Ciba Foundation;
Chapter 1 creation (pages 1–2): R. R. A. Coombs
Chapter 2 The Immune reaction to Parasites (pages 4–19): Sydney Cohen
Chapter three Genetics of Antigenic version in Paramecium: A version method (pages 21–33): G. H. Beale
Chapter four Antigenic version and Immunity to Malaria (pages 35–51): ok. N. Brown
Chapter five Antigenic edition in African Trypanosomes (pages 53–80): Keith Vickerman
Chapter 6 Antigenic edition within the Nematode Nippostrongylus brasiliensis (pages 81–100): Bridget M. Ogilvie
Chapter 7 Immunological Spectra in Infectious illnesses (pages 101–122): J. L. Turk and A. Belehu
Chapter eight Immunodepression Produced by means of Malarial an infection in Mice (pages 123–135): Nina Wedderburn
Chapter nine Immunosuppression in Malaria and Trypanosomiasis (pages 137–159): B. M. Greenwood
Chapter 10 Host Antigens and the Immune reaction in Schistosomiasis (pages 161–183): J. A. Clegg
Chapter eleven Soluble Antigens as blocking off Antigens (pages 185–203): R. J. M. Wilson
Chapter 12 Interactions in vitro among Toxoplasma gondii and Mouse Cells (pages 205–223): James G. Hirsch, Thomas C. Jones and Lucille Len
Chapter thirteen Survival and loss of life of Leishmania in Macrophages (pages 225–241): J. Mauel, R. Behin, Biroum Noerjasin and J. J. Doyle
Chapter 14 Modulation of Immunopathology in Schistosomiasis (pages 243–261): Kenneth S. Warren
Chapter 15 Conclusions (pages 263–272):
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Extra info for Ciba Foundation Symposium 25 - Parasites in the Immunized Host: Mechanisms of Survival
For example, does actinomycin D prevent the antigenic change? Beale: The effects of actinomycin D (as well as of puromycin and chloramphenicol) on antigenic transformation have been studied by Austin et al. (1967) and by Sommerville (1970). The results were not very clear. Austin found that in some cases antigen transformation was stimulated, in others inhibited, by actinomycin D. Sommerville found that actinomycin D did not specifically affect antigen transformation, but had a general detrimental effect on the cells.
I 970a), K. N. Brown et al. (1970b) and Butcher & Cohen (1972) on P. knowlesi; Voller & Rossan (1969b) on P. cynomolgi; and Briggs & Wellde (1969) on P. berghei. Erythrocytic P. knowlesi infection has been studied in most detail using the schizont-infected cell agglutination (SICA), opsonization and multiplication inhibition tests. With these techniques it has been possible to learn much about antigenic variation in this host-parasite combination. Antigenic variation occurs with great frequency in chronic P.
It is highly specific in the sense that paramecia bearing a given surface antigen show very little cross-reaction with antisera against the other antigenic types which can be formed by paramecia belonging to the same stock or genotype. Thus if we may consider the rather fantastic possibility of Paramecium becoming a parasitic organism, variation in its immobilization antigens would be an effective means of evading the response of the host. ). Each gene has the potential ability to determine the formation of a particular antigen.