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H-2 Antigens pp 659–670Cite as

Monoclonal H-2 Class I Specific Antibodies Isolated After Immunization of C57B1/6 Mice with Syngeneic Sendai Virus-Coated Cells

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Part of the book series: NATO ASI Series ((NSSA,volume 144))

Abstract

Two alloreactive H-2 (class I) specific cytotoxic IgM monoclonal antibodies (McAbs), B6-1 and B6-2, were isolated from C57B1/6 (B6) mice after injections of syngeneic Sendai virus-coated (SV+) spleen cells. McAb B6-I recognizes the public H-2 class I specificity H-2.25, shared by the H-2k(Kk) and H-2r haplotypes and cross-reacts with H-2z antigens on SV-infected (SVi) lymphoblasts. McAb B6-2 recognizes the private H-2Kf determinant H-2.26 on normal Sendai virus-negative (SV-) spleen cells but cross-reacts with H-2Kk and H-2Dd antigens on SVi blast cells. A polymorphic reaction pattern, that was dependent on the presence of Sendai virus, as tested on a panel of B10 target cells, was also observed with the cytotoxic immune sera from the mice whose cells were used in fusion experiments. Given the fact that each immune serum is an extensive mixture of anti-H-2 antibodies with different specificities, the isolated McAbs can be seen as illustrative examples which explain the reaction pattern of the immune sera. The recognition of polymorphic determinants on SV-infected, positive cells, is presumably due to a modified exposure of cross-reacting public H-2 class I determinants. Taken together, the lymphocytotoxic McAbs induced by injections of syngeneic SV+ cells recognize neither viral antigen nor self-MHC+X composite determinants, but allogeneic H-2 determinants as presented on normal, SV-coated or SV-infected cells.

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© 1987 Springer Science+Business Media New York

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Kievits, F., Opolski, A., Boerenkamp, W.J., Pla, M., Ivanyi, P. (1987). Monoclonal H-2 Class I Specific Antibodies Isolated After Immunization of C57B1/6 Mice with Syngeneic Sendai Virus-Coated Cells. In: David, C.S. (eds) H-2 Antigens. NATO ASI Series, vol 144. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-0764-9_63

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  • DOI: https://doi.org/10.1007/978-1-4757-0764-9_63

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4757-0766-3

  • Online ISBN: 978-1-4757-0764-9

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