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   <subfield code="a">(NATIONALLICENCE)springer-10.1007/BF01789328</subfield>
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   <subfield code="a">Detection of allogeneic Qa/TL and Ly specificities on murine tumor cells with IgD in tumor-regressor serum</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Takae Tanino, Naohiro Seo, Takahiro Okazaki, Chiemi Nakanishi-Ito, Masayuki Sekimata, Kohji Egawa]</subfield>
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   <subfield code="a">Summary: Serum from C3H/He mice, which show regression of MM2 tumor cells after transplantation and removal (regressor serum, RS) contains non-gammaglobulin components that cross-react with various tumor cells of mice [22, 23]. In addition to tumor cells, various allogeneic lymphocytes are also susceptible to an RS-dependent lymphocyte-mediated cytotoxic reaction. To identify tumor cell surface antigens that cause the cross-reactive host response, the serum components were analyzed by absorption of RS with allogeneic lymphocytes. RS components were found to recognize allogeneic lymphocyte antigens including Qa-2 and Ly6.2. Specificity for the Qa-2 antigen was further tested using Qa-2-congenic mice. The expression of Qa-2 antigen was detected on the surfaces of MM2 and other tumor cells derived from H-2k mice (seven among nine cell lines tested) by a membrane immunofluorescence method using a Qa-2-specific mAb. Physical characteristics of the Qa-2-specific component in RS were determined and found to differ from those of regular IgGs but to be similar to those of IgDs. Using an enzyme-linked immunosorbent assay with an IgD-specific mAb and Qa-2-lacZ fusion protein, the existence of IgD in RS with specificity for Qa-2 was confirmed. These results suggest that the RS component with Qa-2 specificity is an IgD, the specificity and physiological role of which are unknown.</subfield>
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   <subfield code="a">Springer-Verlag, 1992</subfield>
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   <subfield code="a">Tumor antigen</subfield>
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   <subfield code="a">Tanino</subfield>
   <subfield code="D">Takae</subfield>
   <subfield code="u">Department of Tumor Biology, Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, 108, Minatoku, Tokyo, Japan</subfield>
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   <subfield code="u">Department of Tumor Biology, Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, 108, Minatoku, Tokyo, Japan</subfield>
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   <subfield code="a">Okazaki</subfield>
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   <subfield code="u">Department of Tumor Biology, Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, 108, Minatoku, Tokyo, Japan</subfield>
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   <subfield code="a">Nakanishi-Ito</subfield>
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   <subfield code="u">Department of Tumor Biology, Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, 108, Minatoku, Tokyo, Japan</subfield>
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   <subfield code="a">Sekimata</subfield>
   <subfield code="D">Masayuki</subfield>
   <subfield code="u">Department of Tumor Biology, Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, 108, Minatoku, Tokyo, Japan</subfield>
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   <subfield code="u">Department of Tumor Biology, Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, 108, Minatoku, Tokyo, Japan</subfield>
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   <subfield code="t">Cancer Immunology, Immunotherapy</subfield>
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   <subfield code="g">35/4(1992-07-01), 230-236</subfield>
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   <subfield code="a">Metadata rights reserved</subfield>
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