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Journal of Experimental Medicine, Vol 168, 1469-1474, Copyright © 1988 by Rockefeller University Press
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P Hoglund, HG Ljunggren, C Ohlen, L Ahrlund-Richter, G Scangos, C Bieberich, G Jay, G Klein and K Karre
Department of Tumor Biology, Karolinska Institute, Stockholm, Sweden.
The H-2Dd transgenic strain D8 on C57BL background was more resistant to subcutaneous challenge of RBL-5 lymphoma cells than B6 controls. The direct role of the H-2Dd antigen was investigated by the use of (D8 x B6)F1 crosses and (D8 B6) x B6 backcrosses. The latter showed cosegregation with regard to Dd antigen expression and lymphoma resistance, both of which were inherited in a pattern consistent with control by a single dominant gene. The rejection potential in (D8 x B6)F1 mice appeared as strong as that seen in crosses between B6 and MHC congenic mice (on B10 background) carrying H-2Dd. The lymphoma resistance could be abrogated by treatment with anti-asialo GM1 antiserum or anti-NK 1.1 mAb, indicating a role for NK cells.
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