Abnormal anti‐viral immune response in mice is corrected in HLA‐B27.2‐transgenic mice

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Abstract
In contrast to the strong Sendai virus‐specific cytotoxic T‐lymphocyte (CTL) responses in C57BL/6 mice, H‐2Kb mutant bm1 mice are nonresponders to Sendai virus. By appropriate crossings between HLA‐B27 double‐transgenic mice and Kb mutant bm1 mice, and after subsequent selection, H2bm1 homozygous mice were produced expressing the human HLA‐B27.2 and β2−microglobulin genes. Here we show that the introduction of a human HLA classI gene into the genome of the H2bm1 Sendai virus‐nonresponder mutant mice resulted in good responsiveness to Sendai virus, and in normal levels of Sendai virus‐specific CTL precursors. The CTL response in the HLA‐B27.2 double‐transgenic H2bm1 mice against Sendai virus was restricted by the HLA‐B27.2 molecule. These results show the direct involvement of HLA class I molecules inregulation of the anti‐viral CTL repertoire and represent for the first time a correction of abnormal anti‐viral immunity in mice by incorporation of a human MHC class I (HLA‐B27.2) gene.

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