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α1 / α2 domains of H‐2Dd, but not H‐2Ld, induce “missing self” reactivity in vivo – No effect of H‐2Ld on protection against NK cells expressing the inhibitory receptor Ly49G2

Introduction of the MHC class I transgene H‐2Dd on C57BL / 6 (B6) background conveys NK cell‐mediated “missing self” reactivity against transgene‐negative cells, and down‐regulates expression of the inhibitory receptors Ly49A and Ly49G2 in NK cells. We here present an analysis of transgenic mice expressing chimeric H‐2Dd / Ld MHC class I transgenes, and show that the α1 / α2 domains of H‐2Dd were necessary and sufficient to induce “missing self” recognition and to down‐modulate Ly49A and Ly49G2 receptors. In contrast, transgenes containing the α1 / α2 domains of H‐2Ld induced none of these changes, suggesting that not all MHC class I alleles in a host necessarily take part in NK cell education. The lack of effect of the α1 / α2 domains of H‐2Ld on NK cell specificity was surprising, considering that both H‐2Ld and H‐2Dd have been reported to interact with Ly49G2. Therefore, the role of H‐2Ld for protection against NK cells expressing Ly49G2 was re‐investigated in a transfection system. In contradiction to earlier reports, we show that H‐2Dd, but not H‐2Ld, abolished killing by sorted Ly49G2+ NK cells, indicating that H‐2Ld does not inhibit NK cells via the Ly49G2 receptor.