Human cytomegalovirus and natural killer‐mediated surveillance of HLA class I expression: a paradigm of host–pathogen adaptation

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Abstract
Summary: Among various strategies to evade the host immune response, some viruses like human cytomegalovirus (HCMV) interfere with surface MHC class I expression and antigen presentation to T lymphocytes. The ability of natural killer (NK) cells to detect MHC class I molecules through inhibitory receptors can be envisaged as an adaptation of the immune system for responding to such pathological alterations. To fulfil that role, rodents use members of the Ly49 C‐type lectin superfamily, whereas primates employ killer immunoglobulin‐like receptors and the immunoglobulin‐like transcript 2/leucocyte immunoglobulin‐like receptor‐1 receptor. CD94/NKG2 lectin‐like heterodimers represent the most conserved receptor system for MHC class I molecules; by interacting with human HLA‐E or murine Qa‐1b, CD94/NKG2A inhibitory receptors broadly probe the biosynthesis pathway of other class I molecules. Reciprocally, HCMV has developed mechanisms to evade the NK response while modulating HLA class Ia expression. The ability of HCMV to maintain surface levels of HLA‐E and to express an HLA class I surrogate (UL18) are herein discussed in the context of the interplay with human NKR systems.This work was supported by grants FIS 00/0181 and SAF98‐0006. We thank Dr A. Angulo for helpful discussion.

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