NK cell receptors involved in the response to human cytomegalovirus infection.
Human cytomegalovirus (HCMV) infection is a paradigm of the complexity reached by host-pathogen interactions. To avoid recognition by cytotoxic T lymphocytes (CTL) HCMV inhibits the expression of HLA class I molecules. As a consequence, engagement of inhibitory killer immunoglobulin-like receptors (KIR), CD94/NKG2A, and CD85j (ILT2 or LIR-1) natural killer cell receptors (NKR) specific for HLA class I molecules is impaired, and infected cells become vulnerable to an NK cell response driven by activating receptors. In addition to the well-defined role of the NKG2D lectin-like molecule, the involvement of other triggering receptors (i.e., activating KIR, CD94/NKG2C, NKp46, NKp44, and NKp30) in the response to HCMV is being explored. To escape from NK cell-mediated surveillance, HCMV interferes with the expression of NKG2D ligands in infected cells. In addition, the virus may keep NK inhibitory receptors engaged preserving HLA class I molecules with a limited role in antigen presentation (i.e., HLA-E) or, alternatively, displaying class I surrogates. Despite considerable progress in the field, a number of issues regarding the involvement of NKR in the innate immune response to HCMV remain uncertain.
Gumá
M
M
Molecular Immunopathology Unit, DCEXS, Universitat Pompeu Fabra, Dr. Aiguader 80, 08003 Barcelona, Spain.
Angulo
A
A
López-Botet
M
M
D003587:Cytomegalovirus / Q000276:immunology*; D003586:Cytomegalovirus Infections / Q000276:immunology; D006801:Humans; D007113:Immunity, Innate; D007694:Killer Cells, Natural / Q000276:immunology*; D008213:Lymphocyte Activation; D011971:Receptors, Immunologic / Q000378:metabolism*
D011971:Receptors, Immunologic