Emergency immune suppression: a possible impact of HLA-G trogocytosis on immune responses. Within the microenvironment of a tumor, for example, in which some cells express HLA-G and some do not (A), the function of activated natural killer (NK) cells is directly blocked by the interaction of tumor cell HLA-G and NK-cell immunoglobulin-like transcript 2 (ILT2). This results in the immune escape of the HLA-G–positive tumor cell. (B) During this cell-to-cell contact, tumor cell-membrane patches containing HLA-G are acquired by activated NK cells within minutes (through a process known as trogocytosis). (C) This results in the generation of HLA-G–positive activated NK cells, which can inhibit other HLA-G–positive (cross-inhibition) or HLA-G–negative NK cells through HLA-G and ILT2 cross-linking (D). This suppressive function of HLA-G–positive NK cells results in the immune escape of HLA-G–negative tumor cells. (E) Immune suppression does not spread as NK cells do not translate HLA-G de novo and lose its surface expression quickly if not in the vicinity of HLA-G–positive tumor cells. Emergency immune suppression and in situ generation of regulatory cells, which is fast, local and temporary, might constitute an efficient mechanism of immune escape.