{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nHLA‐G is a nonclassical major histocompatibility complex class I molecule characterized by restricted tissue distribution, low polymorphism, and the production of multiple isoforms through alternative splicing. Notably, the soluble HLA‐G5 isoform and disulfide‐linked dimer forms have been shown to play key roles in immune regulation. Its expression is tightly controlled at multiple levels—including genetic variants in the coding region and in regulatory sequences (promoter and 3′ untranslated region), epigenetic modifications, and microRNA‐mediated posttranscriptional regulation—which together influence mRNA stability and the balance between membrane‐bound and soluble forms. Interestingly, HLA‐G expression is even detected in early hematopoietic and endothelial precursors, suggesting additional roles in angiogenesis and primitive erythropoiesis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nFunctionally, HLA‐G engages several inhibitory receptors—including ILT2, ILT4, and KIR2DL4—on natural killer cells, T lymphocytes, B cells, and antigen‐presenting cells to attenuate immune responses. This receptor–ligand interaction mediates suppression of alloreactive T cell proliferation, inhibition of natural killer cell cytotoxicity, and even the up‐regulation of inhibitory receptors on immune cells, thereby raising activation thresholds. In addition to its tolerogenic role at the maternal–fetal interface (mediated by extravillous trophoblasts and associated exosomes), HLA‐G expression by mesenchymal stem cells and dendritic cell subsets has been demonstrated to induce regulatory T cells and type 1 T regulatory (Tr1) cells, further contributing to an immunosuppressive environment. Such multifaceted actions not only facilitate maternal–fetal tolerance but are also implicated in tumor immune evasion and in the control of autoimmune processes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "12", "end_ref": "27"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nClinically, the level and allelic variation of HLA‐G have important implications. Certain polymorphisms—such as the 14‐base pair insertion/deletion and other single‐nucleotide variants in the promoter and 3′UTR—are associated with differential expression of soluble HLA‐G and have been correlated with reproductive outcomes (including successful embryo implantation, recurrent miscarriage, and pre‐eclampsia) as well as with tumor progression (for example, in breast and renal cancers) and even asthma susceptibility. These findings underscore the dual role of HLA‐G as a tolerogenic molecule that facilitates fetal acceptance and transplant tolerance, while its aberrant expression may enable immune escape in pathological conditions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "28", "end_ref": "39"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jonathan E Boyson, Robert Erskine, Mary C Whitman, et al. 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