title: Soluble HLA-G molecules increase during acute leukemia, especially in subtypes affecting monocytic and lymphoid lineages.
abstract: Human leukocyte antigen G (HLA-G) molecules exhibit immunomodulatory properties corresponding to nonclassic class I genes of the major histocompatibility complex. They are either membrane-bound or solubly expressed during certain tumoral malignancies. Soluble human leukocyte antigen G (sHLA-G) molecules seem more frequently expressed than membrane-bound isoforms during hematologic malignancies, such as lymphoproliferative disorders. Assay of these molecules by enzyme-linked immunosorbent assay in patients suffering from another hematologic disorder (acute leukemia) highlights increased sHLA-G secretion. This increased secretion seems more marked in acute leukemia subtypes affecting monocytic and lymphoid lineages such as FABM4 and FABM5, as well as both B and T acute lymphoblastic leukemia (ALL). Moreover, this study uses in vitro cytokine stimulations and reveals the respective potential roles of granulocyte-macrophage colony-stimulating factor and interferon-gamma in increasing this secretion in FABM4 and ALL. Correlations between sHLA-G plasma level and clinical biologic features suggest a link between elevated sHLA-G level and 1) the absence of anterior myelodysplasia and 2) high-level leukocytosis. All these findings suggest that sHLA-G molecules could be a factor in tumoral escape from immune survey during acute leukemia.
authors.affiliation: UPRES EA 3889, Immunologie/Hématologie, Université de Rennes 1, Rennes Cedex, France.
authors.forename: Frédéric
authors.initials: F
authors.lastname: Gros
authors.forename: Yasmine
authors.initials: Y
authors.lastname: Sebti
authors.forename: Sophie
authors.initials: S
authors.lastname: de Guibert
authors.forename: Bernard
authors.initials: B
authors.lastname: Branger
authors.forename: Marc
authors.initials: M
authors.lastname: Bernard
authors.forename: Renée
authors.initials: R
authors.lastname: Fauchet
authors.forename: Laurence
authors.initials: L
authors.lastname: Amiot
mesh_terms: D000208:Acute Disease; D000951:Antigens, Neoplasm / Q000096:biosynthesis / Q000097:blood* / Q000235:genetics; D014408:Biomarkers, Tumor / Q000097:blood; D002051:Burkitt Lymphoma / Q000097:blood / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D045744:Cell Line, Tumor / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism; D016207:Cytokines / Q000097:blood / Q000494:pharmacology; D004797:Enzyme-Linked Immunosorbent Assay; D015973:Gene Expression Regulation, Leukemic / Q000187:drug effects; D006680:HLA Antigens / Q000096:biosynthesis / Q000097:blood* / Q000235:genetics; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I / Q000096:biosynthesis / Q000097:blood* / Q000235:genetics; D006801:Humans; D007938:Leukemia / Q000097:blood* / Q000145:classification / Q000235:genetics / Q000378:metabolism; D007951:Leukemia, Myeloid / Q000097:blood / Q000145:classification / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D015459:Leukemia-Lymphoma, Adult T-Cell / Q000097:blood / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma / Q000097:blood / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D012189:Retrospective Studies; D012995:Solubility; D019139:Tumor Escape
chemical_list: D000951:Antigens, Neoplasm; D014408:Biomarkers, Tumor; D016207:Cytokines; D006680:HLA Antigens; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I