Analysis of HLA-G expression in malignant hematopoetic cells from leukemia patients

Poláková, K; Krcova, Martina; Kuba, Daniel; Russ, G

doi:10.1016/s0145-2126(02)00228-x

Cited by 37 publications

(29 citation statements)

References 23 publications

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“…In addition to its inhibitory function, KIR2DL4 can also have an activating function that may depend on the type of cell. 22 Despite the presence of HLA-G transcription in mature lymphoid cells, HLA-G antigens are not expressed at the cell surface of normal lymphocytes or leukemic cells in the absence of IFN-g. [23][24][25] This finding is at variance with a study published by Nuckel et al 26 showing that a variable percentage of CLL-B cells aberrantly expressed the nonclassical HLA-G molecule. The surface expression of HLA-E depends on the binding of peptides derived from HLA class I molecules.…”

Section: Cell Surface Expression Of Hla Class I Moleculesmentioning

confidence: 68%

NK cell receptors and their ligands in leukemia

Verheyden

Demanet

2007

Leukemia

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Human natural killer (NK) cells are built to kill abnormal cells but to preserve autologous normal cells. To accomplish this task, they are equipped with a large number of inhibiting and activating receptors. Ligation with corresponding ligands will determine whether the NK cell becomes activated to destroy the abnormal cell. This review will focus on the abnormalities of NK cell receptors and their putative ligands found in patients with leukemia, which can lead to an inadequate function of NK cells allowing these malignant cells to escape from NK cell destruction. In recent years it has become clear that NK cells in the haploidentical hematopoietic stem cell transplantation (HSCT) setting are very effective in eliminating residual acute myeloid, but not acute lymphoid, leukemic cells. In this regard, we also reviewed published studies of retrospective cohorts of HSCT investigating the potential beneficial effect of killer-cell immunoglobulin-like receptors (KIRs) and human leukocyte antigen (HLA) ligands on NK alloreactivity. Manipulating NK cell inhibition or activation could lead to new forms of immunotherapy, ultimately leading to the elimination of resistant leukemic cells.

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Section: Cell Surface Expression Of Hla Class I Moleculesmentioning

confidence: 68%

NK cell receptors and their ligands in leukemia

Verheyden

Demanet

2007

Leukemia

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“…26,27 HLA-G expression has also been studied in patients with non-Hodgkin lymphoma (NHL). Although one study showed no expression, 28 other studies reported 65%-100% HLA-G expression in B-NHL, 29 and 58% expression in T-NHL. 30 Similar results for MM are now reported in this study.…”

Section: Discussionmentioning

confidence: 88%

CD86+ or HLA-G+ can be transferred via trogocytosis from myeloma cells to T cells and are associated with poor prognosis

Brown

Kabani

Favaloro

et al. 2012

Blood

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The transfer of membrane proteins between cells during contact, known as trogocytosis, can create novel cells with a unique phenotype and altered function. We demonstrate that trogocytosis is more common in multiple myeloma (MM) than chronic lymphocytic leukemia and Waldenstrom macroglobulinaemia; that T cells are more probable to be recipients than B or natural killer cells; that trogocytosis occurs independently of either the T-cell receptor or HLA compatibility; and that after trogocytosis, T cells with acquired antigens can become novel regulators of T-cell proliferation. We screened 168 patients with MM and found that CD86 and human leukocyte antigen G (HLA-G) were antigens commonly acquired by T cells from malignant plasma cells. CD3+CD86acq+ and CD3+ HLA-Gacq+ cells were more prevalent in bone marrow than peripheral blood samples. The presence of either CD86 or HLA-G on malignant plasma cells was associated with a poor prognosis. CD38++ side population cells expressed HLA-G, suggesting that these putative myeloma stem cells could generate immune tolerance. HLA-G+ T cells had a regulatory potency similar to natural Tregs, thus providing another novel mechanism for MM to avoid effective immune surveillance.

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“…To date, the expression of HLA-G in hematological malignancies has been investigated in a number of studies [39][40][41][42][43] with conflicting findings, presumably due to the heterogeneity of the studied population or technical factors. Amiot et al 39 investigating HLA-G expression in normal and malignant hematopoiesis found HLA-G transcripts only in T and B lymphocytes and a variable proportion of their malignant counterparts (6/15 ALL, 100% of B-NHLs, 20/30 CLL), no protein antigens were detected at the cell surface or in the cytosol of any of these cells.…”

Section: Discussionmentioning

confidence: 99%

“…40 A retrospective study investigating 51 leukemia samples, including 8 CLL did not detect HLA-G surface expression nor transcripts in CLL. 41 Notably, HLA-G expression has recently been reported in B-CLL and associated with an unfavorable outcome. 42 Flow cytometry analysis of CLL samples (n ¼ 47) showed surface expression of HLA-G in a variable proportion of tumor cells in all CLL samples examined that correlated with survival.…”

Section: Discussionmentioning

confidence: 99%

NK resistance of tumor cells from multiple myeloma and chronic lymphocytic leukemia patients: implication of HLA-G

et al. 2008

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Exploiting the antitumor effect of natural killer (NK) cells has regained interest in light of data from preclinical and clinical work on the potential of alloreactive NK cells. Multiple myeloma (MM) and chronic lymphocytic leukemia (CLL) represent the two most prevalent adult hematological malignancies in the western hemisphere. To evaluate the role of NK cells in the immune surveillance and their therapeutic potential for CLL and MM, tumor cell susceptibility to NK-mediated killing was investigated. Results show relative resistance of tumor cells from CLL as well as MM (73 and 70% of the patients, respectively) to NK-mediated killing. To gain insight into molecular mechanisms of this resistance, the expression of the tolerogenic HLA-G molecule in CLL and MM and its relevance to susceptibility to NK-mediated killing were investigated. HLA-G transcript was found in tumor cells from 89% (n ¼ 19) of CLL and 100% (n ¼ 9) of MM patients examined. HLA-G1 surface expression was observed in CLL and was very low or undetectable in MM. Notably, blocking of HLA-G1 with specific antibody on CLL samples increased their susceptibility to NK-mediated killing, demonstrating that HLA-G participates in protecting CLL cells from NK-mediated killing and may thus contribute to their immune escape in vivo.

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Analysis of HLA-G expression in malignant hematopoetic cells from leukemia patients

Cited by 37 publications

References 23 publications

NK cell receptors and their ligands in leukemia

NK cell receptors and their ligands in leukemia

CD86+ or HLA-G+ can be transferred via trogocytosis from myeloma cells to T cells and are associated with poor prognosis

NK resistance of tumor cells from multiple myeloma and chronic lymphocytic leukemia patients: implication of HLA-G

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