scholarly journals HDAC Inhibition Increases HLA Class I Expression in Uveal Melanoma

Cancers ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3690
Author(s):  
Zahra Souri ◽  
Aart G. Jochemsen ◽  
Mieke Versluis ◽  
Annemijn P.A. Wierenga ◽  
Fariba Nemati ◽  
...  
Keyword(s):  
Cell Surface ◽  
Cell Lines ◽  
Uveal Melanoma ◽  
Hdac Inhibitor ◽  
Mrna Level ◽  
Hla Class I ◽  
Class I ◽  
In Vitro Tests ◽  
Hla Class I Antigens

The treatment of uveal melanoma (UM) metastases or adjuvant treatment may imply immunological approaches or chemotherapy. It is to date unknown how epigenetic modifiers affect the expression of immunologically relevant targets, such as the HLA Class I antigens, in UM. We investigated the expression of HDACs and the histone methyl transferase EZH2 in a set of 64 UMs, using an Illumina HT12V4 array, and determined whether a histone deacetylase (HDAC) inhibitor and EZH2 inhibitor modified the expression of HLA Class I on three UM cell lines. Several HDACs (HDAC1, HDAC3, HDAC4, and HDAC8) showed an increased expression in high-risk UM, and were correlated with an increased HLA expression. HDAC11 had the opposite expression pattern. While in vitro tests showed that Tazemetostat did not influence cell growth, Quisinostat decreased cell survival. In the three tested cell lines, Quisinostat increased HLA Class I expression at the protein and mRNA level, while Tazemetostat did not have an effect on the cell surface HLA Class I levels. Combination therapy mostly followed the Quisinostat results. Our findings indicate that epigenetic drugs (in this case an HDAC inhibitor) may influence the expression of immunologically relevant cell surface molecules in UM, demonstrating that these drugs potentially influence immunotherapy.

HLA Influence on NK Cell Expansion

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 4924-4924
Author(s):  
Jennifer Schellekens ◽  
Anna Stserbakova ◽  
Madis Tõns ◽  
Hele Everaus ◽  
Marcel GJ Tilanus ◽  
...  
Keyword(s):  
Nk Cells ◽  
Cell Lines ◽  
Cell Expansion ◽  
Nk Cell ◽  
Killer Cell ◽  
Hla Class I ◽  
Class I ◽  
Haematopoietic Stem Cell ◽  
Specific Priming

Abstract Natural Killer (NK) cells are effector cells in the innate immune system. The anti-leukaemic capacities of NK cells in haematopoietic stem cell transplantation make these cells a potential treatment modality to improve clinical outcome. Immunotherapy with NK cells requires transfusion of large quantities, which obviates the need for an in vitro culture system for NK cells. The killer cell immunoglobulin-like receptors (KIR) on NK cells recognise defined groups of HLA class I alleles. To elucidate the influence of these interactions on proliferation, the peripheral blood mononuclear cells (PBMCs) of 29 patients and donors were cultured in CellGro SCGM with IL-2 and OKT3 antibody to expand the NK cell fraction. The killer cell immunoglobulin-like receptor (KIR) and HLA repertoire were determined by sequence specific priming and sequence based typing respectively. The percentage of NK cell expansion from the total PBMC fraction varied between 5.4% and 71.6%. A significantly better NK cell expansion was observed for individuals homozygous for HLA-C epitope group 2 (p<0.05). For evaluation of cytolytic competence of the cultured NK cells, specific killing of an HLA class I expression deficient LCL 721.221 cell line and three 721.221 cell lines transfected with different HLA-C alleles was determined. A significantly better NK cell-induced specific cytotoxicity was observed towards the untransfected 721.221 cells compared to the HLA-C transfected 721.221 cells. No significant differences were observed between killing of the three HLA-C transfected 721.221 cell lines. We have shown that cytolytic capacities of the cultured NK cells are maintained and in vitro expansion of NK cells is dependant on the presence of HLA-C alleles.

NKG2D ligand expression in AML increases in response to HDAC inhibitor valproic acid and contributes to allorecognition by NK-cell lines with single KIR-HLA class I specificities

Blood ◽  
2008 ◽  
Vol 111 (3) ◽  
pp. 1428-1436 ◽  
Author(s):  
Stefan Diermayr ◽  
Heike Himmelreich ◽  
Bojana Durovic ◽  
Arina Mathys-Schneeberger ◽  
Uwe Siegler ◽  
...  
Keyword(s):  
Valproic Acid ◽  
Cell Surface ◽  
Nk Cells ◽  
Cell Lines ◽  
Nk Cell ◽  
Human Leukocyte ◽  
Hla Class I ◽  
Inhibitory Effect ◽  
Class I ◽  
The Impact

Abstract This study exploited alloreactivity of natural killer (NK) cells for augmenting the recognition of human acute myeloid leukemia (AML). To circumvent the inhibitory effect of killer immunoglobulin receptor (KIR) signaling, we generated NK-cell lines with single KIR specificities for major human leukocyte antigen (HLA) class I allotypes. We demonstrated efficient cytolysis of KIR-HLA class I–mismatched primary AML blasts even at low effector-to-target ratios. To define the impact of tumor-associated activating NKG2D-ligands (NKG2D-L), 66 AML patients at diagnosis were analyzed. NKG2D-L were selectively expressed on monoblastic cells in AML M4 and M5 yet absent or weakly expressed on myeloblastic cells in all AML subtypes. Paucity of cell-surface NKG2D-L was not the result of shedding because levels of soluble ULBP1 ligand measured in AML plasma were in the normal range. Notably, purified NKG2D-L+ monoblastic cells were more susceptible to NK-mediated killing than NKG2D-L− myeloblastic cells. Accordingly, induction of cell-surface NKG2D-L by treatment with the histone deacetylase inhibitor, valproic acid, rendered cells more sensitive to NK cytolysis. These data suggest that adoptive transfer of selected populations of alloreactive HLA class I–mismatched NK cells in combination with pharmacologic induction of NKG2D-L merits clinical evaluation as novel approaches to immunotherapy of human AML.

844 Immunomodulatory activity of epigenetic drugs combinations in mesothelioma: laying the ground for new immunotherapeutic strategies

2020 ◽  
Vol 8 (Suppl 3) ◽  
pp. A896-A896
Author(s):  
Sara Cannito ◽  
Health Biology ◽  
Ornella Cutaia ◽  
Carolina Fazio ◽  
Maria Fortunata Lofiego ◽  
...  
Keyword(s):  
Cell Line ◽  
Cell Lines ◽  
Hla Class I ◽  
Class I ◽  
Immunomodulatory Activity ◽  
Epigenetic Drugs ◽  
Hla Class I Antigens ◽  
Hla Class I Molecules ◽  
Mesothelioma Cell Line ◽  
Mesothelioma Cell

BackgroundGrowing evidence are demonstrating the therapeutic efficacy of immune checkpoint inhibitors (ICI) in mesothelioma; however, a limited percentage of patients benefits from this therapeutic approach. Epigenetic modifications play a relevant role in negatively regulating the cross-talk between neoplastic and immune cells, and in contributing to the highly immunosuppressive mesothelioma microenvironment. A better understanding of mesothelioma epigenetic landscape could open the path to novel and potentially more effective approaches combining ICI and epigenetic drugs. We investigated the immunomodulatory potential of epigenetic agents by comparing the activity of DNA hypomethylating agents (DHA) with histone deacetylases inhibitors (HDACi) and EZH2 inhibitors (EZH2i), alone or combined with DHA, in mesothelioma cells.MethodsFour mesothelioma cell lines were treated with the DHA guadecitabine 1μM, or with the HDACi, Valproic Acid (VPA) 1mM, or the EZH2i, EPZ-6438 1μM, alone or combined with guadecitabine. We investigated the expression of HLA class I molecules by flow-cytometry and of PD-L1, cancer testis antigens (CTA: NY-ESO, MAGE-A1), Natural Killer Group 2 member D Ligands (NKG2DLs: MIC-A, MIC-B, ULBP2) and EMT-regulating cadherins (CDH1, CDH2) by quantitative Real-Time PCR. Fold change (FC) expression for each treatment vs untreated cells was reported as mean values (FCm) among investigated cell lines. A positive modulation of the expression was considered if FCm>1.5.ResultsGuadecitabine upregulated the expression of HLA class I antigens (FCm=1.75), PD-L1 (FCm=2.38), NKG2DLs (MIC-A FCm=1.96, MIC-B FCm=2.57, and ULBP2 FCm=3.56), and upregulated/induced CTA expression. Similarly, VPA upregulated HLA class I antigens (FCm=1.67), PD-L1 (FCm=3.17), NKG2DLs (MIC-A FCm=1.78, MIC-B FCm=3.04, and ULBP2 FCm=3.75) expression; however, CTA expression was modulated only in 1 mesothelioma cell line. Conversely, EPZ-6438 up-regulated only NY-ESO-1 and MIC-B expression in 1 mesothelioma cell line.The addition of both VPA and EPZ-6483 to guadecitabine strengthened its immunomodulatory activity. Specifically, guadecitabine plus VPA or EPZ-6438 upregulated the expression of HLA class I antigens FCm=2.55 or 2.69, PD-L1 FCm=8.04 or 2.65, MIC-A FCm=3.81 or 2.26, MIC-B FCm=8.00 or 3.03, ULBP2 FCm=6.24 or 4.53, respectively. Higher levels of CTA upregulation/induction were observed with combination treatments vs guadecitabine alone.Cadherins modulation was mesothelioma histotype-related: CDH1 expression was induced in the 2 constitutively-negative sarcomatoid mesothelioma cells by guadecitabine alone or combined with VPA or EPZ-6438; CDH2 expression was upregulated by VPA alone (FCm=1.53) or plus guadecitabine (FCm=2.54).ConclusionsCombination of DHA-based immunotherapies with other classes of epigenetic drugs could be an effective strategy to be pursued in the mesothelioma clinic.

Expression of Classic and Nonclassic HLA Class I Antigens in Uveal Melanoma

2003 ◽  
Vol 44 (5) ◽  
pp. 2016 ◽  
Author(s):  
Gerasimos Anastassiou ◽  
Vera Rebmann ◽  
Stephan Wagner ◽  
Norbert Bornfeld ◽  
Hans Grosse-Wilde
Keyword(s):  
Uveal Melanoma ◽  
Hla Class I ◽  
Class I ◽  
Hla Class I Antigens

A Novel Mechanism of Action of Bortezomib: Proteasome Inhibition Down-Regulates HLA-Class I on Myeloma and Enhances NK Cell-Mediated Lysis.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 1525-1525
Author(s):  
Jumei Shi ◽  
Guido J. Tricot ◽  
Priyangi A. Malaviarachchi ◽  
Tarun K. Garg ◽  
Susann M. Szmania ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Cell Surface ◽  
Nk Cells ◽  
Cell Lines ◽  
Nk Cell ◽  
Cell Activity ◽  
Hla Class I ◽  
Class I ◽  
Target Cells ◽  
Down Regulation

Abstract Introduction: Natural killer (NK) cell activity is regulated by a dynamic balance between inhibitory and activating receptors that recognize ligands on target cells. Human leukocyte antigen (HLA)-class I, particularly HLA-C and -Bw4 molecules, are key ligands transmitting inhibitory signals to NK cells. NK cells avidly lyse tumor cells that do not display such inhibitory KIR-ligands. The proteasome is responsible for the generation of peptides that bind to and stabilize class I molecules at the cell surface. We hypothesized that bortezomib, a partial proteasome inhibitor that is clinically approved for the treatment of refractory/relapsed myeloma (MM), could reduce HLA expression on MM cells and thus enhance NK cell-mediated cytotoxicity. Methods: HLA-class I or HLA-C expression was assessed using flow cytometry, after gating on AnnexinV/PI double negative cells, and/or confocal microscopy. Expression of other proteins was measured by flow cytometry using specific mAb. NK cell-mediated lysis of myeloma cells was measured by 51Cr-release. Results: Bortezomib at clinically attainable concentrations down-regulated HLA-class I expression on MM cells in a time- and dose-dependent fashion. Reduction of class I post-10 nM bortezomib treatment was observed in all myeloma cell lines tested (n=10), by a median of 49% (range: 19–66%). A similar decrease of HLA-class I was obtained in 10–50 nM bortezomib treated primary MM cells (n=6). Bortezomib significantly enhanced the sensitivity of MM cells to allogeneic and autologous NK cell-mediated lysis. Further, the level of reduction in HLA-class I expression correlated well with increased susceptibility to lysis by NK cells. The level of down-regulation of HLA-class I induced by bortezomib was reproduced by incubating MM cells with HLA-blocking antibody and resulted in equipotent enhancement of NK cell-mediated lysis (Figure 1). The extent of HLA-class I down-regulation by bortezomib was therefore biologically relevant. Down-regulation of HLA-class I was also observed in vivo on purified MM cells 48 hours after a single dose of bortezomib, by a median of 47% (range: 16–63%, n=6, P= .002). HLA-C expression (the principal NK cell inhibitory ligand) was rescued by exogenous provision of HLA-C binding peptides providing a mechanistic explanation for the effect of bortezomib on HLA-class I expression. Finally, we did not observe bortezomib-mediated enhancement of NK cell-mediated lysis of myeloma through receptors other than the KIR receptor family, including tumor necrosis factor related apoptosis-inducing ligand, NKG2D and natural cytotoxicity receptors. HLA-class I down-regulation was not observed in renal cell and breast carcinoma cell lines, which is in keeping with the remarkable activity of bortezomib in myeloma. Our findings have clear therapeutic implications for MM and other NK cell-sensitive malignancies in the context of both allogeneic and autologous adoptively transferred NK cells. Figure 1. Reduced class I on MM cell surface results in NK cell-mediated recognition and lysis Figure 1. Reduced class I on MM cell surface results in NK cell-mediated recognition and lysis

Specific PML Isoforms and SATB1 Affect HLA Expression In Classical Hodgkin Lymphoma

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 4234-4234
Author(s):  
Yuxuan Liu ◽  
Anke Van Den Berg ◽  
Bea Rutgers ◽  
Rianne Veenstra ◽  
Debora de Jong ◽  
...  
Keyword(s):  
Cell Lines ◽  
Mrna Level ◽  
Hla Class I ◽  
Class Ii ◽  
Hla Class Ii ◽  
Class I ◽  
Expression Levels ◽  
Hla Genes ◽  
Enhanced Expression ◽  
Positive Correlations

Abstract Introduction Hodgkin Reed-Sternberg (HRS) cells are characterized by a general loss of B cell phenotype, whereas antigen presenting properties are commonly retained. HLA class I and class II are expressed in most EBV+ cHL cases, with an even enhanced expression in some cases. The mechanisms underlying enhanced or lost HLA expression are unknown. Promyelocytic leukemia protein (PML) is the main component of nuclear bodies (NBs) and it organizes the chromatin structure into loops by anchoring matrix attachment regions to the nuclear matrix. The PML transcript can be processed into seven different isoforms. Downregulation of PML isoform III or V results in a reduced HLA-A and HLA-G expression in Jurkat T cells, whereas PML enhances HLA class II expression by upregulating the class II transactivator (CIITA). Special AT-rich region binding protein 1 (SATB1) has been shown to be associated with PML-NBs in the HLA region. Downregulation of SATB1 in Jurkat cells results in an enhanced expression of HLA-A, HLA-G and HLA-H. Aim To determine if specific PML isoforms and SATB1 regulate HLA expression in cHL cell lines. Methods We stained HLA class I, HLA class II, PML-NBs and SATB1 in 54 EBV+ cHL cases and in 27 EBV- cHL cases. We analyzed HLA class I, HLA class II, PML isoforms I to V and SATB1 mRNA expression levels by qRT-PCR in cHL cell lines (n=6). Next, we inhibited SATB1 and PML expression in the cHL cell line L1236 using shRNA constructs. The effects of the shRNA constructs on HLA protein expression levels were assessed by Western blot and flow cytometry. Results We observed a normal HLA class I membrane expression in 40% of EBV+ and 20% of EBV- cases. There was a stronger than normal HLA class I protein expression in approximately 40% of EBV+ cHL and not in EBV- cHL patients. The number of PML-NBs was positively correlated to the level of HLA class I expression (p<0.01), whereas the percentage of SATB1 positive cells was inversely correlated with the level of HLA class I expression in EBV+ cHL cases (p<0.05). We observed normal HLA class II expression in 50% of EBV+ and 50% of EBV- cases. A stronger than normal HLA class II expression was observed in 4 EBV+ and 1 EBV- cHL patients. The number of PML-NBs and the percentage of SATB1 positive cells were not correlated with classical HLA class II expression in EBV+, EBV- or the total cHL patient group. We further investigate the association of PML, SATB1 and HLA class I and II in six cell lines. At the mRNA level, significant positive correlations were found between PML-III and HLA-C and between PML-III and β2M. Borderline significant positive correlations were found between PML-V and CIITA and between PML-V and HLA-DPB1. Suggestive, though not significant, correlations were observed of various PML isoforms and SATB1 for several HLA genes. The limited number of cell lines, precluded more definitive conclusions for the other comparisons. To further study the role of specific PML isoforms and SATB1 in regulation of HLA gene expression, we inhibited PML-III, PML-V or SATB1 in L1236 by shRNA-based knockdown. The PML-III shRNA induced a ∼80% reduction at the PML-III mRNA level, but did not affect membranous HLA class I expression and possibly affected HLA class II expression levels in L1236. The shRNA for PML-V was not effective and needs to be optimized and experiments with a pan-PML shRNA are ongoing. The SATB1 shRNA1 induced a ∼75% at the SATB1 mRNA level and a ∼80% reduction at the protein level, while SATB1 shRNA2 showed a ∼75% reduction and a ∼25% reduction, respectively. Inhibition of SATB1 by shRNA1 significantly upregulated HLA class II expression (P=0.02) and no significant effect on HLA class I expression. Inhibition of SATB1 by shRNA2 showed no significant effect on HLA class I and II expression. Conclusion PML and SATB1 protein levels are associated with HLA class I in HRS cells. Various negative associations of SATB1 with HLA genes at the mRNA level support a possible regulatory effect. This was indeed observed upon inhibition of SATB1 in L1236 that induced enhanced HLA-DR/DP/DQ expression. The PML regulation appears to be complex with different PML isoforms showing different associations with specific HLA genes. Disclosures: No relevant conflicts of interest to declare.

Expression of HLA class I antigens in transporter associated with antigen processing (TAP)-deficient mutant cell lines

1998 ◽  
Vol 52 (4) ◽  
pp. 368-373 ◽  
Author(s):  
N.T. Young ◽  
A. Mulder ◽  
V. Cerundolo ◽  
F.H.J. Claas ◽  
K.I. Welsh
Keyword(s):  
Cell Lines ◽  
Antigen Processing ◽  
Mutant Cell ◽  
Hla Class I ◽  
Class I ◽  
Deficient Mutant ◽  
Hla Class I Antigens

Loss of HLA Class-I Expression In Leukemic Cells That Relapsed After HLA-Matched and -Mismatched SCT

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 2541-2541
Author(s):  
Yukio Kondo ◽  
Takamasa Katagiri ◽  
Kohei Hosokawa ◽  
Kinya Ohata ◽  
Hirohito Yamazaki ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Myeloid Leukemia ◽  
Hla Class I ◽  
Class I ◽  
Leukemic Cells ◽  
Leukemia Cells ◽  
Hla Class I Antigens ◽  
Ifn Γ

Abstract Abstract 2541 Background: The loss or down-regulation of HLA class-I antigens often occurs in solid tumors, but it is rarely demonstrated in leukemic cells. This phenomenon may explain why leukemic cells are immunogenic to some degree with allogeneic hematopoietic stem cell transplantation (allo-SCT) or donor leukocyte infusion, because HLA class-I antigens on leukemic cells are thought to present minor histocompatibility antigens (mHAs) and leukemia-associated antigens (LAAs) to donor T cells to elicit anti-leukemic cytotoxic T-cell (CTL) responses. Recent analyses of leukemic cells that relapsed after HLA-haploidentical SCT revealed that the leukemic cells lose their unshared HLA haplotype expression as a result of acquired uniparental disomy (UPD) on the short arm of chromosome 6 (6p). The loss of HLA from leukemic cells may occur after transplantation from HLA-identical donors if CTLs specific to mHAs or LAAs play a substantial role in the eradication of leukemic cells. This study evaluated this hypothesis by investigating HLA class-I expression on leukemic cells from patients at both the time of diagnosis and relapse after allo-SCT from HLA matched and mismatched donors. Objectives/Methods: Leukemic cells were obtained from five patients with myeloid leukemia (1 CML, 4 AML) both at diagnosis and relapse after allo-SCT. HLA class-I expression on leukemic cells was determined by flow cytometry using monoclonal Abs specific for the HLA-A allele. SCT donors were an HLA-matched sibling, an HLA-A locus-mismatched mother, an HLA-B and C locus-mismatched father, and 2 HLA-matched unrelated donors. The copy number-neutral loss of heterozygosity on 6p in leukemic cells was analyzed by a single-nucleotide polymorphism (SNP) array in patients after haploidentical SCT. The origin of the patients' HLA alleles (paternal or maternal) was determined by family studies on HLA. The post-transplantation donor T-cell responses against the leukemic cells were analyzed with an IFN-γ secretion assay. Results: HLA-A expression of leukemic cells obtained at relapse after allo-SCT was down-regulated in all 5 patients compared to that of leukemic cell obtained at diagnosis. The patient possessing HLA-A2/A11 (Case 1) was the recipient of BM possessing HLA-A24/A11 showed that 66% of leukemic cells at relapse were deficient in HLA-A2 expression. Leukemic cells restored HLA-A2 expression when this patient relapsed after the 2nd SCT using HLA-A2-matched cord blood, but at lower level in comparison to the level at diagnosis (MFI at diagnosis 177 vs. MFI at relapse 101). In vitro, cell-surface HLA-A2 expression was completely restored when leukemic cells at the 2nd relapse were treated in culture with IFN-γ (200 U/mL) for 48 hr. HLA-A2 expression in the shared haplotype (A0206-B3902-Cw0702-DR0405) was unexpectedly missing in 12% of the relapsed leukemic cells in another patient (Case 2) with HLA-2 loci (HLA-B and -C)-mismatched BM (A3101-B5601-Cw0401-DR0901), and this proportion increased to 83% at relapse after 2nd allo-SCT from the same donor (Figure). IFN-γ failed to restore HLA-A2 expression (MFI without IFN-γ 32 vs. MFI with IFN-γ 10) in vitro, and the genomic DNA extracted from leukemic cells at relapse showed a UPD of 6p. Donor-derived T-cells stimulated with leukemia cells from case 2 at diagnosis in vitro secreted IFN-γ in response to leukemia cells at diagnosis better than leukemia cells at relapse (1.67% vs. 0.85%). Conclusion: Loss of HLA-class I antigen occurs frequently in myeloid leukemia cells at relapse after allo-SCT regardless of the HLA disparities. T-cell attacks specific to the major as well as the mHAs, and LAAs may favor proliferation of leukemic cells deficient in the expression of HLA class-I. Disclosures: No relevant conflicts of interest to declare.

MEGAKARYOCYTIC ORIGIN OF PLATELET HLA CLASS I ANTIGEN

1987 ◽  
Author(s):  
N Kieffer ◽  
M Titeux ◽  
A Henri ◽  
J Breton-Gorius ◽  
W Vainchenker
Keyword(s):  
Hla Antigens ◽  
Hla Class I ◽  
Human Platelets ◽  
Class I ◽  
Double Labeling ◽  
Hla Antigen ◽  
Platelet Surface ◽  
Hla Class I Antigens ◽  
Hla Class I Antigen

The existence of HLA class I antigens on human platelets is well established. However, several authors have suggested that platelet HLA antigens are not integral membrane components but are acquired from soluble plasma sources and adsorbed to the platelet surface.In the present study, we used the monoclonal antibody W6/32, directed against a monomorphic epitope of the HLA class I antigen for the immunochemical characterization of platelet HLA. Immunoprecipitation experiments, performed after in vitro metabolic radiolabeling of human platelets revealed a band of molecular weight 44,000 identical to that precipitated from metabolic labeled U937 or HEL cells. When the same antibody was tested by indirected immunofluorescence in a double labeling technique on in vitro cultures of human megakaryocytes, performed in the absence of human serum in the culture medium, megakaryocytes identified by an anti-vWF MoAb revealed a membrane staining with W6/32 identical to that observed on other bone marrow cells, e.g. macrophages. Our results provide evidence that platelet HLA has a megaka-ryocytic origin and that residual biosynthesis of HLA antigen does still occur in circulating platelets. However, our results do not exclude the ability of human platelets to adsord circulating HLA class I antigen from plasma.

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