Differentiation stage of natural killer cell‐lineage lymphoproliferative disorders based on phenotypic analysis

Mori, Kiyoshi; Egashira, Motoki; Oshimi, Kazuo

doi:10.1046/j.1365-2141.2001.03038.x

Cited by 50 publications

(38 citation statements)

References 11 publications

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“…10 Stainings were performed using an ethylenediaminetetraacetic acid-anti-coagulated whole blood stain-lyse-and-then-wash method and a four-color panel of monoclonal antibodies conjugated with fluorescein isothiocyanate, phycoerythrin, phycoerythrin-cyanine 5, or peridin chlorophyll protein and allophycocyanine directed against the following antigens: TCR␣␤, TCR␥␦, CD8, CD4, CD3, CD28, CD2, CD7, CD56, CD5, CD57, CD11c, CD38, CD11b, CD45RA, CD45RO, CD122, CD25, CD11a, HLA-DR, CD158a, CD161, CD16, NKB1, and CD94. 23 In addition, the expression of cytoplasmic granzyme B was evaluated using the Fix and Perm reagent kit (Caltag Laboratories, Burlingame, CA), according to the manufacturer's instructions.…”

Section: Immunophenotypic Studiesmentioning

confidence: 99%

“…Such phenotypic and functional features are similar to those observed in neoplastic NK cells from aggressive NK cell leukemia/lymphoma, nasal, and nasal-type lymphomas. 10 Despite this, few cases of CNKCL and LGL leukemias of CD56 Ϫ/ϩdim NK cells have been sporadically described 10 -13 or used to establish NK cell lines. 14 NK cells showing decreased or no expression of CD56 have not been reported either in healthy individuals or in disease conditions associated to either a transient or persistent increase in the number of NK cells in the peripheral blood (PB); 15 in such cases, the expanded cell population constantly shows co-expression of CD16 and CD56 frequently in association with acute or chronic NK cell activation features.…”

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confidence: 99%

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Clinicobiological, Immunophenotypic, and Molecular Characteristics of Monoclonal CD56−/+dim Chronic Natural Killer Cell Large Granular Lymphocytosis

Lima

Almeida

Montero

et al. 2004

The American Journal of Pathology

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Indolent natural killer (NK) cell lymphoproliferative disorders include a heterogeneous group of patients in whom persistent expansions of mature, typically CD56 ؉ , NK cells in the absence of any clonal marker are present in the peripheral blood. In the present study we report on the clinical, hematological, immunophenotypic, serological, and molecular features of a series of 26 patients with chronic large granular NK cell lymphocytosis, whose NK cells were either CD56 ؊ or expressed very low levels of CD56 (CD56 ؊/؉dim NK cells), in the context of an aberrant activation-related mature phenotype and proved to be monoclonal using the human androgen receptor gene polymerase chain reaction-based assay. As normal CD56 ؉ NK cells, CD56 ؊/؉dim NK cells were granzyme B ؉ , CD3 ؊ , TCR␣␤/ ␥␦ ؊ , CD5 ؊ , CD28 ؊ , CD11a ؉bright , CD45RA ؉bright , CD122 ؉ , and CD25 ؊ and they showed variable and heterogeneous expression of both CD8 and CD57. Nevertheless, they displayed several unusual immunophenotypic features. Accordingly, besides being CD56 ؊/؉dim , they were CD11b ؊/؉dim (heterogeneous), CD7 ؊/؉dim (heterogeneous), CD2 ؉ (homogeneous), CD11c ؉bright (homogeneous), and CD38 ؊/؉dim (heterogeneous). Moreover, CD56 ؊/؉dim NK cells heterogeneously expressed HLA-DR. In that concerning the expression of killer receptors, CD56 ؊/؉dim NK cells showed bright and homogeneous CD94 expression, and dim and heterogeneous reactivity for CD161, whereas CD158a and NKB1 expression was variable. From the functional point of view, CD56 ؊/؉dim showed a typical Th1 pattern of cytokine production (interferon-␥ ؉ , tumor necrosis factor-␣ ؉ ). From the clinical point of view, these patients usually had an indolent clinical course, progression into a massive lymphocytosis with lung infiltration leading to death being observed in only one case. Despite this, they frequently had associated cytopenias as well as neoplastic diseases and/or viral infections. In summary, we describe a unique and homogeneous group of monoclonal chronic large granular NK cell lymphocytosis with an aberrant activation-related CD56 ؊/؉dim /CD11b ؊/؉dim phenotype and an indolent clinical course, whose main clinical features are related to concomitant diseases. (Am J

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Section: Immunophenotypic Studiesmentioning

confidence: 99%

mentioning

confidence: 99%

Clinicobiological, Immunophenotypic, and Molecular Characteristics of Monoclonal CD56−/+dim Chronic Natural Killer Cell Large Granular Lymphocytosis

Lima

Almeida

Montero

et al. 2004

The American Journal of Pathology

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“…[1][2][3][4][5] Chronic NK cell lymphocytosis (CNKL) is characterized by the expansion of NK cells with a chronic indolent course, 6,7 although the morphology and the phenotypes of the NK cells are very similar to the ANKL cells. 8 The importance of chemokine receptors on the normal NK cell surface has been reported. [9][10][11][12] The chemokine receptors are thought to regulate NK cell trafficking and cytotoxicity in a phenotype-specific manner.…”

Section: Introductionmentioning

confidence: 99%

Significance of chemokine receptor expression in aggressive NK cell leukemia

et al. 2005

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Natural killer (NK) cell-type lymphoproliferative diseases of granular lymphocytes can be subdivided into aggressive NK cell leukemia (ANKL) and chronic NK cell lymphocytosis (CNKL). One reason for the poor outcome in ANKL is leukemic infiltration into multiple organs. The mechanisms of cell trafficking associated with the chemokine system have been investigated in NK cells. To clarify the mechanism of systemic migration of leukemic NK cells, we enrolled nine ANKL and six CNKL cases, and analyzed the expression profiles and functions of chemokine receptors by flowcytometry and chemotaxis assay. CXCR1 was detected on NK cells in all groups, and CCR5 was positive in all ANKL cells. Proliferating NK cells were simultaneously positive for CXCR1 and CCR5 in all ANKL patients examined, and NK cells with this phenotype did not expand in CNKL patients or healthy donors. ANKL cells showed enhanced chemotaxis toward the ligands of these receptors. These results indicated that the chemokine system might play an important role in the pathophysiology of ANKL and that chemokine receptor profiling might be a novel tool for discriminating ANKL cells from benign NK cells.

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“…Increased expression of Fas-ligand is commonly seen in ENKL, but this is nonspecific and seen in a number of aggressive lymphomas 55,[60][61][62] . NK inhibitory receptors, such as CD94 or NKG2A are also expressed in NK-cell neoplasms, but such expression is not uniform or consistent [63][64][65][66][67] . However, expression of CD94 is reported to confer a better prognosis in ENKL 67 .…”

mentioning

confidence: 99%

Leukemia and Lymphoma of Natural Killer Cells

Suzuki

2005

J Clin Exp Hematopathol

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Malignant hematolymphoid disorders arising from NK cells have become widely recognized over the past decade. The two forms of NK-cell malignancy, aggressive NK-cell leukemia (ANKL) and extranodal NK-cell lymphoma of nasal type (ENKL) are both characterized by the proliferation of tumor cells with an NK-cell like immunophenotype. ANKL usually presents with bone marrow tumor cells accompanied by circulating leukemic cells, and hepatosplenomegalay is a common clinical feature. ENKL most frequently affects the nasal or paranasal regions, with cutaneous involvement also being common. Approximately 70 percent of ENKL present with localized tumor cells, and follow an indolent clinical course, but, in advanced cases, tumors rapidly expand and are frequently fatal. Tumor cells from both ANKL and ENKL are surface CD3 − and CD56 + but differ in their expression of CD16. Epstein-Barr virus (EBV) is found in most cases of NK-cell leukemia/lymphoma, suggesting an oncogenic role, but patients may have biclonal or polyclonal populations of malignant cells based on differential EBV genome incorporation. NK-cell neoplasms are frequently resistant to chemotherapy due to p-glycoprotein expression and associated multidrug resistance. The prognoses of both localized and advanced stages of NK-cell malignancies are worse than most other lymphoid malignancies, but studies are currently underway to assess the safety and efficacy of novel chemoradiotherapy regimens for the treatment of these neoplasms.

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Differentiation stage of natural killer cell‐lineage lymphoproliferative disorders based on phenotypic analysis

Cited by 50 publications

References 11 publications

Clinicobiological, Immunophenotypic, and Molecular Characteristics of Monoclonal CD56−/+dim Chronic Natural Killer Cell Large Granular Lymphocytosis

Clinicobiological, Immunophenotypic, and Molecular Characteristics of Monoclonal CD56−/+dim Chronic Natural Killer Cell Large Granular Lymphocytosis

Significance of chemokine receptor expression in aggressive NK cell leukemia

Leukemia and Lymphoma of Natural Killer Cells

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