BACKGROUND: CD56 is generally considered to be a natural killer (NK) cell marker, but it is also found in various tissues including acute leukemia. Recently, some reports have showed that positive CD56staining by blast cells is associated with an unfavorable outcome in AML with either t(8;21) or t(15;17)and in some ALL. This study investigated the characteristics of morphology, immunophenotype and cytogenetics and correlated the expression of CD56 of blast cells in 262 acute leukemia patients. METHODS: We analyzed 153 AML and 109 ALL, who underwent flow cytometry for CD56 at diagnosis at Chonnam National University Hospital between January 1999 and May 2003, for morphology, immunophenotype, and cytogenetics, retrospectively. RESULTS: The CD56 antigen was positive in 47 out of 163 AML cases (28.8%) and in 4 out of 109 ALL cases (3.7%). There were no statistically significant differences in the hematological parameters between the CD56+ and CD56- groups in ALL. However, the CD56 expression in AML was significantly high (81.8%) in AML-M2 with t(8;21) and low (5%) in AML-M3 with t(15;17) and was associatedwith the frequent expression of CD34 and HLA-DR. CONCLUSIONS: In conclusion, the CD56 expression in AML is associated with specific translocation, FAB subtype, some antigens CD34 and HLA-DR, and is significantly higher than in ALL.
Antigens, CD56 ; Cytogenetics* ; Diagnosis ; Flow Cytometry ; HLA-DR Antigens ; Humans ; Immunophenotyping ; Jeollanam-do ; Leukemia* ; Retrospective Studies

T cell large granular lymphocytic leukemia (T-LGL leukemia) is defined as a clonal proliferative disorder of CD3+ cytotoxic T cells. T-LGL leukemia usually expresses CD3+, CD4-, CD8+, CD16+, CD56- and CD57+ cell markers, and this represents a rearrangement of the T cell receptor (TCR) gene. The clinical course is indolent in most cases, but on rare occasions, when CD3+ and CD56+ are expressed on the leukemic cells, it can be more aggressive. We experienced a patient with T-LGL leukemia and the disease was indolent at the time of diagnosis, and so any specific treatment was not required. Two years after the initial diagnosis, her clinical course became quite aggressive as the CD 56+ cell surface antigen was expressed. We report here on the first case of T-LGL leukemia in Korea and we review the relevant literature.
Antigens, CD3 ; Antigens, CD56 ; Antigens, Surface ; Humans ; Korea ; Leukemia, Large Granular Lymphocytic ; Receptors, Antigen, T-Cell ; T-Lymphocytes

BACKGROUND AND OBJECTIVE: The natural killer (NK) cells which play an important role in defense immune system are supposed to be involved in the pathogenesis of bronchial asthma. The goal of this study is to analyze the role of NK cells in the pathogenesis of bronchial asthma by examining the proportion of NK cells in peripheral blood mononucler cells (PBMCs) and production of interferon gamma (IFN-gamma) in NK cells between normal group and asthmatic group. METHODS: Ten patients with moderate to severe persistent asthma sensitive to house dust mite were enrolled as asthmatic group. PBMCs were activated by 12-0-tetracanoylphorbol-13-acetate (TPA) and calcium inonophore for 18 hours. Surface CD3 and CD56 antigens with intracytoplasmic IFN-gamma staining were performed simultaneously and the results were analyzed by three color flow cytometer. RESULTS: The percentage of CD56+ positive NK cells in PBMCs from asthma group was lower compared to control group (15.4+/-3.9% vs 19.8+/-4.5%). However, There was no signficant difference of IFN-gamma production in CD56+ NK cells between two groups (30.3+/-3.9% vs 25.9+/-5.8%, p>0.05). IFN-gammaproducing CD3+ T cells were significantly higher in asthma group compared with normal control group (36.3+/-1.8% vs 28.4+/-5.7%, p<0.05). The ratio of TNK cells expressing both CD56 and CD3 was not different between asthma group and control group (4.7+/-1.4 % vs 5.9+/-1.8%, p<0.05). CONCLUSION: The results suggest that aggravation of asthma symptoms in severe asthma may be caused partly by decrease in NK cells. The increased production of IFN-gamma in asthma patients suggest that IFN-gammamay function as inflammatory cytokine.
Antigens, CD56 ; Asthma* ; Calcium ; Humans ; Immune System ; Interferons* ; Killer Cells, Natural* ; Pyroglyphidae ; T-Lymphocytes

With the popularity of flow cytometry, the classification of leukemia become more detailed. Myeloid/natural killer cell precursor acute leukemia and myeloid/natural killer cell acute leukemias are generally recognized as two kinds of rare leukemias and have poor prognosis. The cells expressed both myeloid and lymphatic antigens in these two leukemia and can not be diagnosed by morphology. The only basis to make a definite diagnosis is their unique Immunophenotyping. The role of CD7 and CD56 in these two leukemia are compelling, in the other hand, as the progress of cell differentiation research, there are many new awareness of NK cell differentiation. In this article, the biological origin, clinical manifestation, diagnosis, treatment and the role of CD7 and CD56 in these two leukemia are briefly summarized.
Antigens, CD7 ; CD56 Antigen ; Cell Differentiation ; Humans ; Killer Cells, Natural ; Leukemia, Myeloid, Acute ; classification ; diagnosis ; therapy

BACKGROUND: Asthma is a chronic inflammatory disease of the bronchial mucosa and is associated with excess production of Th2 cytokines (IL-4, IL-5) relative to Th1 cytokine (IFN-V). The NK cell and TNK cell are supposed to be involved in the pathogenesis of allergic inflammation by cytokine regulation. OBJECTIVES: The aim of this study was to investigate the effect of allergen (Der p 2) on the production of IFN-V by CD3+T cell, CD56+NK cell and CD3+CD56+TNK cells in patients with mild persistent asthma. METHOD: Peripheral blood mononuclear cells (PBMCs) from patients with mild persistent asthma (n=12) who were sensitive to dust mite, were cultured with or without Der p 2 for 3 days, and phorbol ester plus calcium ionophore and intracellular protein transport inhibitor were added 4 hours before staining. A three-color flow cytometric analysis was done to detect intracytoplasmic IFN-V, surface DC3 and CD56 antigen simultaneously. RESULTS: When PBMCs were cultured only in media, there were no significant differences in the percentage of IFN-V positive CD3+T cell, CD56+NK cell and CD3+CD56+TNK cells between asthmatic patients and normal subjects. However, there were significant decreases in the percent change of IFN-V positive CD3+T cell, CD56+NK cell and CD3+CD56+TNK cell in asthmatic patients comparde to normal subjects after stimulation of PBMCs with Der p 2. CONCLUSION: This study suggests that NK cell and TNK cell may participate in allergic reaction by IFN-V regulation.
Antigens, CD56 ; Asthma* ; Calcium ; Cytokines ; Dust ; Humans ; Hypersensitivity ; Inflammation ; Interferons* ; Killer Cells, Natural ; Mites ; Mucous Membrane ; Protein Transport

CD4 Antigens ; metabolism ; CD56 Antigen ; metabolism ; Child ; Humans ; Lymphoma, T-Cell, Cutaneous ; diagnosis ; metabolism ; Male ; Skin Neoplasms ; diagnosis ; metabolism

Blastic natural killer (NK) cell lymphoma is a rare neoplasm characterized by blastoid tumor cells expressing CD4 and CD56, with predominant skin involvement. Although this tumor has been regarded as a neoplasm related to NK cell, recent studies suggested that it is derived from plasmacytoid dendritic cells, but not from NK cell. Herein we report 4 cases of CD4+CD56+ lineage marker- blastic NK cell lymphomas with a review of literatures. The patients were 3 men and one woman. Three of them were young (17, 18, and 22 yr old). Three patients had skin lesions, at initial presentation in two patients and during the course of disease in other patient. Histologically, tumors consisted of monotonous medium to large blastoid cells showing no necrosis, angiocentric growth or epidermotrophism. All four tumors were CD4+ and CD56+. Three expressed CD68 antigen. Lineage specific markers for B- and T cell were negative. All tumors did not express myeloperoxidase. T-cell receptor gene rearrangement, EBV, CD13 and CD33 were negative. In one patient, tumor cells arranged in Homer-Wright type pseudorosette and expressed terminal deoxynucleotidyl transferase(TdT). Despite the standard lymphoma chemotherapy, the tumors, except one lost during follow-up, progressed and relapsed. The patients died 8-60 months after diagnosis.
Adolescent ; Antigens, CD4/*analysis ; Antigens, CD56/*analysis ; Cell Lineage ; Female ; Humans ; Killer Cells, Natural/immunology/*pathology ; Lymphoma, T-Cell/immunology/*pathology ; Male ; Middle Aged

Anaplastic myeloma has various synonyms such as dysplastic myeloma, aggressitve phase myeloma, or immunoblastic sarcoma. This is known to be an extremely aggressive subentity of plasma cell myeloma, and the diagnosis can usually be delayed because of the lack of the typical morphologic characteristics of myeloma. We describe here a 45-year-old man with anaplastic myeloma, whom we had difficulties with in initial diagnostic workup. The patient was admitted to the hospital due to gum bleeding for 2 weeks. A few abnormal cells were found in the peripheral blood. In bone marrow aspiration smears, the normal hematopoietic cells were replaced by numerous anaplastic cells. An immunophenotype study showed only a dim expression of CD56 antigen, while other routine surface antigens as well as CD45 were all negative. Additional studies showed a moderate positivity of CD38 and cytoplasmic lambda light chain. Serum immunoelectrophoresis confirmed monoclonal lamda light chain production, which led to the diagnosis of anaplastic myeloma. Because the morphologic feature is confused with other lymphoproliferative disorders, the diagnosis of anaplastic myeloma could be delayed unless a high degree of suspicion is made. Cytoplasmic light chains as well as CD56 will be helpful in initial immunophenotyping workup when the neoplastic cells show anaplastic features.
Antigens, CD56 ; Antigens, Surface ; Bone Marrow ; Cytoplasm ; Diagnosis* ; Gingiva ; Hemorrhage ; Humans ; Immunoelectrophoresis ; Immunophenotyping* ; Lymphoma, Large-Cell, Immunoblastic ; Lymphoproliferative Disorders ; Middle Aged ; Multiple Myeloma

BACKGROUND: The natural killer cell antigen CD56 (NCAM) is a member of the immunoglobulin superfamily and is expressed on neurons, astrocytes, and Schwann cells. Recently, it has been reported that CD56 expression is detected on plasma cells of multiple myeloma by flow cytometry. METHOD: In this study, to test the diagnostic usefulness of the anti-CD56 antibody for plasma cell neoplasm on paraffin-embedded materials, we performed immunohistochemical staining of samples from 19 patients with plasma cell neoplasms. These cases included 14 cases of multiple myeloma, 3 cases of solitary plasmacytoma of the bone, and two cases of extramedullary plasmacytoma. RESULTS: The neoplastic plasma cells from 68 % of the patients with plasma cell neoplasms expressed CD56 highly. CD56 was expressed in all three cases of solitary plasmacytoma of the bone and one of two extramedullary plasmacytoma, and nine out of 14 multiple myeloma cases. In contrast, reactive plasma cells from the 18 patients with miscellaneous lesions were completely negative for CD56. CONCLUSIONS: CD56 is aberrantly expressed on the neoplastic plasma cells, and it may be used as a useful marker for the diagnosis of plasma cell neoplasms in paraffin-embedded tissues.
Antigens, CD56* ; Astrocytes ; Diagnosis ; Flow Cytometry ; Humans ; Immunoglobulins ; Immunohistochemistry ; Killer Cells, Natural ; Multiple Myeloma ; Neoplasms, Plasma Cell* ; Neurons ; Paraffin* ; Plasma Cells* ; Plasma* ; Plasmacytoma ; Schwann Cells

The CD56 antigen is a cell adhesion molecule and its expression on tumor cells is thought to play a role in CD56-positive lymphomas and leukemias with unusual sites of involvement. As to chronic myelogenous leukemia (CML) and related blastic crisis, CD56 expression is not generally considered as a part of the CML phenotype and has rarely been reported in CML and other chronic myeloproliferative dirsorders (CMPD). We reported a case of CML expressing the CD56 antigen on the CD34-negative myeloid cells presented with extramedullary granulocytic sarcoma and examined the CD56 reactivity on bone marrow biopsy sections in 9 patients with CMPD. To assess the abnormal expression of the CD56 antigen on myeloid and progenitor cells from CMPD, immunohistochemical staining and flow cytometric analysis were performed on bone marrow biopsy sections and aspirate specimens, respectively. Of nine patients with CMPD, a case of CML in blastic crisis with extramedullary granulocytic sarcoma showed an abnormal expression of CD56 on CD34-negative myeloid cells. The expression of CD56 on CML myeloid elements seems to represent an aberrant phenomenon that could affect the pattern of tumor cell dissemination.
Antigens, CD56 ; Biopsy ; Bone Marrow ; Cell Adhesion ; Humans ; Leukemia ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive* ; Lymphoma ; Myeloid Cells* ; Phenotype ; Sarcoma, Myeloid ; Stem Cells