Chronic lymphocytic leukemia (CLL) is characterized by the accumulation of monoclonal B cells expressing CD19, CD5 and CD23 together with low surface expression of B-cell receptors and related molecules such as FMC7 [1]. CLL cells grow out of control and accumulate in the bone marrow and blood, where they crowd out healthy blood cells. CLL is the most frequent type of adult leukemia in the Western world, accounting for nearly 30% of all reported leukemias, but its prevalence in Asia is relatively low [2]. CLL is a disease of adults, and the median age of newly diagnosed patients with CLL is 65 years [3]. It is a heterogeneous disease with a highly variable clinical course and prognosis. Clinical staging of CLL and determination of the extent of the disease are conducted with the Rai staging system or Binet classification [4]. The clinical course and survival of patients with B-CLL are quite variable, and the two major clinical staging systems are unable to discriminate prospectively between an indolent or aggressive course within the low and intermediate risk categories. For this reason, some biological parameters have been used for the CLL staging systems to differentiate subsets of prognostics. Recently, several new prognostic markers have been reported for the prediction of disease progression in CLL, such as β 2-microglobulin, immunoglobulin variable heavy chain (IgVH) gene mutational status and the expression of ZAP-70 and CD38 [5, 6]. CD160 is a 27 kDa glycoprotein that is known as an essential natural killer (NK) cell activating receptor [7]. Its expression is associated tightly with peripheral blood NK cells and CD8 T lymphocytes with cytolytic effector activity [8]. Recently, some reports have shown that CD160 is expressed by CLL cells, but not in normal B lymphocytes [9]. It has also been demonstrated that CLL cells can be regulated by the CD160 pathway for in vitro proliferation and activation. Further, activated CD160 protects CLL cells from rapid spontaneous apoptosis in vitro via the phosphatidylinositol 3-kinase (PI3K)/AKT pathway [10]. Thus, we hypothesized that expression of CD160 may be associated with high levels of CLL cells, and it may also be associated with the progression and prognosis of the disease. In this study, therefore, we measured the CD160 expression of CLL, and correlated the positive expression rate of CD160 with CLL cells, immune phenotypes, clinical parameters and other well-established prognostic indicators such as clinical stage, IgVH mutational status, ZAP-70, CD38 and chromosomal abnormalities.

The study population consisted of 57 consecutive patients diagnosed with CLL between January 2008 and June 2013. All patients signed written informed consents and the University and Institutional Review Boards gave their approval for this research. According to the National Cancer Institute (NCI) criteria, the diagnosis of CLL requires persistent B lymphocytosis of more than 5.0 10 9/L, and the typical CLL phenotype includes the coexpression of cell surface markers CD5, CD19 and CD23, weak surface immunoglobulin and negative/weak FMC7. All patients were either untreated or at least 6 months from the last treatment. Biological and clinical data were collected during the first hospitalization: age, gender, white blood cell (WBC) count, lymphocyte (LY) count, Binet stage, IgVH, cytogenetics, β 2-microglobulin, lymphadenopathy and splenomegaly. Cell surface antigens were analyzed by four-color immunofluorescence. Alexa Fluorâ647–CD160 (clone BY55), fluorescein isothiocyanate (FITC)–CD19 (clone 4G7), allophycocyanin (APC)–CD5 (clone L17F12), phycoerythrin (PE)–CD23 (clone M-L233 …