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B-cell chronic lymphocytic leukemia (B-CLL) is characterized by homogeneous coexpression of CD19, CD23 and CD5, and poor expression of membrane Ig. The aim of this study was to evaluate, in B-CLL patients and in healthy subjects by flow cytometry, B cell expression of surface molecules involved in cell activation, differentiation, T-B cooperation and apoptosis.The study population consisted of 29 patients (16 men and 13 women; mean age: 66.5 years) with B-CCL. The control group consisted of 16 sex- and age-matched healthy subjects. The results are reported as percentages and mean fluorescence intensity (MFI) of CD19+ cells coexpressing each analyzed molecule.We found that the lymphocyte activation markers, CD69, CD25 and CD11c, were more expressed in B-CLL patients than controls. CD38 and CD95 expressions were higher on normal B lymphocytes than leukemic B cells. Finally, CD80 and CD86, molecules involved in T-B cooperation, showed an inverse expression between lymphocytes of B-CLL patients and healthy subjects. CD80 was higher on normal than leukemic B cells, while CD86 expression was higher on CLL B cells. Linear regression analysis showed a positive correlation between CD80 and CD95 expression on leukemic B cells; a reverse correlation was observed between CD69 and CD11c.These results suggest that common mechanisms may regulate the simultaneous expression of CD80 and CD95 or the reverse expression of CD69 and CD11c, respectively, in different stages of B cell activation and/or differentiation.

B-cell chronic lymphocytic leukemia (B-CLL) is characterized by a sustained accumulation of long-lived and well-differentiated B lymphocytes in lymphoid tissues, peripheral blood and bone marrow. Although the pathogenesis of this disease is not entirely understood, altered apoptosis is believed to play a relevant role in B-CLL. In this study, we compared the expression of CD95, the best characterized surface molecule involved in triggering the apoptotic machinery, on normal and CLL B cells before and after in vitro activation with polyclonal stimulators. Cell activation was monitored by verifying the induced expression of the early activation antigen CD69. Freshly analyzed CLL B cells showed significantly lower levels of CD95 than normal B cells. Moreover, following in vitro culture with phorbol 12-myristate 13-acetate (PMA) + ionomycin, phytohemagglutinin, or pokeweed mitogen, CLL B cells failed to upregulate CD95 expression as efficiently as normal B cells. Impairment of CD95 upregulation was mainly observed following PMA + ionomycin treatment. In contrast, CLL B cells were shown to express CD69 as well as normal B cells, regardless of the activator used, indicating that CLL B cells retain the ability to respond to activating stimuli but are unable to efficiently implement the CD95-mediated activation-induced cell death (AICD) program. In conclusion, these results suggest that prolonged survival of CLL B cells may be contributed to by alterations in AICD mechanisms.

Aims To evaluate changes in Hepatitis C Virus (HCV) RNA both in plasma and Peripheral Blood Mononuclear Cells (PBMC) in onco-haematological patients. Patients and methods 8 consecutive anti-HCV/HCV RNA-positive patients with onco-haematological diseases (5 with B-cell Non-Hodgkin Lymphoma and 3 with chronic lymphocytic leukaemia) were observed during chemotherapy and after its discontinuation. All were naive to chemotherapy. HCV RNA was sought by Real Time Polymerase Chain Reaction in Light Cycler 1.5 in plasma and PBMC samples collected before, during and after chemotherapy. Results An increase in HCV RNA of at least 1.5 log IU/mL in plasma and 1.1 log IU/ml in PBMC was observed in all 7 patients undergoing Rituximab-based chemotherapy; these patients showed a hepatic flare after discontinuation, life-threatening in one with cirrhosis. Also the 8th patient had cirrhosis, but was treated with Rituximab-sparing chemotherapy and did not show any increase in HCV RNA or a hepatic flare. Conclusion Rituximab-based chemotherapy favours an increase in HCV RNA in onco-haematological patients; this is followed by a hepatic flare, possibly immune-mediated and life threatening in cirrhotic patients.

The aim of the study was to evaluate clinical and virological differences in HBV reactivation between patients with overt and occult HBV infection. Twenty-three consecutive patients with symptomatic HBV reactivation occurring during or after immunosuppressive therapy were enrolled in a retrospective study: 10 with reactivation of overt HBV infection (overt group) and 13 of occult HBV infection (occult group). Twenty-one patients were treated with nucleot(s)ide analogues after HBV reactivation. Regimens including rituximab or fludarabine were administered more frequently in the occult group (61% vs. 31%, respectively). HBV reactivation was severe frequently in the overt (40%) and occult groups (38.4%). Patients in the overt group showed higher HBV-DNA titers (1.1×10 8±1.4×10 8 vs. 5.1×10 5±6.8×10 5IU; P