Biomedical subjects

Elisa Ferretti

Publications and source records attributed to Elisa Ferretti.

4 recordsLinked to original sources

PubMed2005

Human mesenchymal stem cells modulate B-cell functions.

Human mesenchymal stem cells (hMSCs) suppress T-cell and dendritic-cell function and represent a promising strategy for cell therapy of autoimmune diseases. Nevertheless, no information is currently available on the effects of hMSCs on B cells, which may have a large impact on the clinical use of these cells. hMSCs isolated from the bone marrow and B cells purified from the peripheral blood of healthy donors were cocultured with different B-cell tropic stimuli. B-cell proliferation was inhibited by hMSCs through an arrest in the G0/G1 phase of the cell cycle and not through the induction of apoptosis. A major mechanism of B-cell suppression was hMSC production of soluble factors, as indicated by transwell experiments. hMSCs inhibited B-cell differentiation because IgM, IgG, and IgA production was significantly impaired. CXCR4, CXCR5, and CCR7 B-cell expression, as well as chemotaxis to CXCL12, the CXCR4 ligand, and CXCL13, the CXCR5 ligand, were significantly down-regulated by hMSCs, suggesting that these cells affect chemotactic properties of B cells. B-cell costimulatory molecule expression and cytokine production were unaffected by hMSCs. These results further support the potential therapeutic use of hMSCs in immune-mediated disorders, including those in which B cells play a major role.

B-Lymphocytes↗

PubMed2005

Chemokine receptor expression and function in childhood acute lymphoblastic leukemia of B-lineage.

Scanty information is available on chemokine receptor expression and function in childhood B-lineage acute lymphoblastic leukemia (ALL). Thirteen pro-B, 17 early pre-B, 12 pre-B, and 9 B-ALL/Burkitt lymphoma (BL) pediatric cases were tested for CXCR1 to CXCR5 and CCR1 to CCR7 expression. CXCR2, CXCR3, and CXCR4 were expressed in the majority of cases, while the other receptors were variably expressed or absent. CXCR4 mediated chemotaxis of all leukemic cell subtypes. Freshly isolated CCR7(+) early pre-B-ALL cells migrated to CCL19, whereas CCR7(+) pro-B- and pre-B-ALL cells were attracted by CCL19 only following culture with soluble recombinant CD40 ligand.

Burkitt Lymphoma↗

PubMed2004

Recapitulation of B cell differentiation in the central nervous system of patients with multiple sclerosis.

Clonally expanded populations of B cells carrying somatic mutations of Ig variable (V) region genes have been detected in the CNS of subjects with multiple sclerosis (MS), suggesting that a process of B cell affinity maturation with ensuing production of potentially pathogenic autoantibodies may occur inside the CNS. Here, we have characterized the B cell subsets present in the cerebrospinal fluid (CSF) of MS patients and of individuals with other inflammatory neurological disorders by flow cytometry. CD19(+)CD38(high+)CD77(+), Ki67(+), Bcl-2(-) centroblasts, i.e., a B cell subset found exclusively in secondary lymphoid organs, were detected in the CSF but not in paired peripheral blood from both patient groups. CD27(+)IgD(-) memory B cells, i.e., cells with hyper-mutated IgV genes, were significantly increased in the CSF vs. paired peripheral blood and displayed up-regulation of the CD80 and CD86 costimulatory molecules and of CC chemokine receptor (CCR) 1, CCR2, and CCR4 in both patient groups. Lymphotoxin-alpha, CXC ligand (CXCL) 12, and CXCL13, key mediators of lymphoid neogenesis, were present in the CSF from patients with MS and other inflammatory neurological disorders and were expressed in MS brain tissue, with selective localization in the outer layer of the capillary vessel wall. In conclusion, this study suggests that a compartmentalized B cell response occurs within the CNS during an ongoing inflammatory reaction, through a recapitulation of all stages of B cell differentiation observed in secondary lymphoid organs. The presence of lymphotoxin-alpha, CXCL12, and CXCL13 in the CNS may provide favorable microenvironmental conditions for these events.

Antigens, CD↗

PubMed2004

CCL19 and CXCL12 trigger in vitro chemotaxis of human mantle cell lymphoma B cells.

PURPOSE: Few data are available in the literature on chemokine receptor expression and migratory capability of mantle cell lymphoma (MCL) B cells. Information on these issues may allow us to identify novel mechanisms of chemokine-driven tumor cell migration. EXPERIMENTAL DESIGN: The research was designed to investigate: (a) expression of CCR1 to CCR7 and CXCR1 to CXCR5 chemokine receptors; and (b) chemotaxis to the respective ligands in MCL B cells and in their normal counterparts, i.e., CD5+ B cells. RESULTS: Malignant B cells from MCL patients and normal counterparts displayed similar chemokine receptor profiles. MCL B cells were induced to migrate by CXCL12 and CCL19, whereas normal CD5+ B cells migrated to the former, but not the latter chemokine. Overnight culture of MCL B cells and their normal counterparts with CXCL12 cross-sensitized other chemokine receptors to their ligands in some tumor samples but not in CD5+ B cells. CONCLUSIONS: CCR7 and CXCR4 ligands may play a key role in tumor cell migration and spreading in vivo. CXCL12 may additionally contribute by sensitizing MCL B cells to respond to the ligands of other chemokine receptors.

Aged↗