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Titolo:
LIGATION OF CD38 SUPPRESSES HUMAN B-LYMPHOPOIESIS
Autore:
KUMAGAI MA; COUSTANSMITH E; MURRAY DJ; SILVENNOINEN O; MURTI KG; EVANS WE; MALAVASI F; CAMPANA D;
Indirizzi:
ST JUDE CHILDRENS HOSP,DEPT HEMATOL ONCOL,DIV BONE MARROW TRANSPLANTAT,332 N LAUDERDALE ST MEMPHIS TN 38101 ST JUDE CHILDRENS HOSP,DEPT HEMATOL ONCOL,DIV BONE MARROW TRANSPLANTAT MEMPHIS TN 38101 ST JUDE CHILDRENS HOSP,DEPT PHARMACOKINET MEMPHIS TN 38101 ST JUDE CHILDRENS HOSP,DEPT BIOCHEM MEMPHIS TN 38101 ST JUDE CHILDRENS HOSP,DEPT VIROL & MOLEC BIOL MEMPHIS TN 38101 UNIV TENNESSEE,COLL MED MEMPHIS TN 38101 UNIV TURIN,DIPARTIMENTO GENET BIOL & CHIM MED I-10126 TURIN ITALY CNR,CIOS I-10126 TURIN ITALY
Titolo Testata:
The Journal of experimental medicine
fascicolo: 3, volume: 181, anno: 1995,
pagine: 1101 - 1110
SICI:
0022-1007(1995)181:3<1101:LOCSHB>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
CYCLIC ADP-RIBOSE; ACUTE LYMPHOBLASTIC-LEUKEMIA; LYMPHOCYTE ANTIGEN CD38; HUMAN-BONE-MARROW; CELL ACTIVATION; CA2+ RELEASE; SURFACE; MOLECULE; DIFFERENTIATION; EXPRESSION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
42
Recensione:
Indirizzi per estratti:
Citazione:
M.A. Kumagai et al., "LIGATION OF CD38 SUPPRESSES HUMAN B-LYMPHOPOIESIS", The Journal of experimental medicine, 181(3), 1995, pp. 1101-1110

Abstract

CD38 is a transmembrane glycoprotein expressed in many cell types, including lymphoid progenitors and activated lymphocytes. High levels ofCD38 expression on immature lymphoid cells suggest its role in the regulation of cell growth and differentiation, but there is no evidence demonstrating a functional activity of CD38 on these cells. We used stroma-supported cultures of B cell progenitors and anti-CD38 monoclonalantibodies (T16 and IB4) to study CD38 function. In cultures of normal bone marrow CD19(+) cells (n = 5), addition of anti-CD38 markedly reduced the number of cells recovered after 7 d. Cell loss was greatest among CD19(+)sIg(-) B cell progenitors (mean cell recovery +/- SD = 7.2 +/- 11.7% of recovery in control cultures) and extended to CD19(+)CD34(+) B cells (the most immature subset; 7.6 +/- 2.2%). In contrast, CD38 ligation did not substantially affect cell numbers in cultures of normal peripheral blood or tonsillar B cells. In stroma-supported cultures of 22 B-lineage acute lymphoblastic leukemia cases, anti-CD38 suppressed recovery of CD19(+)sIg(-) leukemic cells. CD38 ligation also suppressed the growth of immature lymphoid cell lines cultured on stroma and, in some cases, in the presence of stroma-derived cytokines (interleukin [IL] 7, IL-3, and/or stem cell factor), but did not inhibit growth in stroma- or cytokine- free cultures. DNA content and DNA fragmentation studies showed that CD38 ligation of stroma-supported cells resulted in both inhibition of DNA synthesis and induction of apoptosis. It is known that CD38 catalyzes nicotinamide adenine dinucleotide (NAD+) hydrolysis into cyclic ADP-ribose (cADPR) and ADPR. However, no changes in NAD+ hydrolysis or cADPR and ADPR production after CD38 ligation were found by high-performance liquid chromatography; addition ofNAD+, ADPR, or cADPR to cultures of lymphoid progenitors did not offset the inhibitory effects of anti-CD38. Thus, anti-CD38 does not suppress B lymphopoiesis by altering the enzymatic function of the molecule. In conclusion, these data show that CD38 ligation inhibits the growth of immature B lymphoid cells in the bone marrow microenvironment, and suggest that CD38 interaction with a putative ligand represents a novel regulatory mechanism of B lymphopoiesis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 24/11/20 alle ore 07:42:44