scholarly journals Immune complexes from SLE sera induce IL10 production from normal peripheral blood mononuclear cells by an FcgammaRII dependent mechanism: implications for a possible vicious cycle maintaining B cell hyperactivity in SLE

2003 ◽  
Vol 62 (1) ◽  
pp. 37-42 ◽  
Author(s):  
J Ronnelid
Keyword(s):  
B Cell ◽  
Peripheral Blood Mononuclear Cells ◽  
Immune Complexes ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Vicious Cycle ◽  
Peripheral Blood Mononuclear ◽  
Normal Peripheral Blood ◽  
Blood Mononuclear Cells ◽  
Dependent Mechanism

Monoglycerides induce apoptosis in human leukemic cells while sparing normal peripheral blood mononuclear cells

Blood ◽  
2003 ◽  
Vol 101 (1) ◽  
pp. 292-294 ◽  
Author(s):  
Fabianne Philippoussis ◽  
Chantal Arguin ◽  
Véronique Mateo ◽  
Ann-Muriel Steff ◽  
Patrice Hugo
Keyword(s):  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Human Peripheral Blood ◽  
Lymphocytic Leukemia ◽  
Leukemic Cells ◽  
Major Drawback ◽  
Peripheral Blood Mononuclear ◽  
Normal Peripheral Blood ◽  
Blood Mononuclear Cells

Abstract A major drawback of the current antineoplastic treatments is their lack of specificity toward cancer cells, because they are most often cytotoxic to normal cells, thus creating related side effects. Hence, the identification of new apoptosis-inducing agents, specifically targeting malignant cells while sparing their normal counterparts, is of crucial interest. We show here that monoglycerides, a family of lipids consisting of a single fatty acid attached to a glycerol backbone, induce cell death in several human leukemic cell lines. Importantly, treatment of primary leukemic cells, obtained from B-cell chronic lymphocytic leukemia patients, resulted in rapid apoptosis. In striking contrast, resting or activated human peripheral blood mononuclear cells from healthy individuals were resistant to the same treatment. Therefore, these compounds could represent potential antileukemic drugs or could allow for the design of novel therapeutic agents applied to leukemia.

Downregulating the Fibromodulin Gene by Short Interfering RNA Causes B-CLL Cell Death.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 176-176 ◽  
Author(s):  
Aniruddha Choudhury ◽  
Katja Derkow ◽  
Eva Mikaelsson ◽  
Parviz Kokhaei ◽  
Anders Österborg ◽  
...  
Keyword(s):  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Rt Pcr ◽  
Sirna Transfection ◽  
Peripheral Blood Mononuclear ◽  
Normal Peripheral Blood ◽  
Extracellular Matrix Molecule ◽  
Rnai Technology ◽  
Blood Mononuclear Cells

Abstract Development of targeted therapies against B-CLL is dependent on the identification of molecules that are essential for the proliferation and survival of the leukemic cells. One such molecule investigated by us as a putative leukemia-associated target is Fibromodulin (FIM). FIM is an extracellular matrix molecule belonging to the leucin-rich proteoglycan family. Our laboratory studies have verified that expression of FIM is upregulated in B-CLL cells. Moreover, this molecule is specifically overexpressed in B-CLL cells and not on normal peripheral blood mononuclear cells. Analysis of FIM expression on various other hematological tumor cells have revealed that with the exception of mantle cell lymphoma, FIM is not expressed in other hematological malignancies. RNAi technology has recently emerged as a powerful method to specifically silence the expression of a gene. We have generated three siRNA against various segments of FIM and tested the effects of these siRNA on B-CLL cells. Transfection of B-CLL cells with these siRNA significantly diminished, or completely abrogated the expression of FIM mRNA as detected by RT-PCR. The figure below shows silencing of the FIM gene following siRNA transfection, as assayed by RT-PCR. “Untrans” and “ctrl” represents untransfected and control siRNA-transfected B-CLL cells respectively. As noted, transfection with each of the three siRNA against FIM completely abrogated the expression of FIM siRNA. 24–48 hours after siRNA transfection, a substantial fraction (30–70%) of the B-CLL cells, compared to cells transfected with control non-silencing siRNA, went into apoptosis as assayed by Annexin-V-propidium iodide staining. Time kinetic studies revealed that siRNA mediated silencing and apoptosis occurred between 18 and 48 hours. No such effect was noted when peripheral blood mononuclear cells of healthy donors or FIM-positive fibroblast cell lines were transfected with siRNA. In reconstitution experiments, siRNA treated B-CLL cells were co-cultured with various numbers of FIM-positive fibroblasts. The presence of these fibroblasts greatly diminished the apoptosis of B-CLL cells induced after siRNA treatment. Our results indicate that overexpression of FIM in B-CLL cells are critical for their survival and FIM may serve as a leukemia-specific target for B-CLL therapy. Figure Figure

Lymphotropic Virus Infection of Peripheral Blood Mononuclear Cells in B-Cell Non-Hodgkin’s Lymphoma

1997 ◽  
Vol 98 (2) ◽  
pp. 89-94 ◽  
Author(s):  
Clodoveo Ferri ◽  
Francesca Lo Jacono ◽  
Monica Monti ◽  
Francesco Caracciolo ◽  
Luca La Civita ◽  
...  
Keyword(s):  
Virus Infection ◽  
B Cell ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Hodgkin’S Lymphoma ◽  
Mononuclear Cells ◽  
Hodgkin's Lymphoma ◽  
Peripheral Blood Mononuclear ◽  
Non Hodgkin's Lymphoma ◽  
Blood Mononuclear Cells
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