کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10909510 | 1087905 | 2005 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Signaling capacity of FcγRII isoforms in B-CLL cells
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موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
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چکیده انگلیسی
Two main isoforms of Fcγ receptor II (CD32) have been described in humans: activatory FcγRIIA and inhibitory FcγRIIB. We have previously reported that B cells from a subset of chronic lymphocytic leukemia (B-CLL) patients express not only FcγRIIB, as normal B lymphocytes, but also the myeloid FcγRIIA. The aim of this study was to evaluate the signaling capacity of both FcγRII isoforms in B-CLL cells. We found that FcγRIIA expressed by leukemic cells failed to induce Ca2+ mobilization or protein tyrosine phosphorylation, suggesting that the receptor is not functional. By contrast, FcγRIIB effectively diminished BCR-triggered ERK1 phosphorylation, which indicates that it is able to transduce inhibitory signals in B-CLL cells. Moreover, we found that FcγRIIB homoaggregation in either B-CLL or non-malignant tonsillar B cells did not result in apoptosis as was reported for murine B splenocytes. Together, these results show that FcγRIIB, but not FcγRIIA is biologically active in B-CLL cells and might influence leukemic cell physiology in vivo.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Leukemia Research - Volume 29, Issue 11, November 2005, Pages 1277-1284
Journal: Leukemia Research - Volume 29, Issue 11, November 2005, Pages 1277-1284
نویسندگان
Romina Gamberale, Paula Fernández-Calotti, Julieta Sanjurjo, Guillermo Arrossagaray, Julio Sánchez Avalos, Jorge Geffner, Mirta Giordano,