Revisiting the role of interleukin-8 in chronic lymphocytic leukemia

The proliferation and survival of malignant B cells in chronic lymphocytic leukemia (CLL) depend on signals from the microenvironment in lymphoid tissues. Among a plethora of soluble factors, IL-8 has been considered one of the most relevant to support CLL B cell progression in an autocrine fashion,...

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Publicado: 2017
Acceso en línea:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_20452322_v7_n1_p_Risnik
http://hdl.handle.net/20.500.12110/paper_20452322_v7_n1_p_Risnik
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spelling paper:paper_20452322_v7_n1_p_Risnik2023-06-08T16:33:31Z Revisiting the role of interleukin-8 in chronic lymphocytic leukemia The proliferation and survival of malignant B cells in chronic lymphocytic leukemia (CLL) depend on signals from the microenvironment in lymphoid tissues. Among a plethora of soluble factors, IL-8 has been considered one of the most relevant to support CLL B cell progression in an autocrine fashion, even though the expression of IL-8 receptors, CXCR1 and CXCR2, on leukemic B cells has not been reported. Here we show that circulating CLL B cells neither express CXCR1 or CXCR2 nor they respond to exogenous IL-8 when cultured in vitro alone or in the presence of monocytes/nurse-like cells. By intracellular staining and ELISA we show that highly purified CLL B cells do not produce IL-8 spontaneously or upon activation through the B cell receptor. By contrast, we found that a minor proportion (<0.5%) of contaminating monocytes in enriched suspensions of leukemic cells might be the actual source of IL-8 due to their strong capacity to release this cytokine. Altogether our results indicate that CLL B cells are not able to secrete or respond to IL-8 and highlight the importance of methodological details in in vitro experiments. © 2017 The Author(s). 2017 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_20452322_v7_n1_p_Risnik http://hdl.handle.net/20.500.12110/paper_20452322_v7_n1_p_Risnik
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
description The proliferation and survival of malignant B cells in chronic lymphocytic leukemia (CLL) depend on signals from the microenvironment in lymphoid tissues. Among a plethora of soluble factors, IL-8 has been considered one of the most relevant to support CLL B cell progression in an autocrine fashion, even though the expression of IL-8 receptors, CXCR1 and CXCR2, on leukemic B cells has not been reported. Here we show that circulating CLL B cells neither express CXCR1 or CXCR2 nor they respond to exogenous IL-8 when cultured in vitro alone or in the presence of monocytes/nurse-like cells. By intracellular staining and ELISA we show that highly purified CLL B cells do not produce IL-8 spontaneously or upon activation through the B cell receptor. By contrast, we found that a minor proportion (<0.5%) of contaminating monocytes in enriched suspensions of leukemic cells might be the actual source of IL-8 due to their strong capacity to release this cytokine. Altogether our results indicate that CLL B cells are not able to secrete or respond to IL-8 and highlight the importance of methodological details in in vitro experiments. © 2017 The Author(s).
title Revisiting the role of interleukin-8 in chronic lymphocytic leukemia
spellingShingle Revisiting the role of interleukin-8 in chronic lymphocytic leukemia
title_short Revisiting the role of interleukin-8 in chronic lymphocytic leukemia
title_full Revisiting the role of interleukin-8 in chronic lymphocytic leukemia
title_fullStr Revisiting the role of interleukin-8 in chronic lymphocytic leukemia
title_full_unstemmed Revisiting the role of interleukin-8 in chronic lymphocytic leukemia
title_sort revisiting the role of interleukin-8 in chronic lymphocytic leukemia
publishDate 2017
url https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_20452322_v7_n1_p_Risnik
http://hdl.handle.net/20.500.12110/paper_20452322_v7_n1_p_Risnik
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