Revisiting the role of interleukin-8 in chronic lymphocytic leukemia

BORGE, MERCEDES; FERNÁNDEZ-GRECCO, HORACIO; COLADO, ANA; RISNIK, DENISE; BORGE, MERCEDES; FERNÁNDEZ-GRECCO, HORACIO; COLADO, ANA; RISNIK, DENISE; GIORDANO, MIRTA; SÁNCHEZ-ÁVALOS, JULIO C.; BEZARES, RAIMUNDO F.; ALMEJÚN, MARÍA B.; GIORDANO, MIRTA; SÁNCHEZ-ÁVALOS, JULIO C.; BEZARES, RAIMUNDO F.; ALMEJÚN, MARÍA B.; GAMBERALE, ROMINA; CRANCO, SANTIAGO; ELÍAS, ESTEBAN E.; PODAZA, ENRIQUE; GAMBERALE, ROMINA; CRANCO, SANTIAGO; ELÍAS, ESTEBAN E.; PODAZA, ENRIQUE

Scientific Reports

Springer Nature

Año: 2017 vol. 7

2045-2322

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.