Blockage of Wnt/beta-catenin signaling by quercetin reduces survival and proliferation of B-1 cells in vitro

Author(s)

Tavares Novo, Marilia Campos ^[1] ; Osugui, Lika ^[1] ; dos Reis, Vanessa Oliveira ^[1] ; Longo-Maugeri, Ieda Maria ^[1] ; Mariano, Mario ^[1] ; Popi, Ana Flavia ^[1]

Affiliation

^[1] Univ Fed Sao Paulo, UNIFESP, Dept Microbiol Imunol & Parasitol, Disciplina Imunol, BR-04023900 Sao Paulo - Brazil

• Document type: Journal article
• Source: Immunobiology; v. 220, n. 1, p. 60-67, JAN 2015.
• Web of Science Citations: 20

Abstract

The Wnt/beta-catenin signaling pathway has been shown to play an important role in controlling the proliferation, survival and differentiation of hematopoietic cells. Several Wnt/beta-catenin signaling components influence hematopoietic cells fate. B-1 cells are self-renewing and spontaneously express both myeloid and lymphoid restricted transcription factors. B-1 lymphocytes play a major role in autoimmunity and are related to CD5(+) B-cell lymphomas and leukemias, such as CLL (chronic lymphocytic leukemia). Herein, we demonstrate that Wnt/beta-catenin pathway is important to B-1 cell survival in vitro. The loss of Wnt signals by quercetin treatment induces a reduction in the proliferation and survival of B-1 cells. Furthermore, the quercetin treatment diminishes IL-6 production by peritoneal cells, a cytokine important to the maintenance of B-1 cells in vitro. Importantly, the IL-6 addition to B-1 cell culture prevents cells from apoptosis, even in the presence of quercetin. These data suggest that a deregulation in beta-catenin signals could result in alterations in B-1 cell proliferation and differentiation. The correlation between Wnt/beta-catenin and IL-6 could point out a mechanism for the expansion of B-1 cells in autoimmune disease and neoplasia. (C) 2014 Elsevier GmbH. All rights reserved. (AU)