The development of liver fibrosis constitutes one of the major complications of chronic liver disease with many clinical consequences such as the development of esophageal varices and ascites being directly related to the presence of liver fibrosis (1). The hepatic wound healing response is a concerted action of multiple resident and non-resident cell types that not only provides a scaffold for structural stability but also involves the removal of cellular debris by infiltrating hepatic macrophages (HM) and the regeneration of functional parenchyma (2,3). Hepatic stellate cells (HSCs) are considered the main fibrogenic cell type in the liver, and are responsible for the production of various types of extracellular matrix (ECM) (2,3). HSCs undergo a well-characterized activation process during which they lose their characteristic vitamin A and lipid stores, and obtain a myofibroblastic phenotype (2,3). The activation of HSCs is controlled by multiple soluble mediators including TGFβ and PDGF, and is part of a complex cellular network that controls the hepatic wound healing response. Previous studies have demonstrated that multiple cell populations including HM, myeloid-derived suppressor cell, B cells, T cells and natural killer cells influence the development of liver fibrosis (4-12). Among those, HM exert a profound effect on HSCs and hepatic fibrosis as shown by genetic or pharmacologic models of macrophage depletion (6,7,13). At the same time, HM also contribute to fibrosis resolution through MMP13 and matrix remodeling (6,14,15). However, the mechanisms by which HM promote liver fibrosis remain largely elusive. Dendritic cells (DC) are developmentally closely related to macrophages, and exert a profound effect on liver fibrosis regression (16) and the cytokine microenvironment during fibrogenesis (12), but their contribution to liver fibrosis development remains unknown. In the present study, we uncovered the promotion of HSC/myofibroblast survival as novel and to-date unknown mechanism through which macrophages promote fibrosis. Moreover, we demonstrate for the first time that neither classical DC (cDC) and plasmacytoid DC (pDC) contribute to fibrogenesis.