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Liver diseases remain clinically challenging and exhibit complex cellular interactions, including liver cell–immune cell communications that can shape disease progression.1 During portal injury, biliary epithelial cells (BECs, also known as cholangiocytes) expand excessively, a process termed ‘ductular reaction (DR)’ which promotes fibrogenesis, tumourigenesis and consecutive liver disease progression.2 It is increasingly recognised that reactive BECs are active players in shaping the hepatic inflammatory milieu through the secretion of cytokines, chemokines and chemicals, referred to as cholangiokines.3 4 Indeed, cholangiokines such as Nuclear factor Kappa B (NF-κB)-inducing kinase stimulate liver macrophages and hepatic stellate cells, augmenting liver inflammation and fibrosis.5 However, identifying and understanding the role of cholangiokines in disease is a nascent field and requires more attention.