Recruitment of IL-1β-producing intermediate monocytes enhanced by C5a contributes to the development of malignant pleural effusion.

C5a, activated by the classical and alternative pathways of the complement system, not only mediated the infiltration of intermediate monocytes by enhancing CCL2 production in PMCs but also induced IL-1β release from the recruited monocytes in MPE. The consequence of C5a activation and the subsequent IL-1β overexpression in intermediate monocytes contributed to MPE progression.