Furthermore, the use of a specific C5aR antagonist led to similar attenuation of inflammation signs in immune complex-induced lung injury, indicating the C5aR as a predominant effector of the C5a-mediated inflammation in the lung [117] . A recent study could point out that the cellular responses induced by C5a/C5aR interaction are potentiated by a tight connection between complement and Fcγ receptors [118] . Both C5aR and FcγR are known to be expressed on alveolar macrophages [111] . Shushakova et al. found that C5a causes induction of the activating FcγRIII and suppression of the inhibitory FcγRII during lung injury resulting in a pro-inflammatory reaction. Genetic ablation of C5aR expression in mutant mice completely abolished C5a/C5aR-induced regulation of FcγRs and led to decreased intrapulmonary generation of TNF and neutrophil accumulation [118] . Taken together, C5a seems to have a broader critical function through FcγR regulation, thus augmenting inflammation in the lung. In contrast to the C5aR, the effects of C5a are limited by C5L2 that is co-expressed with the C5aR on many cells including neutrophils [119] . Besides of C5a, C5L2 can also bind C5a desArg and potentially additional complement fragments [120] . Gerard et al. could demonstrate a greater influx of inflammatory cells and an enhanced release of IL-6 and TNF in C5L2-deficient mice in the model of immune complex-induced lung injury [121] . This observation proposes an anti-inflammatory role of C5L2 in the lung that seems to counteract C5a/C5aR-mediated inflammation.