Molecular Immunology 89 (2017) 121–124 Contents lists available at ScienceDirect Molecular Immunology journal homepage: www.elsevier.com/locate/molimm Abstracts 013 Distribution and function of the complement protein C1q in malignant pleural mesothelioma microenvironment Bulla Roberta 1,∗ , Chiara Agostinis 2 , Romana Vidergar 1 , Beatrice Belmonte 3 , Alessandro Mangogna 1 , Leonardo Amadio 2 , Violetta Borelli 1 , Fabrizio Zanconati 4 , Marco Confalonieri 4 , Francesco Tedesco 5 , Claudio Tripodo 3 , Uday Kishore 6 1 Department of Life Sciences, University of Trieste, 34127 Trieste, Italy 2 Institute for Maternal and Child Health, Istituto di Ricovero e Cura a Carattere Scientifico Burlo Garofolo, 34137 Trieste, Italy 3 Department of Human Pathology, University of Palermo, Italy 4 Department of Medical, Surgical and Health Science, University of Trieste 5 Istituto Auxologico Italiano, 20149, Milan, Italy 6 Biosciences, College of Health and Life Sciences, Brunel University London, Uxbridge UB8 3PH, United Kingdom Background: The complement component C1q has been shown to be abundantly expressed in the microenvironment of several solid tumors where it can act as a tumour-promoting factor favou- ring adhesion, migration and proliferation of cancer cells as well as angiogenesis and metastasis. In this study, we have examined the role of C1q in the microenvironment of malignant pleural mesothe- lioma (MPM), a rare form of cancer commonly associated with exposure to asbestos. Materials and methods: MPM human sections were ana- lysed by immunohistochemistry for the presence of C1q and for the presence of hyaluronic acid in the microenvironment. MPM human primary mesothelioma cells were isolated from pleural biopsy, characterized by immunofluorescence and cytofluorimet- ric analysis. These cells were used for adhesion and migration experiments. Human macrophages were incubated with MPM con- ditioned medium and their phenotype and their production of C1q, was evaluated by qPCR and ELISA. The analysis of the activation pathway was investigated by microarray analysis. Results and conclusions: C1q was express in tumor-associated stroma of different histotypes of mesothelioma. M treated with MPM conditioned medium have shown an M2-like phenotypic pro- file (CD206 and IL-10 upregulation) and a significant upregulation in C1q production. No variation was detected for C1s gene. C1q avidly bound high and low molecular weight hyaluronic acid via its globular domain. C1q bound to hyaluronic acid was able to induce adhesion and proliferation of mesothelioma cells via enhancement of ERK1/2, SAPK/JNK and p38 phosphorylation; C1q may bind to hyaluronic acid through ghA module, whereas it may interact with human mesothelioma cells through the ghC. In conclusion, C1q is highly expressed in MPM and promotes cell adhesion and prolif- eration. These data can help develop novel diagnostic markers and molecular targets for MPM. http://dx.doi.org/10.1016/j.molimm.2017.06.052 014 Role of complement in cancer-related inflammation Elena Magrini 1,∗ , Sabrina Di Marco 1 , Kevin Berthenet 1 , Maria Luisa Barbagallo 1 , Nadia Polentarutti 1 , Andrea Ponzetta 1 , Alberto Mantovani 1,2 , Cecilia Garlanda 1,2 1 IRCCS – Humanitas Clinical and Research Center, Rozzano, Milan, Italy 2 Humanitas University, Milan, Italy Background: Cancer related inflammation (CRI) is an essential component of the tumor microenvironment. The complement is a component of the humoral arm of the innate immune system with potential antitumor activity, although no formal evidence support the existence of an effective immune surveillance medi- ated by complement during carcinogenesis. In contrast, recent studies establish an important role for complement activation in sustaining tumor growth, although discordant are the results con- cerning the mechanism/s involved. Our aim is to clarify the function and the mechanisms underlying complement activation in differ- ent inflammatory-driven carcinogenesis models, which show the advantage of representing the entire process of tumor progres- sion and immunoediting, including the development of CRI, in mice through a genetic approach. Materials and methods: We verified the deposition of C3 on different tumor cell lines by in vitro C3 deposition 0161-5890/