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In addition, the IL-34 tumorigenic effect can also be mediated by its other receptors, protein-tyrosine phosphatase zeta, Syndecan-1 (CD138) and triggering receptor expressed on myeloid cells 2. Small tyrosine kinase inhibitors are used to block CSF-1R signaling but lack specificity. Neutralizing anti-CSF-1 and\/or IL-34 antibodies have been proposed, but their effects are limited. Thus, there is a need for a more specific and yet integrative approach.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      A human mutated form of the extracellular portion of CSF-1R was in silico modelized to trap both IL-34 and CSF-1 with higher affinity than the wild-type CSF-1R by replacing the methionine residue at position 149 with a Lysine (\n                      <jats:sub>\n                        <jats:sc>M149K<\/jats:sc>\n                      <\/jats:sub>\n                      ). The extracellular portion of the mutated CSF-1R\n                      <jats:sc>M149K<\/jats:sc>\n                      was dimerized using the immunoglobulin Fc sequence of a silenced human IgG1 (sCSF-1R\n                      <jats:sub>\n                        <jats:sc>M149K<\/jats:sc>\n                      <\/jats:sub>\n                      -Fc). Signaling through CSF-1R, survival of monocytes and differentiation of suppressive macrophages were analyzed using pleural mesothelioma patient's samples and mesothelioma\/macrophage spheroids in vitro and in vivo in the presence of sCSF-1R\n                      <jats:sub>\n                        <jats:sc>M149K<\/jats:sc>\n                      <\/jats:sub>\n                      -Fc or sCSF-1R-Fc wild type control (sCSF-1R\n                      <jats:sub>\n                        <jats:sc>WT<\/jats:sc>\n                      <\/jats:sub>\n                      -Fc).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We defined that the D1 to D5 domains of the extracellular portion of CSF-1R were required for efficient binding to IL-34 and CSF-1. The mutein sCSF-1R\n                      <jats:sub>\n                        <jats:sc>M149K<\/jats:sc>\n                      <\/jats:sub>\n                      -Fc trapped with higher affinity than sCSF-1R\n                      <jats:sub>\n                        <jats:sc>WT<\/jats:sc>\n                      <\/jats:sub>\n                      -Fc both CSF-1 and IL-34 added in culture and naturally produced in mesothelioma pleural effusions. sCSF-1R\n                      <jats:sub>\n                        <jats:sc>M149K<\/jats:sc>\n                      <\/jats:sub>\n                      -Fc inhibited CSF-1R signaling, survival and differentiation of human suppressive macrophage in vitro and in vivo induced by pleural mesothelioma cells. Neutralization of IL-34 and CSF-1 by sCSF-1R\n                      <jats:sub>\n                        <jats:sc>M149K<\/jats:sc>\n                      <\/jats:sub>\n                      -Fc also resulted in higher killing of pleural mesothelioma cells by a tumor-specific CD8\n                      <jats:sup>+<\/jats:sup>\n                      T cell clone in mesothelioma\/macrophage spheroids.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      sCSF-1R\n                      <jats:sub>\n                        <jats:sc>M149K<\/jats:sc>\n                      <\/jats:sub>\n                      -Fc efficiently traps both CSF-1 and IL-34 and inhibits CSF-1R signaling, monocyte survival and suppressive macrophage differentiation induced by pleural mesothelioma cells producing CSF-1 and IL-34, as well as restores cytotoxic T-cell responses. sCSF-1R\n                      <jats:sub>\n                        <jats:sc>M149K<\/jats:sc>\n                      <\/jats:sub>\n                      -Fc has therapeutic potential vs other therapies under development targeting single components of this complex cytokine pathway involved in cancer.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/jitc-2024-010112","type":"journal-article","created":{"date-parts":[[2025,3,19]],"date-time":"2025-03-19T13:58:06Z","timestamp":1742392686000},"page":"e010112","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":7,"title":["New soluble CSF-1R-dimeric mutein with enhanced trapping of both CSF-1 and IL-34 reduces suppressive tumor-associated macrophages in pleural mesothelioma"],"prefix":"10.1136","volume":"13","author":[{"given":"No\u00e9mie","family":"Joalland","sequence":"first","affiliation":[{"name":"INSERM, Center for Research in 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