{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,30]],"date-time":"2026-10-30T09:39:54Z","timestamp":1793353194784,"version":"4.5.0"},"reference-count":52,"publisher":"BMJ","issue":"9","license":[{"start":{"date-parts":[[2022,9,16]],"date-time":"2022-09-16T00:00:00Z","timestamp":1663286400000},"content-version":"unspecified","delay-in-days":15,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001655","name":"Deutscher Akademischer Austauschdienst","doi-asserted-by":"publisher","award":["57516591"],"award-info":[{"award-number":["57516591"]}],"id":[{"id":"10.13039\/501100001655","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100002347","name":"Bundesministerium f\u00fcr Bildung und Forschung","doi-asserted-by":"publisher","award":["01KU2017"],"award-info":[{"award-number":["01KU2017"]}],"id":[{"id":"10.13039\/501100002347","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["259332240\/RTG"],"award-info":[{"award-number":["259332240\/RTG"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["bmj.com"],"crossmark-restriction":true},"short-container-title":["J Immunother Cancer"],"accepted":{"date-parts":[[2022,9,1]]},"published-print":{"date-parts":[[2022,9]]},"abstract":"<jats:sec>\n                  <jats:title>Background<\/jats:title>\n                  <jats:p>Tumor cells modulate host immunity by secreting extracellular vesicles (EV) and soluble factors. Their interactions with myeloid cells lead to the generation of myeloid-derived suppressor cells (MDSC), which inhibit the antitumor function of T and NK cells. We demonstrated previously that EV derived from mouse and human melanoma cells induced immunosuppressive activity via increased expression of programmed cell death ligand 1 (PD-L1) on myeloid cells that was dependent on the heat-shock protein 90\u03b1 (HSP90\u03b1) in EV. Here, we investigated whether soluble HSP90\u03b1 could convert monocytes into MDSC.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>CD14 monocytes were isolated from the peripheral blood of healthy donors, incubated with human recombinant HSP90\u03b1 (rHSP90\u03b1) alone or in the presence of inhibitors of TLR4 signaling and analyzed by flow cytometry. Inhibition of T cell proliferation assay was applied to assess the immunosuppressive function of rHSP90\u03b1-treated monocytes. HSP90\u03b1 levels were measured by ELISA in plasma of patients with advanced melanoma and correlated with clinical outcome.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>We found that the incubation of monocytes with rHSP90\u03b1 resulted in a strong upregulation of PD-L1 expression, whereas reactive oxygen species (ROS) and nitric oxide (NO) production as well as the expression of arginase-1, ectoenzymes CD39 and CD73 remained unchanged. The PD-L1 upregulation was blocked by anti-TLR4 antibodies and a nuclear factor-\u03baB inhibitor. rHSP90\u03b1-treated monocytes displayed the downregulation of HLA-DR expression and acquired the resistance to apoptosis. Moreover, these monocytes were converted into MDSC as indicated by their capacity to inhibit T cell proliferation, which was mediated by TLR4 signaling as well as PD-L1 and indoleamine 2,3-dioxygenase (IDO) 1 expression. Higher levels of HSP90\u03b1 in plasma of patients with melanoma correlated with augmented PD-L1 expression on circulating monocytic (M)-MDSC. Patients with melanoma with high levels of HSP90\u03b1 displayed shorter progression-free survival (PFS) on the treatment with immune checkpoint inhibitors (ICIs).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>Our findings demonstrated that soluble rHSP90\u03b1 increased the resistance of normal human monocytes to apoptosis and converted them into immunosuppressive MDSC via TLR4 signaling that stimulated PD-L1 and IDO-1 expression. Furthermore, patients with melanoma with high concentrations of HSP90\u03b1 displayed increased PD-L1 expression on M-MDSC and reduced PFS after ICI therapy, suggesting HSP90\u03b1 as a promising therapeutic target for overcoming immunosuppression in melanoma.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1136\/jitc-2022-005551","type":"journal-article","created":{"date-parts":[[2022,9,16]],"date-time":"2022-09-16T13:08:36Z","timestamp":1663333716000},"page":"e005551","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":39,"title":["HSP90\u03b1 induces immunosuppressive myeloid cells in melanoma via TLR4 signaling"],"prefix":"10.1136","volume":"10","author":[{"given":"Ihor","family":"Arkhypov","sequence":"first","affiliation":[{"name":"Skin Cancer Unit, German Cancer Research Center (DKFZ), Heidelberg, Germany"},{"name":"Department of Dermatology, Venereology and Allergology, University Medical Centre, Ruprecht-Karl University 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