{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T02:48:57Z","timestamp":1793155737373,"version":"4.5.0"},"reference-count":55,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,4,21]],"date-time":"2026-04-21T00:00:00Z","timestamp":1776729600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100011033","name":"Agencia Estatal de Investigaci\u00f3n","doi-asserted-by":"publisher","award":["PID2021-125415OB-I00"],"award-info":[{"award-number":["PID2021-125415OB-I00"]}],"id":[{"id":"10.13039\/501100011033","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Tyrosine kinases and phosphatases regulate protein phosphorylation and maintain cellular homeostasis. The phosphoprotein tyrosine phosphatase SHP-1 (encoded by the\n                      <jats:italic>Ptpn6<\/jats:italic>\n                      gene) has been proposed as an immune checkpoint in CD8\n                      <jats:sup>+<\/jats:sup>\n                      T cells in preclinical models, yet its pharmacological inhibition has shown no efficacy against tumor growth in clinical trials. This suggests that SHP-1 may play opposing roles in different cell types within the tumor microenvironment. Here, we investigated the effect of depleting SHP-1 in CD11c\n                      <jats:sup>+<\/jats:sup>\n                      cells on the anti-tumoral response.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      To dissect the specific role of SHP1 in CD11c\n                      <jats:sup>+<\/jats:sup>\n                      antigen-presenting cells, or specifically in conventional type 1 dendritic cells (cDC1s) or macrophages, we subcutaneously inoculated different tumors in\n                      <jats:italic>Itgax\u0394Ptpn6<\/jats:italic>\n                      ,\n                      <jats:italic>Xcr1<\/jats:italic>\n                      \u0394\n                      <jats:italic>Ptpn6<\/jats:italic>\n                      and\n                      <jats:italic>Lyz2<\/jats:italic>\n                      \u0394\n                      <jats:italic>Ptpn6<\/jats:italic>\n                      mice, respectively. Tumor growth and survival were monitored, and immune infiltrates were analyzed using flow cytometry or scRNA-seq.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Tumor rejection was impaired when SHP-1 was depleted in CD11c\n                      <jats:sup>+<\/jats:sup>\n                      cells, as well as in XCR1\n                      <jats:sup>+<\/jats:sup>\n                      or Lyz2\n                      <jats:sup>+<\/jats:sup>\n                      cells. scRNA-seq analysis revealed that both tumor-associated macrophages and cDC1s exhibited downregulation of interferon response pathways in tumor-bearing\n                      <jats:italic>Itgax\u0394Ptpn6<\/jats:italic>\n                      mice compared with controls. Reduced MHC-II expression in tumor-associated macrophages was validated by flow cytometry, supporting impaired antigen presentation in these cells, whereas cDC subsets displayed heterogeneous alterations in co-stimulatory marker expression rather than a defect. Consistent with these findings, flow cytometry analysis showed that\n                      <jats:italic>Itgax\u0394Ptpn6<\/jats:italic>\n                      mice injected with MC38 tumor and treated with anti-PD1 displayed a reduction in CD8\n                      <jats:sup>+<\/jats:sup>\n                      IFN-\u03b3 cells in comparison with\n                      <jats:italic>\n                        Ptpn6\n                        <jats:sup>f\/f<\/jats:sup>\n                      <\/jats:italic>\n                      littermates.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      These results show that SHP-1 depletion in CD11c\n                      <jats:sup>+<\/jats:sup>\n                      cells impairs anti-tumor immunity and suggest that both cDC1s and macrophages contribute to this effect.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2026.1710547","type":"journal-article","created":{"date-parts":[[2026,4,21]],"date-time":"2026-04-21T09:46:57Z","timestamp":1776764817000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Loss of SHP-1 in CD11c+ cells impairs anti-tumor immunity"],"prefix":"10.3389","volume":"17","author":[{"given":"Miguel","family":"Gal\u00e1n","sequence":"first","affiliation":[{"name":"Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC)","place":["Madrid, Spain"]},{"name":"Escuela de Doctorado, Universidad Aut\u00f3noma de Madrid","place":["Madrid, Spain"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elena","family":"Hern\u00e1ndez-Garc\u00eda","sequence":"additional","affiliation":[{"name":"Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC)","place":["Madrid, Spain"]},{"name":"Fundaci\u00f3n Inmunotek","place":["Alcal\u00e1 de Henares, Spain"]},{"name":"Department of Immunology, Ophthalmology and Ear, Nose and Throat (ENT), School of Medicine, Universidad Complutense de Madrid","place":["Madrid, Spain"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pablo","family":"Munn\u00e9","sequence":"additional","affiliation":[{"name":"Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC)","place":["Madrid, Spain"]},{"name":"Escuela de Doctorado, Universidad Aut\u00f3noma de Madrid","place":["Madrid, Spain"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ana","family":"Redondo-Urzainqui","sequence":"additional","affiliation":[{"name":"Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC)","place":["Madrid, Spain"]},{"name":"Escuela de Doctorado, Universidad Aut\u00f3noma de Madrid","place":["Madrid, Spain"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Francisco J.","family":"Cueto","sequence":"additional","affiliation":[{"name":"Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC)","place":["Madrid, Spain"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jon","family":"Sicilia","sequence":"additional","affiliation":[{"name":"Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC)","place":["Madrid, Spain"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sergio Callejas","family":"Alejano","sequence":"additional","affiliation":[{"name":"Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC)","place":["Madrid, Spain"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. 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