{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,17]],"date-time":"2026-04-17T14:01:21Z","timestamp":1776434481454,"version":"3.51.2"},"reference-count":75,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,3,17]],"date-time":"2026-03-17T00:00:00Z","timestamp":1773705600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>Immune checkpoint receptors, including Sialic-acid-binding immunoglobulin-like lectins (Siglecs), are critical regulators of immune homeostasis. Siglecs can serve as negative regulators of Toll-like receptor (TLR) signaling, promoting the resolution of inflammatory signaling through feedback inhibition mechanisms. Previous studies demonstrated that Siglec-E, the murine homolog of the human inhibitory receptor Siglec-7, negatively regulates TLR4 signaling by controlling receptor endocytosis. This regulatory mechanism suggests that Siglec-7 may also limit TLR signaling. Here we reveal a novel mechanism whereby Siglec-7 represses endosomal TLR3 activation, compared to other TLRs, in human myeloid cells. Crosslinking Siglec-7 with antibody clone QA79 significantly reduced TNF\u03b1 secretion in U937 cells, primary monocytes, and macrophages following Poly(I:C) stimulation. Mechanistically, QA79 triggers rapid Fc\u03b3R-independent internalization and endolysosomal trafficking of surface Siglec-7, which enables the direct co-localization of Siglec-7 with TLR3 within the endolysosome. This co-localization between Siglec-7 and TLR3 suppresses NF-\u03baB phosphorylation, a key pro-inflammatory signaling node downstream of TLR3. These findings establish a previously unrecognized negative regulatory role of Siglec-7 for TLR3-mediated inflammation in myeloid cells, where a disrupted interaction could contribute to autoimmune disease pathogenesis. Targeting this pathway represents a promising therapeutic approach for TLR3-driven autoimmune diseases.<\/jats:p>","DOI":"10.3389\/fimmu.2026.1764343","type":"journal-article","created":{"date-parts":[[2026,3,17]],"date-time":"2026-03-17T05:25:36Z","timestamp":1773725136000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Siglec-7 inhibits TLR3-induced pro-inflammatory cytokine production from human monocytes and macrophages"],"prefix":"10.3389","volume":"17","author":[{"given":"Justin N.","family":"Keeney","sequence":"first","affiliation":[{"name":"Immunology & Inflammation Research, Sanofi R&D","place":["Cambridge, MA, United States"]},{"name":"Sanofi Global Postdoctoral Fellowship Program","place":["Cambridge, MA, United States"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Janina","family":"Schwarte","sequence":"additional","affiliation":[{"name":"Target, Disease & Systems Biology, Sanofi R&D","place":["Cambridge, MA, United States"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bo","family":"Yang","sequence":"additional","affiliation":[{"name":"Translational Medicine Unit, Sanofi R&D","place":["Cambridge, MA, United States"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hendrik","family":"Wesseling","sequence":"additional","affiliation":[{"name":"Translational Medicine Unit, Sanofi R&D","place":["Cambridge, MA, United States"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bailin","family":"Zhang","sequence":"additional","affiliation":[{"name":"Translational Medicine Unit, Sanofi R&D","place":["Cambridge, MA, United States"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrew J.","family":"McKnight","sequence":"additional","affiliation":[{"name":"Immunology & Inflammation Research, Sanofi R&D","place":["Cambridge, MA, United 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