{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T20:21:06Z","timestamp":1785442866279,"version":"3.56.0"},"reference-count":65,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,3,25]],"date-time":"2026-03-25T00:00:00Z","timestamp":1774396800000},"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:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>Spontaneous abortion (SA) is closely associated with immune homeostasis of decidual natural killer (dNK) cells at the maternal-fetal interface, yet how decidual stromal cells (DSCs) educate NK cells remains incompletely understood. Here, we showed that DSC-derived hyaluronic acid (HA) shapes NK cell residency and cytotoxicity in early pregnancy.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Reanalysis of single-cell RNA sequencing data and functional assays identified DSCs as the major source of HAS2-dependent HA. We assessed dNK phenotypes and functions in SA versus normal pregnancies, and tested HA -CD44 effects using high-molecular-weight HA (HMW-HA) stimulation, HAS2 knockdown in DSCs, and CD44 blockade, with partial rescue by exogenous HMW-HA. Canonical Wnt activation and\n                      <jats:italic>FOSL2<\/jats:italic>\n                      upregulation were further evaluated by western blotting to examine downstream signaling.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Our findings revealed a reduced proportion of dNK cells, impaired adhesion molecule expression, and increased cytotoxicity in SA compared with normal pregnancies. HMW-HA from DSCs, via engagement of CD44 on NK cells, promoted the phenotypic transition of peripheral NK cells into CD49a\n                      <jats:sup>+<\/jats:sup>\n                      tissue-resident dNK-like cells, increased adhesion, and shifted cytokine production toward an immune-tolerant profile. HAS2 knockdown in DSCs or CD44 blockade reduced CD49a expression, expanded highly cytotoxic CD44\n                      <jats:sup>high<\/jats:sup>\n                      subset, and disrupted the balance among dNK1\/dNK2\/dNK3-like subsets, effects that were partially rescued by exogenous HMW-HA. Mechanistically, HA\/CD44 signaling activated canonical Wnt pathways and upregulated the dNK1-associated transcription factor\n                      <jats:italic>FOSL2<\/jats:italic>\n                      , driving differentiation toward a low-cytotoxic dNK1-like phenotype.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>\n                      These findings define a DSC-centered HA\/HAS2 -CD44 -Wnt -\n                      <jats:italic>FOSL2<\/jats:italic>\n                      axis that remodels NK cells and supports maternal-fetal immune tolerance, providing potential targets for preventing SA and related pregnancy complications.\n                    <\/jats:p>\n                  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