{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,28]],"date-time":"2026-05-28T07:03:03Z","timestamp":1779951783784,"version":"3.53.1"},"reference-count":112,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,5,28]],"date-time":"2026-05-28T00:00:00Z","timestamp":1779926400000},"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>Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. \u201cLymphocyte homing\u201d\u2014the targeted migration of lymphocytes between organs\u2014serves as the physiological foundation for immune surveillance and local immune homeostasis. Under septic conditions, this precisely regulated process is severely disrupted, leading to failed recruitment of immune cells to infection\/injury sites and exacerbated depletion of lymphoid tissues, ultimately inducing systemic immune imbalance. This review elaborates on three core aspects: the physiological basis of intestinal lymphocyte homing, the mechanisms by which sepsis disrupts this pathway (including immune microenvironment remodeling, abnormal homing signaling, and regulatory T cell dysfunction), and targeted interventional strategies (chemokine receptor antagonists, integrin-directed regulation, and microbiota-immune crosstalk modulation). Understanding lymphocyte homing disorder provides a novel breakthrough for deciphering septic immunosuppression and improving clinical outcomes.<\/jats:p>","DOI":"10.3389\/fimmu.2026.1827322","type":"journal-article","created":{"date-parts":[[2026,5,28]],"date-time":"2026-05-28T06:20:07Z","timestamp":1779949207000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Lymphocyte homing disorder: a concealed driver of intestinal immune collapse in sepsis"],"prefix":"10.3389","volume":"17","author":[{"given":"Huixian","family":"Geng","sequence":"first","affiliation":[{"name":"Hebei Medical University","place":["Shijiazhuang, China"]},{"name":"High Dependency Unit, Hebei General Hospital","place":["Shijiazhuang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dacheng","family":"Xiong","sequence":"additional","affiliation":[{"name":"Hebei Medical University","place":["Shijiazhuang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xuechun","family":"L\u00fc","sequence":"additional","affiliation":[{"name":"Hebei Medical University","place":["Shijiazhuang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jing","family":"Wang","sequence":"additional","affiliation":[{"name":"High Dependency Unit, Hebei General Hospital","place":["Shijiazhuang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hua","family":"Chen","sequence":"additional","affiliation":[{"name":"High Dependency Unit, Hebei General Hospital","place":["Shijiazhuang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lijing","family":"Jia","sequence":"additional","affiliation":[{"name":"Hebei Medical University","place":["Shijiazhuang, China"]},{"name":"High Dependency Unit, Hebei General Hospital","place":["Shijiazhuang, 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