{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,15]],"date-time":"2026-04-15T06:46:05Z","timestamp":1776235565243,"version":"3.50.1"},"reference-count":65,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,4,15]],"date-time":"2026-04-15T00:00:00Z","timestamp":1776211200000},"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>Background and objective<\/jats:title>\n                    <jats:p>Sepsis is a life-threatening condition characterized by increasing global incidence, fundamentally driven by immune dysregulation. The liver, crucial for pathogen clearance and inflammatory modulation during sepsis, frequently exhibits functional impairment. Mucosal-associated invariant T (MAIT) cells bridge innate and adaptive immunity and are integral to antimicrobial defense. Their specific role in sepsis-related liver injury (SRLI) remains unclear. This study aims to elucidate MAIT cell alterations and function in SRLI using clinical cohorts and murine models.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      The cohort comprised 47 SRLI patients, 37 with non-septic acute liver injury (NSLI), 34 patients with non-associated liver injury in sepsis (NLIS), and 115 healthy controls (HC). Peripheral blood MAIT cells were characterized by flow cytometry for frequency, phenotype, and cytokine production.\n                      <jats:italic>In vitro<\/jats:italic>\n                      experiments assessed effects of bilirubin and cytokines on MAIT cells. A murine SRLI model was established via intraperitoneal lipopolysaccharide (LPS) injection. Liver injury severity, inflammatory cytokines, and histopathology were compared between wild-type and MAIT cell-deficient mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      In the SRLI group, the proportion of peripheral blood MAIT cells was significantly decreased compared to the HC group. Regarding activation (CD69\n                      <jats:sup>+<\/jats:sup>\n                      , CD25\n                      <jats:sup>+<\/jats:sup>\n                      ) and exhaustion (PD-1\n                      <jats:sup>+<\/jats:sup>\n                      , Tim-3\n                      <jats:sup>+<\/jats:sup>\n                      ) phenotypes, the expression levels of CD69 and PD-1 were markedly upregulated relative to all other groups, while the expression of CD25 and Tim-3 was increased compared to the HC and NSLI groups.\n                      <jats:italic>In vitro<\/jats:italic>\n                      assays indicated that upon stimulation, these MAIT cells preferentially produced IL-17A, TNF-\u03b1, and granzyme B, suggesting a bias toward Th17-like differentiation. Elevated concentrations of bilirubin exacerbated both the activation and exhaustion of MAIT cells through a TCR-dependent mechanism. In the septic murine model, MAIT cells deficiency led to more severe liver injury, and higher serum levels of transaminases, bilirubin, and pro-inflammatory cytokines compared to wild-type.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>In the context of SRLI, peripheral blood MAIT cells exhibit a diminished frequency, functional impairment, and a phenotypic shift toward a Th17-like profile. Among these, bilirubin plays a key role. Ultimately, MAIT cells exert a protective role in sepsis-induced liver injury by suppressing excessive inflammatory responses.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2026.1779656","type":"journal-article","created":{"date-parts":[[2026,4,15]],"date-time":"2026-04-15T05:44:39Z","timestamp":1776231879000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Protective role of mucosa-associated invariant T cells in sepsis-related liver injury"],"prefix":"10.3389","volume":"17","author":[{"given":"Wei","family":"Bu","sequence":"first","affiliation":[{"name":"Department of Critical Care Medicine, The First Affiliated Hospital of Anhui Medical University, Anhui Medical University","place":["Hefei, Anhui, China"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Qiang","family":"Ji","sequence":"additional","affiliation":[{"name":"Department of Critical Care Medicine, The First Affiliated 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China"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nian","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Critical Care Medicine, The First Affiliated Hospital of Anhui Medical University, Anhui Medical University","place":["Hefei, Anhui, China"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Min","family":"Shao","sequence":"additional","affiliation":[{"name":"Department of Critical Care Medicine, The First Affiliated Hospital of Anhui Medical University, Anhui Medical University","place":["Hefei, Anhui, China"]},{"name":"Center for Big Data and Population Health of IHM, Anhui Medical University","place":["Hefei, China"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1965","published-online":{"date-parts":[[2026,4,15]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.7554\/eLife.55615","article-title":"Mucosal-associated invariant T (Mait) cells mediate protective host responses in 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