{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,3]],"date-time":"2026-02-03T03:26:18Z","timestamp":1770089178944,"version":"3.49.0"},"reference-count":73,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2003,7,1]],"date-time":"2003-07-01T00:00:00Z","timestamp":1057017600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2003,7,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Challenge with low doses of LPS together with d-galactosamine causes severe liver injury, resulting in lethal shock (low dose LPS-induced shock). We examined the role of LFA-1 in low dose LPS-induced shock. LFA-1\u2212\/\u2212 mice were more resistant to low dose LPS-induced shock\/liver injury than their heterozygous littermates, although serum levels of TNF-\u03b1 and IL-12 were higher in these mice. C57BL\/6 mice were not rescued from lethal effects of LPS by depletion of NK1+ cells, granulocytes, or macrophages, and susceptibility of NKT cell-deficient mice was comparable to that of controls. High numbers of platelets were detected in the liver of LFA-1+\/\u2212 mice after low dose LPS challenge, whereas liver accumulation of platelets was only marginal in LFA-1\u2212\/\u2212 mice. Following low dose LPS challenge, serum levels of IL-10 were higher in LFA-1\u2212\/\u2212 mice than in LFA-1+\/\u2212 mice, and susceptibility to low dose LPS-induced shock as well as platelet accumulation in the liver of LFA-1\u2212\/\u2212 mice were markedly increased by IL-10 neutralization. Serum levels of IL-10 in LFA-1+\/\u2212 mice were only marginally affected by macrophage depletion. However, in LFA-1\u2212\/\u2212 mice macrophage depletion markedly reduced serum levels of IL-10, and as a corollary, susceptibility of LFA-1\u2212\/\u2212 mice to low dose LPS-induced shock was markedly elevated despite the fact that TNF-\u03b1 levels were also diminished. We conclude that LFA-1 participates in LPS-induced lethal shock\/liver injury by regulating IL-10 secretion from macrophages and that IL-10 plays a decisive role in resistance to shock\/liver injury. Our data point to a novel role of LFA-1 in control of the proinflammatory\/anti-inflammatory cytokine network.<\/jats:p>","DOI":"10.4049\/jimmunol.171.2.584","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T19:29:26Z","timestamp":1398022166000},"page":"584-593","source":"Crossref","is-referenced-by-count":20,"title":["Increased Resistance of LFA-1-Deficient Mice to Lipopolysaccharide-Induced Shock\/Liver Injury in the Presence of TNF-\u03b1 and IL-12 Is Mediated by IL-10: A Novel Role for LFA-1 in the Regulation of the Proinflammatory and Anti-Inflammatory Cytokine Balance"],"prefix":"10.1093","volume":"171","author":[{"given":"Masashi","family":"Emoto","sequence":"first","affiliation":[{"name":"Department of Immunology, Max-Planck-Institute for Infection Biology , Berlin ,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yoshiko","family":"Emoto","sequence":"additional","affiliation":[{"name":"Department of Immunology, Max-Planck-Institute for Infection Biology , Berlin ,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Volker","family":"Brinkmann","sequence":"additional","affiliation":[{"name":"Central Core Facility Microscopy, Max-Planck-Institute for Infection Biology , Berlin ,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mamiko","family":"Miyamoto","sequence":"additional","affiliation":[{"name":"Department of Immunology, Max-Planck-Institute for Infection Biology , Berlin ,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Izumi","family":"Yoshizawa","sequence":"additional","affiliation":[{"name":"Department of Immunology, Max-Planck-Institute for Infection Biology , Berlin ,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Manuela","family":"Sta\u0308ber","sequence":"additional","affiliation":[{"name":"Department of Immunology, Max-Planck-Institute for Infection Biology , Berlin ,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nico","family":"van Rooijen","sequence":"additional","affiliation":[{"name":"Department of Cell Biology and Immunology, Faculty of Medicine, Vrije Universiteit , Amsterdam ,","place":["The Netherlands"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alf","family":"Hamann","sequence":"additional","affiliation":[{"name":"Experimental Rheumatology, Medical Clinic, Charite\u0301, Humboldt University , Berlin ,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stefan H E","family":"Kaufmann","sequence":"additional","affiliation":[{"name":"Department of Immunology, Max-Planck-Institute for Infection Biology , Berlin ,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2003,7,15]]},"reference":[{"key":"2026020210191755200_R1","first-page":"732","volume-title":"Lancet","year":"1991"},{"key":"2026020210191755200_R2","first-page":"625","volume-title":"Annu. 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