{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T05:00:34Z","timestamp":1782882034757,"version":"3.54.5"},"reference-count":55,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation Research"],"published-print":{"date-parts":[[2015,4,10]]},"abstract":"<jats:sec>\n            <jats:title>\n              <jats:underline>Rationale:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>Lymphotoxin \u03b2 receptor (LTbR) regulates immune cell trafficking and communication in inflammatory diseases. However, the role of LTbR in atherosclerosis is still unclear.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\n              <jats:underline>Objective:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>The aim of this study was to elucidate the role of LTbR in atherosclerosis.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\n              <jats:underline>Methods and Results:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>\n              After 15 weeks of feeding a Western-type diet, mice double-deficient in apolipoprotein E and LTbR (apoE\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              \/LTbR\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              ) exhibited lower aortic plaque burden than did apoE\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              littermates. Macrophage content at the aortic root and in the aorta was reduced, as determined by immunohistochemistry and flow cytometry. In line with a decrease in plaque inflammation, chemokine (C\u2013C motif) ligand 5 (\n              <jats:italic>Ccl5<\/jats:italic>\n              ) and other chemokines were transcriptionally downregulated in aortic tissue from apoE\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              \/LTbR\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice. Moreover, bone marrow chimeras demonstrated that LTbR deficiency in hematopoietic cells mediated the atheroprotection. Furthermore, during atheroprogression, apoE\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice exhibited increased concentrations of cytokines, for example, Ccl5, whereas apoE\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              \/LTbR\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice did not. Despite this decreased plaque macrophage content, flow cytometric analysis showed that the numbers of circulating lymphocyte antigen 6C (Ly6C)\n              <jats:sup>low<\/jats:sup>\n              monocytes were markedly elevated in apoE\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              \/LTbR\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice. The influx of these cells into atherosclerotic lesions was significantly reduced, whereas apoptosis and macrophage proliferation in atherosclerotic lesions were unaffected. Gene array analysis pointed to chemokine (C\u2013C motif) receptor 5 as the most regulated pathway in isolated CD115\n              <jats:sup>+<\/jats:sup>\n              cells in apoE\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              \/LTbR\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice. Furthermore, stimulating monocytes from apoE\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice with agonistic anti-LTbR antibody or the natural ligand lymphotoxin-\u03b11\u03b22, increased\n              <jats:italic>Ccl5<\/jats:italic>\n              mRNA expression.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\n              <jats:underline>Conclusions:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>These findings suggest that LTbR plays a role in macrophage-driven inflammation in atherosclerotic lesions, probably by augmenting the Ccl5-mediated recruitment of monocytes.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/circresaha.116.305723","type":"journal-article","created":{"date-parts":[[2015,3,5]],"date-time":"2015-03-05T03:22:44Z","timestamp":1425525764000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":37,"title":["Deficiency in Lymphotoxin \u03b2 Receptor Protects From Atherosclerosis in apoE-Deficient Mice"],"prefix":"10.1161","volume":"116","author":[{"given":"Maria","family":"Grandoch","sequence":"first","affiliation":[{"name":"From the Institut f\u00fcr Pharmakologie und Klinische Pharmakologie (M.G., K.F., L.S.D., S.H., C.K., J.K.B., J.N.W., B.R., N.N., J.W.F.), Cardiovascular Research Institute D\u00fcsseldorf (CARID) (M.G., K.F., L.S.D., S.H., C.K., J.K.B., J.N.W., B.R., N.N., J.W.F.), Klinik f\u00fcr Gef\u00e4\u00df- und Endovaskularchirurgie (A.O.), Biologisch-Medizinisches Forschungszentrum (BMFZ) (R.D., K.K.), Hautklinik (B.H.), and Institut f\u00fcr Medizinische Mikrobiologie und Krankenhaushygiene (K.P.), Universit\u00e4tsklinikum der Heinrich..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kathrin","family":"Feldmann","sequence":"additional","affiliation":[{"name":"From the Institut f\u00fcr Pharmakologie und Klinische Pharmakologie (M.G., K.F., L.S.D., S.H., C.K., J.K.B., J.N.W., B.R., N.N., J.W.F.), Cardiovascular Research Institute D\u00fcsseldorf (CARID) (M.G., K.F., L.S.D., S.H., C.K., J.K.B., J.N.W., B.R., N.N., J.W.F.), Klinik f\u00fcr Gef\u00e4\u00df- und Endovaskularchirurgie (A.O.), Biologisch-Medizinisches Forschungszentrum (BMFZ) (R.D., K.K.), Hautklinik (B.H.), and Institut f\u00fcr Medizinische Mikrobiologie und Krankenhaushygiene (K.P.), Universit\u00e4tsklinikum der Heinrich..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joachim R.","family":"G\u00f6thert","sequence":"additional","affiliation":[{"name":"From the Institut f\u00fcr Pharmakologie und Klinische Pharmakologie (M.G., K.F., L.S.D., S.H., C.K., J.K.B., J.N.W., B.R., N.N., J.W.F.), Cardiovascular Research Institute D\u00fcsseldorf (CARID) (M.G., K.F., L.S.D., S.H., C.K., J.K.B., J.N.W., B.R., N.N., J.W.F.), Klinik f\u00fcr Gef\u00e4\u00df- und Endovaskularchirurgie (A.O.), Biologisch-Medizinisches Forschungszentrum (BMFZ) (R.D., K.K.), Hautklinik (B.H.), and Institut f\u00fcr Medizinische Mikrobiologie und Krankenhaushygiene (K.P.), Universit\u00e4tsklinikum der Heinrich..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lena S.","family":"Dick","sequence":"additional","affiliation":[{"name":"From the Institut f\u00fcr Pharmakologie und Klinische Pharmakologie (M.G., K.F., L.S.D., S.H., C.K., J.K.B., J.N.W., B.R., N.N., J.W.F.), Cardiovascular Research Institute D\u00fcsseldorf (CARID) (M.G., K.F., L.S.D., S.H., C.K., J.K.B., J.N.W., B.R., N.N., J.W.F.), Klinik f\u00fcr Gef\u00e4\u00df- und Endovaskularchirurgie (A.O.), Biologisch-Medizinisches Forschungszentrum (BMFZ) (R.D., K.K.), Hautklinik (B.H.), and 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