{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,9,25]],"date-time":"2023-09-25T05:48:44Z","timestamp":1695620924447},"reference-count":32,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2015,10,28]],"date-time":"2015-10-28T00:00:00Z","timestamp":1445990400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"National Health and Medical Research Council of Australia"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Nephrology"],"published-print":{"date-parts":[[2015,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Aim<\/jats:title><jats:p>Interactions between the co\u2010stimulatory molecule programmed death 1 (<jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\u20101) and its ligands, <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">L<\/jats:styled-content>1 and <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">L<\/jats:styled-content>2, constrain <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\u2010cell responses and help maintain peripheral tolerance. Glomerulonephritis can result from a variety of antigens, both self and foreign, and from humoural and cellular effector responses. These studies aimed to define the role of <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>1 and its ligands in circulating immune complex glomerulonephritis induced by immunity to a foreign antigen.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Immune complex glomerulonephritis was initiated by injecting BALB\/c mice with horse spleen apoferritin intraperitoneally daily for 14 days. Inhibitory anti\u2010mouse <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\u20101, anti\u2010<jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">L<\/jats:styled-content>1 or anti\u2010<jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">L<\/jats:styled-content>2 antibodies were administered every other day. Renal disease and immune responses were studied.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Daily injection of horse spleen apoferritin\u2010induced proliferative immune complex glomerulonephritis in control antibody\u2010treated mice, but inhibiting <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\u20101 did not augment renal injury. Specifically, blocking <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\u20101 did not increase serum antigen\u2010specific antibodies or increase glomerular immunoglobulin <jats:styled-content style=\"fixed-case\">G<\/jats:styled-content> deposition, the hallmark of injury in this model. Furthermore, <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>3 deposition was unaffected and glomerular macrophages were reduced after anti\u2010<jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\u20101 antibodies. However, anti\u2010<jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\u20101 administration did increase splenocyte proliferation and cytokine production including interferon\u2010\u03b3, interleukin (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>)\u20104, and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017, but not <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201010. Neutralizing either <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">L<\/jats:styled-content>1 or <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">L<\/jats:styled-content>2 alone did not result in major alterations in renal injury.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>The endogenous <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\u20101\/<jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">L<\/jats:styled-content> pathway does not limit acute experimental foreign antigen\u2010induced circulating immune complex glomerulonephritis.<\/jats:p><\/jats:sec>","DOI":"10.1111\/nep.12532","type":"journal-article","created":{"date-parts":[[2015,6,5]],"date-time":"2015-06-05T07:36:30Z","timestamp":1433489790000},"page":"892-898","update-policy":"http:\/\/dx.doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Programmed death 1 and its ligands do not limit experimental foreign antigen\u2010induced immune complex glomerulonephritis"],"prefix":"10.1111","volume":"20","author":[{"given":"Joshua D","family":"Ooi","sequence":"first","affiliation":[{"name":"Centre for Inflammatory Diseases Monash University Department of Medicine  Melbourne Victoria Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ming","family":"Li","sequence":"additional","affiliation":[{"name":"Centre for Inflammatory Diseases Monash University Department of Medicine  Melbourne Victoria 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