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Article: Up-regulation of macrophage migration inhibitory factor in acute renal allograft rejection in the rat

TitleUp-regulation of macrophage migration inhibitory factor in acute renal allograft rejection in the rat
Authors
KeywordsMacrophage migration inhibitory factor
Transplantation
Macrophage
T cell
Immunohistochemistry
Issue Date1999
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CEI
Citation
Clinical and Experimental Immunology, 1999, v. 118 n. 2, p. 329-36 How to Cite?
AbstractRecent studies have identified a key role for macrophage migration inhibitory factor (MIF) in a number of immune cell-mediated diseases. The current study investigated the potential role of MIF in acute allograft rejection. Lewis rats underwent bilateral nephrectomy and then received an orthotopic DA renal allograft or an orthotopic Lewis renal isograft. Groups of six animals were killed at day 1 or 5 after transplantation. No immunosuppression was used. Animals receiving a renal allograft exhibited severe rejection on day 5, as shown by high levels of serum creatinine, very low rates of creatinine clearance, and severe tubulitis with a dense macrophage and T cell infiltrate. In contrast, isografts had normal renal function on day 5 with no histological evidence of rejection. Northern blotting showed that renal MIF mRNA expression was unchanged at day 1, but was increased 3.5-fold on day 5. In situ hybridization showed a marked increase in MIF mRNA expression by tubular cells and MIF mRNA expression by many infiltrating mononuclear cells in day 5 allografts. Immunostaining confirmed an increase in tubular MIF protein expression, particularly in areas of severe tubular damage with prominent leucocytic infiltration. Double staining showed that many infiltrating macrophages and T cells expressed the MIF protein in day 5 allografts. There was only a minor increase in MIF expression in day 5 isografts, demonstrating that neither surgical injury nor stress cause significant up-regulation of MIF expression in allograft rejection. In conclusion, this study has demonstrated that local MIF production is specifically increased in acute renal allograft rejection. These results suggest that MIF may play an important role in the cellular immune response mediating acute allograft rejection.
Persistent Identifierhttp://hdl.handle.net/10722/49102
ISSN
2015 Impact Factor: 3.148
2015 SCImago Journal Rankings: 1.369
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorBrown, FGen_HK
dc.contributor.authorNikolic-Paterson, DJen_HK
dc.contributor.authorMetz, Cen_HK
dc.contributor.authorBucala, Ren_HK
dc.contributor.authorAtkins, RCen_HK
dc.contributor.authorLan, HYen_HK
dc.date.accessioned2008-06-12T06:34:28Z-
dc.date.available2008-06-12T06:34:28Z-
dc.date.issued1999en_HK
dc.identifier.citationClinical and Experimental Immunology, 1999, v. 118 n. 2, p. 329-36en_HK
dc.identifier.issn0009-9104en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49102-
dc.description.abstractRecent studies have identified a key role for macrophage migration inhibitory factor (MIF) in a number of immune cell-mediated diseases. The current study investigated the potential role of MIF in acute allograft rejection. Lewis rats underwent bilateral nephrectomy and then received an orthotopic DA renal allograft or an orthotopic Lewis renal isograft. Groups of six animals were killed at day 1 or 5 after transplantation. No immunosuppression was used. Animals receiving a renal allograft exhibited severe rejection on day 5, as shown by high levels of serum creatinine, very low rates of creatinine clearance, and severe tubulitis with a dense macrophage and T cell infiltrate. In contrast, isografts had normal renal function on day 5 with no histological evidence of rejection. Northern blotting showed that renal MIF mRNA expression was unchanged at day 1, but was increased 3.5-fold on day 5. In situ hybridization showed a marked increase in MIF mRNA expression by tubular cells and MIF mRNA expression by many infiltrating mononuclear cells in day 5 allografts. Immunostaining confirmed an increase in tubular MIF protein expression, particularly in areas of severe tubular damage with prominent leucocytic infiltration. Double staining showed that many infiltrating macrophages and T cells expressed the MIF protein in day 5 allografts. There was only a minor increase in MIF expression in day 5 isografts, demonstrating that neither surgical injury nor stress cause significant up-regulation of MIF expression in allograft rejection. In conclusion, this study has demonstrated that local MIF production is specifically increased in acute renal allograft rejection. These results suggest that MIF may play an important role in the cellular immune response mediating acute allograft rejection.en_HK
dc.format.extent388 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CEIen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsClinical and Experimental Immunology. Copyright © Blackwell Publishing Ltd.en_HK
dc.rightsThe definitive version is available at www.blackwell-synergy.comen_HK
dc.subjectMacrophage migration inhibitory factoren_HK
dc.subjectTransplantationen_HK
dc.subjectMacrophageen_HK
dc.subjectT cellen_HK
dc.subjectImmunohistochemistryen_HK
dc.titleUp-regulation of macrophage migration inhibitory factor in acute renal allograft rejection in the raten_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0009-9104&volume=118&issue=2&spage=329&epage=36&date=1999&atitle=Up-regulation+of+macrophage+migration+inhibitory+factor+in+acute+renal+allograft+rejection+in+the+raten_HK
dc.identifier.emailLan, HY: hylan@hku.hken_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1046/j.1365-2249.1999.01048.xen_HK
dc.identifier.pmid10540199-
dc.identifier.pmcidPMC1905421en_HK
dc.identifier.scopuseid_2-s2.0-0011019505-
dc.identifier.hkuros48887-
dc.identifier.isiWOS:000083539000023-

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