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Article: Macrophage migratory inhibitory factor (MIF) expression in acute graft-versus-host disease (GVHD) in allogeneic hemopoietic stem cell transplant recipients

TitleMacrophage migratory inhibitory factor (MIF) expression in acute graft-versus-host disease (GVHD) in allogeneic hemopoietic stem cell transplant recipients
Authors
KeywordsAcute GVHD
Allogeneic stem cell transplantation
MIF
Issue Date2002
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/bmt
Citation
Bone Marrow Transplantation, 2002, v. 30 n. 6, p. 375-380 How to Cite?
AbstractGraft-versus-host disease (GVHD) is a major complication after hemopoietic stem cell transplantation (HSCT), but its pathogenesis remains uncertain. Macrophage migratory inhibitory factor (MIF) is an important mediator in the allo-immune reaction during renal transplantation, yet its role in hemopoietic stem cell transplantation (HSCT) remains unexplored. This study investigated the potential role of MIF in acute graft-versus-host disease (aGVHD) following allogeneic HSCT. Forty-six randomly selected patients undergoing autologous or allogeneic HSCT were studied. Immunohistochemistry and in situ hybridization were performed to examine tissue MIF mRNA and protein expression on skin and colonic biopsy specimens. The associated T cell and macrophage activation was also studied by immunohistochemical studies. A semi-quantitative method was used to assess MIF staining, as well as T cell and macrophage staining. Serial blood samples were analyzed by ELISA for serum MIF levels. Immunohistochemistry and in situ hybridization performed in 15 skin and 19 colonic biopsies from 17 patients who developed moderate to severe aGVHD showed a significant increase in MIF mRNA and protein expression compared with normal controls (seven skin and five colonic biopsies). MIF was localized within the epidermis and the vascular area of skin, but diffusely expressed in the entire thickness of colon. Macrophage and T lymphocyte infiltration was confined to areas of strong MIF expression. Serial analysis by ELISA showed that only patients who developed aGVHD (n = 19) exhibited an increase (two- to three-fold) in serum MIF during HSCT, but not in the allogeneic HSCT recipients without aGVHD (n = 7) or those who received autologous HSCT (n = 8). In 14 out of 19 patients, serum MIF peaked before the onset of aGVHD. Local and systemic up-regulation of MIF expression is associated with the occurrence of acute GVHD. Its pathogenetic role remains to be further determined.
Persistent Identifierhttp://hdl.handle.net/10722/76751
ISSN
2015 Impact Factor: 3.636
2015 SCImago Journal Rankings: 1.585
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLo, JWSen_HK
dc.contributor.authorLeung, AYHen_HK
dc.contributor.authorHuang, XRen_HK
dc.contributor.authorLie, AKWen_HK
dc.contributor.authorMetz, Cen_HK
dc.contributor.authorBucala, Ren_HK
dc.contributor.authorLiang, Ren_HK
dc.contributor.authorLan, HYen_HK
dc.date.accessioned2010-09-06T07:24:32Z-
dc.date.available2010-09-06T07:24:32Z-
dc.date.issued2002en_HK
dc.identifier.citationBone Marrow Transplantation, 2002, v. 30 n. 6, p. 375-380en_HK
dc.identifier.issn0268-3369en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76751-
dc.description.abstractGraft-versus-host disease (GVHD) is a major complication after hemopoietic stem cell transplantation (HSCT), but its pathogenesis remains uncertain. Macrophage migratory inhibitory factor (MIF) is an important mediator in the allo-immune reaction during renal transplantation, yet its role in hemopoietic stem cell transplantation (HSCT) remains unexplored. This study investigated the potential role of MIF in acute graft-versus-host disease (aGVHD) following allogeneic HSCT. Forty-six randomly selected patients undergoing autologous or allogeneic HSCT were studied. Immunohistochemistry and in situ hybridization were performed to examine tissue MIF mRNA and protein expression on skin and colonic biopsy specimens. The associated T cell and macrophage activation was also studied by immunohistochemical studies. A semi-quantitative method was used to assess MIF staining, as well as T cell and macrophage staining. Serial blood samples were analyzed by ELISA for serum MIF levels. Immunohistochemistry and in situ hybridization performed in 15 skin and 19 colonic biopsies from 17 patients who developed moderate to severe aGVHD showed a significant increase in MIF mRNA and protein expression compared with normal controls (seven skin and five colonic biopsies). MIF was localized within the epidermis and the vascular area of skin, but diffusely expressed in the entire thickness of colon. Macrophage and T lymphocyte infiltration was confined to areas of strong MIF expression. Serial analysis by ELISA showed that only patients who developed aGVHD (n = 19) exhibited an increase (two- to three-fold) in serum MIF during HSCT, but not in the allogeneic HSCT recipients without aGVHD (n = 7) or those who received autologous HSCT (n = 8). In 14 out of 19 patients, serum MIF peaked before the onset of aGVHD. Local and systemic up-regulation of MIF expression is associated with the occurrence of acute GVHD. Its pathogenetic role remains to be further determined.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/bmten_HK
dc.relation.ispartofBone Marrow Transplantationen_HK
dc.subjectAcute GVHDen_HK
dc.subjectAllogeneic stem cell transplantationen_HK
dc.subjectMIFen_HK
dc.titleMacrophage migratory inhibitory factor (MIF) expression in acute graft-versus-host disease (GVHD) in allogeneic hemopoietic stem cell transplant recipientsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0268-3369&volume=30&issue=6&spage=375&epage=80&date=2002&atitle=Macrophage+migratory+inhibitory+factor+(MIF)+expression+in+acute+graft-versus-host+disease+(GVHD)+in+allogeneic+hemopoietic+stem+cell+transplant+recipientsen_HK
dc.identifier.emailLeung, AYH:ayhleung@hku.hken_HK
dc.identifier.emailLiang, R:rliang@hku.hken_HK
dc.identifier.authorityLeung, AYH=rp00265en_HK
dc.identifier.authorityLiang, R=rp00345en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/sj.bmt.1703639en_HK
dc.identifier.scopuseid_2-s2.0-0036750609en_HK
dc.identifier.hkuros78427en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036750609&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume30en_HK
dc.identifier.issue6en_HK
dc.identifier.spage375en_HK
dc.identifier.epage380en_HK
dc.identifier.isiWOS:000178545700007-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLo, JWS=7201650905en_HK
dc.identifier.scopusauthoridLeung, AYH=7403012668en_HK
dc.identifier.scopusauthoridHuang, XR=7410248090en_HK
dc.identifier.scopusauthoridLie, AKW=24284842400en_HK
dc.identifier.scopusauthoridMetz, C=7102876220en_HK
dc.identifier.scopusauthoridBucala, R=7102379822en_HK
dc.identifier.scopusauthoridLiang, R=26643224900en_HK
dc.identifier.scopusauthoridLan, HY=7102710832en_HK

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