Linked Life Data

16869802

Source:http://linkedlifedata.com/resource/pubmed/id/16869802

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2006-8-25
pubmed:abstractText
One of the defining lesions of kidney allograft rejection is epithelial deterioration and invasion by inflammatory cells (tubulitis). We examined epithelial changes and their relationship to effector T cells and to CD103/E-cadherin interactions in mouse kidney allografts. Rejecting allografts showed interstitial mononuclear infiltration from day 5. Loss of epithelial mass, estimated by tubular surface area, and tubulitis were minimal through day 7 and severe by day 21. Tubules in day 21 allografts manifested severe reduction of E-cadherin and Ksp-cadherin by immunostaining with redistribution to the apical membrane, indicating loss of polarity. By flow cytometry T cells isolated from allografts were 25% CD103+. Laser capture microdissection and RT-PCR showed increased CD103 mRNA in the interstitium and tubules. However, allografts in hosts lacking CD103 developed tubulitis, cadherin loss, and epithelial deterioration similar to wild-type hosts. The loss of cadherins and epithelial mass was also independent of perforin and granzymes A and B. Thus rejection is characterized by severe tubular deterioration associated with CD103+ T cells but not mediated by CD103/cadherin interactions or granzyme-perforin cytotoxic mechanisms. We suggest that alloimmune effector T cells mediate epithelial injury by contact-independent mechanisms related to delayed type hypersensitivity, followed by invasion of the altered epithelium to produce tubulitis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1600-6135
pubmed:author
pubmed:issnType
Print
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2109-20
pubmed:dateRevised
2007-2-14
pubmed:meshHeading
pubmed-meshheading:16869802-Animals, pubmed-meshheading:16869802-Antigens, CD, pubmed-meshheading:16869802-Epithelial Cells, pubmed-meshheading:16869802-Graft Rejection, pubmed-meshheading:16869802-Granzymes, pubmed-meshheading:16869802-Immunoenzyme Techniques, pubmed-meshheading:16869802-Integrin alpha Chains, pubmed-meshheading:16869802-Kidney Transplantation, pubmed-meshheading:16869802-Kidney Tubules, pubmed-meshheading:16869802-Male, pubmed-meshheading:16869802-Membrane Proteins, pubmed-meshheading:16869802-Mice, pubmed-meshheading:16869802-Mice, Inbred C57BL, pubmed-meshheading:16869802-Mice, Inbred CBA, pubmed-meshheading:16869802-Mice, Knockout, pubmed-meshheading:16869802-Nephritis, pubmed-meshheading:16869802-Pore Forming Cytotoxic Proteins, pubmed-meshheading:16869802-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:16869802-Serine Endopeptidases, pubmed-meshheading:16869802-T-Lymphocytes, pubmed-meshheading:16869802-Transplantation, Homologous
pubmed:year
2006
pubmed:articleTitle
Tubulitis and epithelial cell alterations in mouse kidney transplant rejection are independent of CD103, perforin or granzymes A/B.
pubmed:affiliation
Department of Medicine, Division of Nephrology and Transplantation Immunology, University of Alberta, Edmonton, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't