Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1991-8-19
pubmed:abstractText
We investigated the clearance kinetics and tissue distribution of different sized IgA in normal and macrophage-depleted rats. Rats were injected iv with liposomes containing dichloromethylene diphosphonate (DMDP). DMDP treatment resulted in complete depletion of liver macrophages 24-48 h after administration. Normal and macrophage depleted rats were injected intravenously with monomeric, dimeric, polymeric or aggregated polymeric IgA (AIgA) and assessed for blood clearance and tissue distribution. In normal rats, clearance of IgA was size dependent, i.e. a faster clearance with increasing size. No differences in clearance kinetics were observed of the different sized IgA between normal and DMDP-treated rats. TCA non-precipitable radioactivity, a measure for degradation of IgA, was found in the circulation of normal and DMDP-treated rats after AIgA administration. The liver was the main organ responsible for the clearance of IgA in normal and DMDP-treated rats. Immunofluorescence studies on liver biopsies indicated that AIgA was associated with Kupffer cells in normal rats. Electron microscopical studies revealed that the AIgA was internalized and located in vesicles in Kupffer cells. In DMDP-treated rats the AIgA was associated with endothelial cells and electron microscopy studies showed that this AIgA was taken up by endothelial cells. These data show that rat liver endothelial cells are able to bind, internalize and degrade AIgA in situations where Kupffer cells are absent, and that these cells may play an important role in the handling of AIgA and IgA-immune complexes.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/1829990-2141546, http://linkedlifedata.com/resource/pubmed/commentcorrection/1829990-2192437, http://linkedlifedata.com/resource/pubmed/commentcorrection/1829990-2454258, http://linkedlifedata.com/resource/pubmed/commentcorrection/1829990-2473956, http://linkedlifedata.com/resource/pubmed/commentcorrection/1829990-2530286, http://linkedlifedata.com/resource/pubmed/commentcorrection/1829990-2644483, http://linkedlifedata.com/resource/pubmed/commentcorrection/1829990-2651270, http://linkedlifedata.com/resource/pubmed/commentcorrection/1829990-2723442, http://linkedlifedata.com/resource/pubmed/commentcorrection/1829990-2770118, http://linkedlifedata.com/resource/pubmed/commentcorrection/1829990-2796287, http://linkedlifedata.com/resource/pubmed/commentcorrection/1829990-2816927, http://linkedlifedata.com/resource/pubmed/commentcorrection/1829990-3308622, http://linkedlifedata.com/resource/pubmed/commentcorrection/1829990-3329736, http://linkedlifedata.com/resource/pubmed/commentcorrection/1829990-3518044, http://linkedlifedata.com/resource/pubmed/commentcorrection/1829990-3518747, http://linkedlifedata.com/resource/pubmed/commentcorrection/1829990-3576132, http://linkedlifedata.com/resource/pubmed/commentcorrection/1829990-3704558, http://linkedlifedata.com/resource/pubmed/commentcorrection/1829990-3882559, http://linkedlifedata.com/resource/pubmed/commentcorrection/1829990-4018843, http://linkedlifedata.com/resource/pubmed/commentcorrection/1829990-6219575, http://linkedlifedata.com/resource/pubmed/commentcorrection/1829990-6388998, http://linkedlifedata.com/resource/pubmed/commentcorrection/1829990-6436366, http://linkedlifedata.com/resource/pubmed/commentcorrection/1829990-6715019, http://linkedlifedata.com/resource/pubmed/commentcorrection/1829990-6736868, http://linkedlifedata.com/resource/pubmed/commentcorrection/1829990-6781799, http://linkedlifedata.com/resource/pubmed/commentcorrection/1829990-7076275, http://linkedlifedata.com/resource/pubmed/commentcorrection/1829990-7286581, http://linkedlifedata.com/resource/pubmed/commentcorrection/1829990-915301
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0009-9104
pubmed:author
pubmed:issnType
Print
pubmed:volume
85
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
128-36
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Kupffer cell depletion in vivo results in clearance of large-sized IgA aggregates in rats by liver endothelial cells.
pubmed:affiliation
Department of Nephrology, University Hospital Leiden, The Netherlands.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't