Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1996-11-22
pubmed:abstractText
The IL-4R exists in two forms, either membrane bound or as a soluble (s) molecule. Since the sIL-4R binds to its ligand with high affinity, thereby acting as an immunoregulatory molecule, we were interested in the processes leading to its release. First, the release of sIL-4R in the model of murine leishmaniosis was analyzed. Infection of mice with Leishmania major resulted in up-regulation of sIL-4R production by Ag-stimulated CD4+ T cells, with a maximum around 7 days after infection. To clarify the mechanisms underlying sIL-4R release, in vitro studies were performed. After stimulation of naive lymphoid cells with IL-4, sIL-4R release was dependent on up-regulation of spliced IL-4R mRNA, as shown by inhibition with specific antisense oligonucleotides. In contrast to this, no increase in the spliced IL-4R mRNA and no inhibitory influence of antisense oligonucleotides were observed after stimulation of T cells from IL-4-deficient mice with anti-CD3 mAb. Thus, TCR stimulation can lead to IL-4-independent sIL-4R production. Under these conditions proteolytic shedding of membrane-bound IL-4R appears to be the principal mechanism of release, since in contrast to stimulation with IL-4, iodinated sIL-4R could only be immunoprecipitated after cell surface labeling and subsequent TCR stimulation. The common gamma-chain, a component of the IL-4R complex, did not appear to be involved in the pathways leading to sIL-4R expression. This analysis suggests the existence of two differentially regulated pathways of sIL-4R release, possibly having different consequences for the regulation of IL-4 bioactivity.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
157
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1846-53
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:8757301-Alternative Splicing, pubmed-meshheading:8757301-Animals, pubmed-meshheading:8757301-Antigens, CD, pubmed-meshheading:8757301-Female, pubmed-meshheading:8757301-Interleukin-4, pubmed-meshheading:8757301-Leishmaniasis, Cutaneous, pubmed-meshheading:8757301-Lymphocyte Activation, pubmed-meshheading:8757301-Mice, pubmed-meshheading:8757301-Mice, Inbred BALB C, pubmed-meshheading:8757301-Mice, Inbred C3H, pubmed-meshheading:8757301-Mice, Inbred C57BL, pubmed-meshheading:8757301-Mice, Inbred CBA, pubmed-meshheading:8757301-Mice, Inbred DBA, pubmed-meshheading:8757301-Mice, SCID, pubmed-meshheading:8757301-RNA, Messenger, pubmed-meshheading:8757301-Receptors, Interleukin, pubmed-meshheading:8757301-Receptors, Interleukin-4, pubmed-meshheading:8757301-Solubility, pubmed-meshheading:8757301-T-Lymphocytes
pubmed:year
1996
pubmed:articleTitle
Two distinct stimulus-dependent pathways lead to production of soluble murine interleukin-4 receptor.
pubmed:affiliation
Institute of Clinical Microbiology and Immunology, University of Erlangen-Nurnberg, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't