Linked Life Data

1671403

Source:http://linkedlifedata.com/resource/pubmed/id/1671403

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1991-3-8
pubmed:abstractText
The CD45 Ag family is comprised of at least five isoforms generated by the alternative splicing of three exons encoded by a single leukocyte common Ag gene. These isoforms, differentially expressed on subsets of T cells, are widely believed to delineate maturational status. Thus, cells expressing the high molecular mass CD45RA+ isoforms (220 and 205 kDa) are believed to represent naive cells, whereas those lacking CD45RA and expressing high density CD45RO (180 kDa) represent memory cells. This is based on findings that after activation, CD45RA+ cells "convert" to the CD45RA- phenotype, losing CD45RA and gaining CD45RO. This conversion is believed to be both unidirectional and irreversible. We now report a strategy for the development of polyclonal CD45RA+ cell lines derived from peripheral blood CD4+CD45RA+ cells. However, in such cell lines, CD45RA expression was not constant, but varied cyclically with restimulation. After restimulation, CD45RA expression decreased significantly, nadiring on days 5 to 7. However, CD45RA was fully re-expressed by days 14 to 16. These cells coexpressed high density CD45RO, which did not vary through the stimulatory cycle. Cells sorted CD45RA- on day 7 of the cycle rapidly reexpress CD45RA. Metabolic labeling revealed that the 220 kDa CD45RA isoform is no longer synthesized. Synthesis of the 205 kDa (CD45RA) isoform decreased significantly early after stimulation, but then increased back to baseline after day 12. The 180-kDa (CD45RO) isoform followed an opposite pattern. Our results document that alternative splicing of the different CD45 isoforms is highly regulated after activation and that conversion from CD45RA+ to CD45RA- is neither unidirectional, nor irreversible.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
146
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1175-83
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:1671403-Antibodies, Monoclonal, pubmed-meshheading:1671403-Antigens, CD, pubmed-meshheading:1671403-Antigens, CD2, pubmed-meshheading:1671403-Antigens, CD3, pubmed-meshheading:1671403-Antigens, CD45, pubmed-meshheading:1671403-Antigens, Differentiation, pubmed-meshheading:1671403-Antigens, Differentiation, T-Lymphocyte, pubmed-meshheading:1671403-Blotting, Southern, pubmed-meshheading:1671403-Cell Cycle, pubmed-meshheading:1671403-Cell Line, pubmed-meshheading:1671403-Concanavalin A, pubmed-meshheading:1671403-Flow Cytometry, pubmed-meshheading:1671403-Gene Expression Regulation, pubmed-meshheading:1671403-Gene Rearrangement, beta-Chain T-Cell Antigen Receptor, pubmed-meshheading:1671403-Histocompatibility Antigens, pubmed-meshheading:1671403-Humans, pubmed-meshheading:1671403-Lymphocyte Activation, pubmed-meshheading:1671403-Molecular Weight, pubmed-meshheading:1671403-Receptors, Antigen, T-Cell, pubmed-meshheading:1671403-Receptors, Immunologic, pubmed-meshheading:1671403-T-Lymphocyte Subsets, pubmed-meshheading:1671403-Time Factors
pubmed:year
1991
pubmed:articleTitle
Cyclic regulation of CD45 isoform expression in a long term human CD4+CD45RA+ T cell line.
pubmed:affiliation
Division of Tumor Immunology, Dana Farber Cancer Institute, Harvard Medical School Boston, MA 02115.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.