Linked Life Data

1352459

Source:http://linkedlifedata.com/resource/pubmed/id/1352459

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1992-8-7
pubmed:abstractText
Clonal deletion and anergy are two major mechanisms of self-tolerance. However, the molecular mechanisms underlying clonal deletion and anergy, as well as the threshold of TCR affinity/avidity required for these processes, are not known. Expression of the V beta 8.1 TCR correlates with the reactivity of the T cells to the minor lymphocyte stimulating locus-1a (Mls-1a) and T cells expressing this TCR are deleted in the thymus of Mls-1a mice. Similarly, in TCR V beta 8.1 transgenic mice, the number of CD4+CD8-T cells is reduced in Mls-1a mice. However, small numbers of CD4+CD8-T cells remain in the periphery of adult Mls-1a transgenic mice. We have generated T cell clones from TCR V beta 8.1 transgenic mice by stimulation of lymph node T cells with C57BL/6 alloantigens. Interestingly, CD4+CD8-V beta 8.1+ clones isolated from the transgenic mice of Mls-1a background responded to the self-antigen Mls-1a, to which they did not respond in primary assay. Reactive patterns of the clones were compared with clones derived from Mls-1b mice. Proliferation and cytokine production of the clones from Mls-1a mice to the self-antigen Mls-1a were generally reduced when compared with clones from Mls-1b mice. More importantly, T cell clones from Mls-1a mice required more Mls-1a antigen for their activation, and were more susceptible to the inhibitory effects of anti-CD4 antibody on the proliferative responses to Mls-1a than those from Mls-1b mice. These results suggest that the T cell receptor on clones derived from Mls-1a mice have functional but reduced affinity/avidity for self-antigen Mls-1a.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0953-8178
pubmed:author
pubmed:issnType
Print
pubmed:volume
4
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
125-33
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:1352459-Animals, pubmed-meshheading:1352459-Antigens, CD2, pubmed-meshheading:1352459-Antigens, CD4, pubmed-meshheading:1352459-Antigens, Differentiation, T-Lymphocyte, pubmed-meshheading:1352459-Autoimmunity, pubmed-meshheading:1352459-CD4-Positive T-Lymphocytes, pubmed-meshheading:1352459-Clone Cells, pubmed-meshheading:1352459-Flow Cytometry, pubmed-meshheading:1352459-Interleukins, pubmed-meshheading:1352459-Isoantigens, pubmed-meshheading:1352459-Lymphocyte Activation, pubmed-meshheading:1352459-Lymphocyte Function-Associated Antigen-1, pubmed-meshheading:1352459-Mice, pubmed-meshheading:1352459-Mice, Inbred Strains, pubmed-meshheading:1352459-Mice, Transgenic, pubmed-meshheading:1352459-Minor Lymphocyte Stimulatory Antigens, pubmed-meshheading:1352459-Minor Lymphocyte Stimulatory Loci, pubmed-meshheading:1352459-Receptors, Antigen, T-Cell, alpha-beta, pubmed-meshheading:1352459-Receptors, Immunologic
pubmed:year
1992
pubmed:articleTitle
Response of V beta 8.1+ T cell clones to self Mls-1a: implications for the origin of autoreactive T cells.
pubmed:affiliation
Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia 19104-6082.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't